Procedimiento

In obstructive lung dz, no prob getting air in, but have a problem in getting the air out. Why don’t you have a problem getting it in? B/c the elastic tissue support is destroyed, so it is very ez to fill up the lungs. However, b/c the elastic tissue support is destroyed, it is very difficult hard to get it out b/c it collapses on expiration, so you can get air in, but cannot get air out. In a pt with obstructive air dz, they breathe in with no

problem, but have trouble getting it out. So, something is left over in the lung – cannot get all the air out, therefore the residual volume is increased (whenever something is left over, it is called the ‘residual’). So, if you cannot get air out, then the residual volume increases, which means that the TLC will increase, which means that the diaphragm will go down b/c as the lungs are over inflated, and the AP diameter will go out. So, with obstructive lung dz, you have increased AP diameter and diaphragms go down (depressed). There is only a certain amount of expansion your chest can go. Eventually, the chest starts to compress other volumes (as you trap air and residual volumes go up). So, tidal volume starts decreasing, vital capacity goes down b/c the residual vol is increasing and you are

compressing other volumes. So, TLC and RV increases, everything else decreases.

On spirometer, FEV1 is very low (usually 1 – normally it is 4). In other words, you have a better FEV1 with restrictive lung dz b/c you can get air in. The FVC (total amt they can get out) is 3 liters (vs. 5 liters). When you do a ratio of FEV1/FVC, the ratio has

decreased, hence distinguishing restrictive from obstructive dz’s.

Classic COPD x-ray: hard to see the heart, with depressed diaphragms (at level of umbilicus), increased AP diameter – dx? Classic obstructive dz x-ray – prob getting air out, therefore the diaphragm is down and AP diameter is increased. Example: 3 month old can have this same finding due to RSV

Example: Newborn with Chlamydia trachomatis pneumonia b/c he is trapping air.

B. There are 4 type of obstructive lung dz’s: chronic bronchitis, bronchiectasis, emphysema, asthma. The ones associated with smoking are bronchitis and emphysema.

1. Chronic Bronchitis

Purely a clinical dx = Pt has productive cough for 3 months out of the year for 2 consecutive years. Where is the dz? Terminal bronchioles (you have main stem bronchus, segmental bronchi, terminal bronchioles, resp bronchioles, alveolar ducts,

alveoli). As soon as you hit the terminal bronchioles, these are small airway; it is all turbulent air up to terminal bronchioles. After that, it is parallel branching of the airways. The turbulent air hits the terminal bronchioles and then hits a massive cross sectional airway where you can go diff path’s b/c parallel branching of the small airways.

So, the airflow changes from turbulent to laminar airflow. By the time you hit the resp unit, it is not moving the air. Most small airway dz’s are inflammation of the terminal bronchioles, leads to wheeze. Terminal bronchioles are the site of chronic bronchitis. This is the same area as asthma and bronchiolitis. More prox to the terminal bronchioles, in bronchitis, you will get a mucus gland hyperplasia, and a lot of crap is coming up (that’s the productive part). The actual area of obstruction is the terminal bronchiole. Have goblet cell metaplasia and mucous plugs. Think about having one terminal bronchiole and one mucous plug – this is affecting a major cross sectional area of lung b/c all the parallel branches that derive from here will not have CO2 in them, and they are trying to get air past the mucous plug, but cannot. So, there is a HUGE vent-perfusion mismatch. This is why they are called blue boaters – they are

cyanotic. They have mucous plugs in the terminal bronchioles and cannot rid CO2.

2. Emphysema

Not in the terminal bronchioles. It is in the resp unit (resp unit is where gas exchange occurs – cannot exchange gas in the terminal bronchioles – aka nonresp bronchiole); it is the primary place for expiratory wheeze and small airway dz, however.

Gas exchange occurs in the resp bronchiole, resp alveolar duct and alveoli.

Only need to know 2 emphysemas: centrolobular and panacinar. Emphysema affects gas exchange and where it affects the airway is more distal, compared to chronic bronchitis (proximal). So, when you have emphysema with all the inflammation

associated with it, not only destroy the resp unit, but also the vasculature associated with it. Therefore, there is an even loss of ventilation and perfusion. So, will NOT have retention of CO2 in these pts. When you have a problem with a mucous plug in the terminal bronchiole, which is way more prox and a great cross sectional area of the lung is affected, there is gonna be a problem there; however when you are out this far (in emphysema) and also destroying the vessels, you will not have an increase in CO2. This is why they are called pink puffers, and this is why many of them have resp alkalosis.

a) Centrolobular – most associated with smoking and involved with the upper lobes. So, it is an upper lobe emphysema, and the primary portion of the resp unit that is destroyed is the resp bronchiole (this is the very first thing that smoke hits). Neutrophils will damage it b/c all people that smoke have more neutrophils in their lungs, and smoke is chemotactic for neutrophils. ALL smokers have increased neutrophils in their lungs. What does alpha-1 antitrypsin do? It’s an antielastase (its only purpose is to destroy elastases produced by neutrophils – that is its function. If you are a smoker, that is denatured. So, you also have an acquired alpha-1 antitrypsin def). Don’t have adequate alpha-1 antitrypsin, and have too many neutrophils in the lungs. This is a terrible combo. This why neutrophils have no problem in destroying the elastic tissue support of the respiratory bronchioles.

So, you breath air in, which is no problem; but you try to get it out, and there is no elastic tissue support and leads to lung expansion – this is why blebs are found – there are big cystic spaces in the lung – it has trapped air in there b/c there is no

elastic tissue, so when it tries to get by, it just expands. This is centrolobular emphysema of the UPPER lobes.

b) Panacinar Emphysema (remember ‘pan’ means everything – ie in pancytopenia, ALL the cells decreased). So, panacinar means that the ENTIRE resp unit is decreased b/c it is associated with NO alpha 1 antitrypsin. This is a genetic dz – auto rec – the LIVER does not make it. So, at a young age, you develop destruction of entire resp unit of the LOWER lobes, so this is a LOWER lobe emphysema. So, you can see that the resp bronchioles are knocked out, the alveolar ducts are knocked out, alveoli

knocked out. So, you breathe in, and this entire resp unit catches it – this is in the lower lobes.

Smokers, which have an acquired alpha-1 antitrypsin def, can get an element of panacinar emphysema in the lower lobes, too. So, smokers can get 2 emphysema’s:

centrolobular emphysema in the upper lobes (which knocks off the resp bronchiole) and in the lower lobes, get a panacinar type of pattern. Therefore, can get upper AND lower lobe emphysema, and 2 diff types of emphysema.

3. Bronchiectasis

Have bronchiectasis – see bronchi going out to the pleura (abnormal). When you see bronchi going out further than the hilum, this is bronchiectasis.

Mech: infection, destruction of the elastic tissue support, dilatation of the airways. Segmental bronchi; fill with pus. Example: pt has a productive cough of

“cupfuls” (not just a tablespoon) of pus, b/c they are trapped.

a) Causes:

1) MCC bronchiectasis in USA = cystic fibrosis. If parent with child has cystic fibrosis, will see huge pus coming out of bronchi, a couple times per day.

2) MCC bronchiectasis in 3^rd world countries = TB.

3) Kartagener’s syndrome (aka immotile cilia syndrome). 9+2 configuration arrangement with cilia and microtubules. The problem with immotile cilia syndrome is an absent dynein arm. The 9 microtubules on the outside have arms that keep them together – these dynein arms are missing. So, when these arms are missing, the cilia cannot move. So, the places with cilia not moving are affected: these places are sinuses (why sinusitis is a problem), bronchiectasis (b/c there is cilia –

psuedostratified columnar epithelium is affected), males and females are infertile (b/c the tail on the sperm cannot move – the tail is a modified cilia – they head is moving, but the tail is weak. Women are infertile; too, b/c the fallopian tube needs cilia to carry the egg down. Organs are located on the opposite side

(dextrocardia, withOUT transposition of great vessels).

4. Asthma

Can be extrinsic (type 1 HPY) and intrinsic: Involves chemicals – people in the

workplace can get triad asthma, which involves people taking NSAIDs Many people, ie athletes will get exertional asthma and wheeze – cromolyn Na is the DOC for these patients. Cold temps can cause asthma. Type I HPY has nothing to do with these causes of asthma. The wheezing is due to inflammation of the terminal bronchioles – it

is not due to smoking, but b/c factors like LT C4, D4, E4, PG’s causing inflammation and narrowing of the airways.

IX. Lung Cancer

A. Peripherally located vs. centrally located 1. Centrally located (mainstem bronchus):

Have the highest association with smoking. Include squamous cell carcinoma and small cell carcinoma. These are generally centrally located, hence mainstem bronchus types of locations. Squamous cell are more common than small cell carcinomas.

2. Peripherally located:

Adenocarcinomas (the more common primary lung cancer, more common than

squamous) are more peripheral than central. Shifted to the periphery b/c of the filters of the cigarettes. The filters prevented the large carcinogens from passing in, but the small carcinogens still passed through, and they are not trapped in the main stem, but trapped in the periphery.

There are at least 3 or 4 types of adenocarcinoma. One obviously does have a smoking relationship, while the others do not. The ones that do not have a smoking relationship include bronchiolar alveolar carcinoma, and large cell adenocarcinoma of the lung (scar cancers).

B. Cytology: know what squamous cancer looks like with a pap smear. A lot of people think that the Papanicolaou stain is only done for cervical carcinoma. This is not the case. This is a famous stain (pap smear) used for all cytological specimens on for all organs. The stain stain’s keratin bright red. Slide: (pic) pt that is a smoker with a centrally located mass. Showing sputum sample with a Papanicolaou (pap smear) stain – has red keratin, which is squamous cell carcinoma. If this were a cervical pap smear from a woman that is 40 years of age, this is squamous cell carcinoma. The keratin is staining bright red! (bright red cytoplasm = keratin = squamous cell carcinoma). Papanicolaou stains keratin bright red.

Example: small cells that look like lymphocytes – this is small cell carcinoma. This is more difficult to dx, b/c sometimes diff to tell the difference from lymphocytes. Slide shows malignant cells. Small cell carcinoma is the most malignant cancer of the lung. Rx? Radiation and chemo (not surgery). These are auput tumors with neurosecretory granules and S-100 Ag positive. They can make ADH and ACTH.

A slightly less malignant tumor with auput origin is the bronchiocarcinoid. It is a low grade malignancy of the same types of cells that produce small cell carcinoma. So, they can invade, met, and produce carcinoid syndrome if they make increased amount of serotonin. They don’t have to mets to produce carcinoid syndrome – it just goes straight into the bloodstream. It is very uncommon.

C. Cancer:

MC cancer of lung = mets – ie see many metastatic nodules all over lung; if you play odds, what is the primary cancer? breast (which the MC met to the lung, or in other words, it is the MC cancer of the lung).

Summary of lung cancer in the lung:

MC cancer = mets

MC primary cancer = primary adenocarcinoma of the lung, followed by squamous and small cell carcinoma.

Worst cancer (worst prognosis): small cell carcinoma.

Horner’s syndrome – pancoast tumor/superior sulcus tumor – tumors that are in the upper lobe posteriorly (in post mediastinum); most of the time is caused by squamous carcinoma in that area.

What’s happening here? Tumor is locally invading into the local part of the lower trunk of the brachial plexus, so can get lower trunk brachial plexus like findings, and can also affect the superior cervical ganglion. This is in the posterior mediastinum, therefore will end up with Horner’s

syndrome; as a result, will end up knocking OFF sympathetic activity – ptosis (lid is lower), anhydrous (lack of sweating), miosis (in sympathetic, which is fight or flight, normally have mydriasis, which dilates the pupil – with fight or flight, want as much light as possible, therefore dilating pupil, but this is cut off, leading to miosis). Do not confuse with SVC syndrome; this is just blocking off SVC.

Myasthenia has to do with thymoma, which is located in the anterior mediastinum.

Exudate vs. transudate (< 3 grams, without many cells in it) MCC pleural effusion due to transudate = HF

Exudate = protein > 3 grams, and has cells in it (ie pneumonia’s, pulmonary infarction)

CHAPTER 9: GI