Pathoma COPD

Question 1

COPD conditions involve what general principle?

Answer 1

Can’t get air out of the lungs

Question 2

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

Answer 2

FVC. FVC is decreased.

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

Question 3

FVC?

Answer 3

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

Question 4

FEV1?

Answer 4

Amount of air expired in 1 second maximally.

Question 5

Relationship between FEV1 and FVC with airway obstruction

Answer 5

Decrease your FEV1:FVC ratio because FEV1 is more affected

Question 6

What value increases with airway obstruction?

Answer 6

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

Question 7

TLC?

Answer 7

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

Question 8

Chronic Bronchitis is defined exactly in what ways

Answer 8

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

Question 9

Patient complaint related to chronic bronchitis?

Answer 9

“Coughing up buckets of mucus”

Question 10

Cause of chronic bronchitis?

Answer 10

Smoking

Question 11

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

What is in them?

Answer 11

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

Question 12

Mucinous glands take up ____% of the wall

Answer 12

40%

Question 13

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

Answer 13

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

Question 14

What is the Reid index

Answer 14

Measure of wall thickness in regards to the mucinous glands

Question 15

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

Answer 15

More than 50%

Question 16

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

Answer 16

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

Question 17

Clinical features of Chronic Bronchitis?

Answer 17

Productive cough, cyanosis, increased PaCO2 and decreased PaO2.

Increased risk of infection and cor pulmonale

Question 18

Emphysema

Answer 18

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

Question 19

What really causes emphysema?

Answer 19

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.

Question 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.

Answer 20

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

Question 21

Centriacinar emphysema

Answer 21

Hitting the central portion of the acinus.

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

Question 22

What is the acinus?

Answer 22

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

Question 23

What is panacinar emphysema?

Answer 23

Full acinus emphysema which we see in A1AT emphysema

Question 24

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

Answer 24

Upper

Question 25

What other condition do we see with A1AT deficiency?

Answer 25

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

Question 26

A1AT gene comes in multiple alleles. What are they?

Answer 26

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

Question 27

PiMZ (heterozygotes) present how?

Answer 27

Uusually asymptomatic with decreased circulating llevels of A1AT. Significant risk for emphysema with smoking

Question 28

PiZZ (homozygous) presents how?

Answer 28

Panacinar emphysema with cirrhosis

Question 29

Clinical features of emphysema

Answer 29

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

Question 30

Late complications of emphysema?

Answer 30

Hypoxemia | Cor pulmonale

Question 31

What is asthma?

Answer 31

Reversible airway bronchoconstriction

Question 32

Asthma most often due to what?

Answer 32

Allergic reaction with Type I hypersentitivity

Question 33

Presentation of asthma

Answer 33

Allergic rhinits Eczema Family history of atopy

Question 34

Pathogenesis of Asthma

Answer 34

1. Allergens induce TH2 phenotype in CD4+ T cells of genetically suceptible individuals 2. TH2 cells secrete IL-4, IL-5, and IL-10

Question 35

IL-4 does what?

Answer 35

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

Question 36

IL-5?

Answer 36

Calls in eosinophils

Question 37

IL-10?

Answer 37

Inhibits TH1 and boosts TH2

Question 38

Re-exposure to allergen involved with asthma?

Answer 38

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

Question 39

Presentation of asthma

Answer 39

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)

Question 40

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

Answer 40

Aspirin (called asthma intolerant asthma)

Question 41

Bronchiectasis

Answer 41

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

Question 42

Causes of bronchiectasis

Answer 42

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

Question 43

Common diseases that can cause bronchiectasis

Answer 43

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

Question 44

What is allergic bronchopulmonary aspergillosis? Who gets it? What does it lead to?

Answer 44

Allergic reaction to aspergillis seen in two types of patients 1. asthma 2. CF patients Leads to bronchiectasis!

Question 45

Clinical features of Bronchiectasis?

Answer 45

Cough, dyspnea, foul smelling sputum

Question 46

Complications of bronchiectasis?

Answer 46

Complications include hypoxemia with cor pulmonale and secondary amyloidosis

Question 47

Amyloidosis

Answer 47

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