Pathology Scribes Jan and Kristina

Pathology Scribes Jan and Kristina

1/16/01

9:00 am Dr. Jumper/ Graham

Respiratory CPC-1

-Today we are going to be doing cases on emphysema and pulmonary fibrosis. We will clarify the diseases that make holes in your lung and why they act different physiologically. This will be on the exam. Case 1 is airway disease with the prototype being asthma, and Case 2 is loss of parenchyma, which is emphysema. Starts on pg. 81 of your notes.

-Dr. Jumper showed a slide of a skinny old man. He was resting is weight on his forearms while he was sitting down, and his lips were pursed. She asked what his condition was. The answer is emphysema. If he comes to your clinic he will complain to you about having difficulty breathing. This old mans problem could have been going on for years. Although if you ask this patient about any pain 2 months prior to seeing you he would say that he didn’t have any. Not because the pain or difficulty breathing was not there, but rather the man probably stopped any kind of exertion that caused him the pain and shortness of breath. Emphysema is a progressive disease so ask them what made them finally come to the clinic. These patients are usually middle-aged to elderly, male or female, have chronic progressive shortness of breath.

-So, if you put your stethoscope on this patient’s chest what will you hear? Probably crackles and wheezing. Also, you don’t really hear any air come out when they take a breath for you. They generally have an increased anterior/ posterior ration (AP ratio) and will present very barrel-chested. This is due to gas trapping. When they breath in they are fine (negative pressure during this process), however, when they breath out the positive pressure causes their airways to close off and they get air trapped in their lungs. This gas trapping pushes their diaphragm down, and over years their chest wall remodels due to the pressure from having huge lungs. This guy is a big bag of air, and can float if you put him in water.

-What do you think this guy’s appetite is like? Well, he gets hungry, but there is no way he could hang with Jan-jan at Hong Kong Super Buffet. He doesn’t really have room for that due to his depressed diaphragm so he will have to settle for drinking Ensure. He probably can’t eat three meals a day, so part of the treatment for a patient with emphysema is putting them on a schedule where they eat six times a day. Another reason why these patients are thin is the lack of gas exchange when they breath in and out. It is inefficient.

-In a physical exam you will see little air movement, when you percuss down his back you will feel huge lungs. Also, you can palpate their liver pretty easily due to the fact that it is pushed down. These patients use their accessory respiratory muscles readily in order to breath. “These guys don’t like to use their arms.”

-There was a question, but I could not hear what it was. The answer was “ Yes, COPD which emphysema is a part of can lead to chronic right heart failure which causes anatomy to back up on the right side and will get backed up to the liver. That is how they can get liver disease. Then she moved on to the respiratory equipment, but we won’t be tested on this stuff.

-Dr. Jumper began discussing test standards that you compare your data with. Race, age, sex, ect… Then she showed a slide of some data gathered from a patient who did pulmonary function testing. A 40 year old male, 6’ 7”, 200 lbs. She did a flow volume rate on him. He took a big breath in blew it out hard and fast. He got out the majority of the volume out in the first second. There are three numbers that you will focus on. His forced vital capacity which was 6.39 L, the standard was 6.16 L. This patient was above 100%, therefor, this patient is not obstructed. In order to be obstructed you have to have a decreased FEV1 when compared to an FEC. This is pretty normal.

-Then Dr. Jumper showed a slide of what someone with emphysema would look like on these tests. His FVC (forced vital capacity) was 2.56 where predicted was 3.87 L. His predicted is low. This individual could breath out for a long time so you would have to cut him off at some point. With a normal person it would be difficult to breath out for 5-6 seconds unless you breath out slowly. FEV1 is 1.34 and predicted is 2.99 L. He only blew out 30% of what you should be able to do. This man is obstructed. Just by knowing that this individual is obstructed you can not tell which disease he has, whether it’s emphysema, chronic bronchitis ect… These patients get very little volume out per time compared to a normal person.

-Dr. Jumper then asked how could someone tell a severe asthmatic from someone with emphysema. You look at their diffusion capacity. In someone with emphysema the diffusion capacity is going to be low. That is due to loss of the interstitial space and increased alveolar space. A person with asthma will have a normal diffusion capacity.

-Dr. Graham began her slide show at this time. She began by stating that right heart failure occurs earlier in chronic bronchitis than emphysema. This is due to reaching a chronic hypoxic state in chronic bronchitis and their ventilation perfusion mismatch. There was some question at this time from one of the students, but I couldn’t make it out. The answer was that you have to remember that chronic bronchitis is purely an airway disorder whereas emphysema also deals with loss of the lung parenchyma.

-They described a person with emphysema as a pink puffer and someone with chronic bronchitis as a blue bloater. These terms are used by Netter’s to describe the physical characteristics of the two diseases we discussed today. At this point Dr. Graham stated that a smoker who comes in with these respiratory problems does not come in with just one of these problems, but rather a mixture of both.

-Dr. Graham showed a picture of centrilobular emphysema, the most common type. Centrilobular emphysema is the dilation of the respiratory bronchioles, and it is most often localized to the upper part of the pulmonary lobes. Then she showed a cross section of a lung floated in water. The lung is holy and dishrag or jellyfish like. Anything that is considered holy, floppy, and dishrag-like is emphysema. Now if it was a holy, and hard it is fibrotic.

-Dr. Graham showed a high power gross picture of centrilobular emphysema. This has pretty normal parenchyma with small alveolar sacks. The primary site of injury in central lobular emphysema is the respiratory bronchiole.

-She showed a high power view of a panacinar (acinar and lobule mean the same thing) emphysema. Panacinar emphysema is dilation of the entire acinus, including the alveoli, alveolar ducts, respiratory bronchioles, and terminal bronchioles. It is generally distributed evenly through the entire lung. You have a loss of elasticity that is associated with a deficiency in alpha-1 antitrypsin. Have a fairly holy lung with the entire lobule being involved. This is alpha-1 antitrypsin deficiency. Dr. Graham then stated that people who seem to get emphysema early have a heterozygous pattern for alpha-1 antitrypsin expression. If you are heterozygous for alpha-1 antitrypsin and don’t smoke you can live a normal life. The smoking is what gets these people.

-Dr. Graham wants us to know that emphysema is not a fibrosing disease. There is only a minimal bit of scarring, it is more of a loss of parenchyma.

-At this point in the lecture Dr. Jumper came back to the podium and showed a flow volume loop. Volume is the y-axis and flow is the x-axis. And yet another question from a student. I couldn’t hear that either, but I think he asked something about treatment of emphysema. Dr. Jumper stated that you really can’t do much to treat it. And now another question from a student, something about COPD. Dr. Jumpers answer is that COPD has big vital capacity, big residual volume, big total lung capacity.

-Dr. Jumper showed a picture of a normal chest X-ray. The diaphragm is nice and curved. Heart is normal, and has space between the ribs. Now a person with COPD, emphysema, will have to bring four X-rays because they can’t get it all on one. They have huge lungs, skinny heart, stomach pushed down, gas trapping. When you listen to the lungs you don’t hear anything.

-Dr. Jumper starts talking about bolus lung disease, something bigger than 2cm, holes everywhere. I’m thinking this isn’t that important.

-Dr. Jumper goes to #5 on page 82. She discusses the differential Dx. She shows a slide of a pulmonary abscess. See a lot of abscesses in drunks because they aspirate a bunch of anaerobic stuff into their lungs.

-She showed a slide of an old scar that is now filled with aspirgillus (aspirgiloma). She will now show the last few slides. Another slide of bolus lung disease which is a disease with holes in the lungs that are greater than 2cm. Mostly in the upper pulmonary lobes.

-Dr. Graham begins to talk about scar emphysema. See this in the ICU and autopsies where people have been on a ventilator.This is the end of the first hour of the CPC.

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