Path- Pulmonary System

Front 1

Where is cartilage present in the respiratory tree?

Back 1

Present only in the trachea and bronchi.

Front 2

What type of muscle do the walls of conducting airways contain?

Back 2

Smooth muscle.

Front 3

Describe the structures of the respiratory tree from the mouth down to the alveoli.

Back 3

Mouth and nose, pharnyx, trachea, bronchi, bronchioles, terminal bronchiole, alveoli.

Front 4

What Type of cells line alveoli and make up 97% of the alveolar surface?

Back 4

Squamous epithelium lines 97% of the alveolar surface and is optimal for gas diffusion.

Front 5

What are Type II cells? What do they secrete and what can they differentiate into? When do they proliferate most?

Back 5

Type II cells make up 3% of the alveolar surface and they secrete surfactant (dipalmitoyl phosphatidylcholine). Type II cells also serve as precursor Type I cells and other Type II cells, thus they can differentiate into both. Type II cells proliferate during lung damage

Front 6

Describe the in index of amniotic fluid indicates fetal lung maturity?

Back 6

A lecithin-to-sphingomyelin ratio of >2.0 in amniotic fluid is indicative of fetal lung maturity.

Front 7

Explain what clara cells are, where they are found in the repiratory tree, and what their job is.

Back 7

One of the main functions of Clara cells is to protect the bronchiolar epithelium. They do this by secreting Clara cell secretory protein (CCSP) and a component of the lung surfactant. They also detoxify harmful substances inhaled into the lungs. Clara cells do this using cytochrome P450 in their smooth ER. Clara cells also multiply and differentiate into ciliated cells to regenerate the bronchiolar epithelium

Front 8

Describe the gross morphology of the left and right lungs in terms of lobes and lingulas.

Back 8

The right lung has three lobes and the left lung has two lobes and a lingula.

Front 9

What does the acronym RALS mean and what is it used for?

Back 9

RALS= right anterior, left superior

This refers to the relation of the pulmonary artery to the bronchus at each lung hilus.

Front 10

Which lung is the more common site for inhaled foreign bodies and why?

Back 10

The right lung is the more common site because the main stem bronchus of the right lung is wider and more vertical than the main stem bronchus of the left lung.

Front 11

If you were to aspirate a peanut while upright, which portion of the right inferior lobe is it more likely to travel into?

Back 11

The lower portion of the right inferior lobe.

Front 12

If you were to aspirate a peanut while supine, which portion of the right inferior lobe is it more likely to travel into?

Back 12

The superior portion of the right inferior lobe.

Front 13

Name the structures that perforate the diaphragm and the vertebral levels they cross at.

Back 13

The IVC(T8), esophagus, vagus (2 trunks) (T10),
aorta, thoracic duct, and azygous vein(T12).

Front 14

Which nerves innervate the diaphragm?

Back 14

C3,4,5 keep the diaphragm alive!

Front 15

Where does pain from the diaphragm usually refer to?

Back 15

The shoulder.

Front 16

Describe the muscle(s) used during quiet inspiration.

Back 16

The diaphragm.

Front 17

Describe the muscle(s) used during quiet expiration.

Back 17

No muscles are used here. This is a passive process.

Front 18

Describe the muscle(s) used during exercise inspiration.

Back 18

External intercostals, Scalene muscles, Sternomastoids

Front 19

Describe the muscle(s) used during exercise expiration.

Back 19

Rectus abdominis, Internal and External obliques, Transversus abdominis, Internal intercostals

Front 20

Describe the physiologic jobs that surfactant does in the lungs. Which cells produce it.

Back 20

Surfactant serves to decrease alveolar Surface Tension, increase Compliance, and decrease the Work of inspiration. Surfactant is secreted by Type II pneumocytes.

Front 21

Describe is the equation that dictates collapsing pressureof alveoli? Is collapse more likely on inspiration or expiration/why?

Back 21

Collapsing pressure = 2(surface tension)/alveolar radius

Collapse is more likely to occur expiration because the radius of the alveoli decreases

Front 22

Define Residual Volume (RV). Can this volume be measured with spirometry?

Back 22

This is the amount of air in your lungs after maximal expiration. This volume CANNOT BE MEASURED with SPIROMETRY

Front 23

Define Expiratory Reserve Volume (ERV).

Back 23

This is the air that can still be breathed out after normal expiration.

Front 24

Define Tidal Volume (TV).

Back 24

This is the air that moves into the lungs with each quiet inspiration. The typical tidal volume is 500 ml.

Front 25

Define Inspiratory Reserve Volume (IRV).

Back 25

This is the air in excess of Tidal Volume that moves into the lungs upon maximal inspiration.

Front 26

Define Vital Capacity (VC).

Back 26

This is ERV + TV + IRV

Front 27

Define Functional Residual Capacity (FRC) (volume in lungs after normal inspiration).

Back 27

This is RV + ERV

Front 28

Define Inspiratory Capacity (IC).

Back 28

This is TV + IRV

Front 29

Define Total Lung Capacity (TLC).

Back 29

This is RV + ERV + TV + IRV

Front 30

Define the equation for physiological dead space.

Back 30

VD = VT x (PaCO2 - PeCO2)/ PaCO2

VD = physiological dead space = anatomical dead space of conducting airways plus functional dead space in alveoli; apex of healthy lung is the largest contributor of functional dead space (volume of air that does not take part in gas exchange)

VT = tidal volume

PaCO2 = arterial PCO2

PeCO2 = expired air PCO2

Front 31

Describe the physical properties of the physical properties of bodies structures that determine FRC.

Back 31

The elastic properties of both the chest wall and lungs determine their combined volume.

Front 32

Describe the two states that hemoglobin is found in and define the affinity for oxygen of each.

Back 32

Hemoglobin is found in the Taut (low affinity for O2) and Relaxed (high affinity for O2) states.

Front 33

Describe are the main functional differences between hemoglobin and myoglobin?

Back 33

Hemoglobin exhibits positive cooperativity and negative allostery, unlike myoglobin.

Front 34

What are the subunits of Adult hemoglobin (HbA)? Fetal hemoglobin (HbF)? Describe the main functional difference between HbA and HbF.

Back 34

Adult Hemoglobin = 2 alpha, 2 beta

Fetal Hemoglobin = 2 alpha, 2 gamma

The main functional difference between HbA and HbF is that HbF has a lower affinity for 2,3 BPG than HbA and thus has a higher affinity for O2.

Front 35

What are the conditions that shift the O2 binding curve to the right and increase HbA's O2 unloading ability. Which state (T or R) do they promote?

Back 35

Increased Cl-, H+, CO2, 2,3-BPG and temperature. These promote the T state of HbA, which leads to increased unloading.

Front 36

What form is the CO2 transported in the blood, not bound to hemoglobin, found in?

Back 36

It is found primarily in bicarbonate form.

Front 37

What form of CO2 binds RBCs? Which molecules does it bind to and where on the molecules does it bind (heme vs. globin)?

Back 37

The carbamate form of CO2 binds to amino acids in the globin chain of RBCs, at the N-terminus. It does not bind the heme.

Front 38

At which week of gestation do the alveoli develop?

Back 38

They do not form until the 24th week of gestation.

Front 39

What are the seven types of pneumonia?

Back 39

Community Acquired Typical pneumonia, Community Acquired Atypical pneumonia, Hospital Acquired Pneumonia, Aspiration Pneumonia, Necrotizing pneumonias (lung abscess), Chronic pneumonias (histoplasmosis, blastomycosis, coccidioidomycosis), Pneumonia in the immunocompromised host.

Front 40

What are the smoking related diseases?

Back 40

Obstructive: COPD (emphysema), Lung cancer

Restrictive: Desquamative Interstitial Pnuemonitis (abnormal proliferation of macrophage in the alveoli), Respiratory Bronchiolitis Interstitial Lung Disease.

Front 41

What is the tonicity of the solution produced in the secretory coil down in the base of a sweat gland? Describe what happens to the secretions as they exit the gland in a normal person. In a patient with CF?

Back 41

The normal sweat gland produces an isotonic solution relative to blood in the secretory coil. As the secretions make their way out of the gland Na+ and Cl- are normally reabsorbed in the ducts to make hypotonic them hypotonic. In a patient with CF there is a defect in the CFTR channels and chloride can not be reabsorbed so their secretions have a high salt content.

Front 42

How does the sweat test for CF patients work? How much sweat is collected over what period of time? What is a common salt concentration for patients with CF?

Back 42

It uses pilocarpine and iontophoresis to cause the patient to produce sweat. The sweat is then tested for its Na+ and Cl- levels. Ideally, 75mg of sweat is collected over 30min. A common salt level for CF patients is >60mmol/L.

Front 43

What is the most common fatal autosomal recessive disease in Caucasians?

Back 43

Cystic fibrosis.

Front 44

What are some key GI and Nutritional abnormalities found in children with CF?

Back 44

Meconium ileus, Pancreatic insufficiency, Focal biliary or Multilobular Cirhosis, Failure to thrive

Front 45

What reproductive problems exist for male patients with cystic fibrosis? What about female patients?

Back 45

Almost all male patients are infertile due to obstruction of the vas deferens. Females are not completely infertile but may have a very hard time becoming pregnant due to thickened mucous secretions in the vagina.

Front 46

Describe some of the phenotypic features of the airways in a patient with CF.

Back 46

There is commonly persistent infection with particular pathogens such as pseudomonas aeruginosa, chronic cough and sputum production, persistent chest radiograph abnormalities, airway OBSTRUCTION manifested by wheezing and/or air trapping, nasal polyps or imaging evidence of sinusitis, and digital clubbing.

Front 47

Explain why Na+ not reabsorbed in the ducts of sweat glands in patients with CF.

Back 47

Na+ is not reabsorbed because there is an excess of Cl- in the lumen creating a negative charge that the Na+ cannot move against. There is excess Cl- because the CFTR channel is not functional and will not allow the reabsorption of Cl- in the ducts of sweat glands like it normally would.

Front 48

How many classes of mutations of the CFTR channels are there?

Back 48

There are 6 classes of mutations.

Front 49

Name the most common gene mutation in the CFTR gene.

Back 49

The most common gene mutation is deltaF508.

Front 50

What is a normal O2 saturation for and infant?

Back 50

95-100%.

Front 51

What is the most common cause of bronchiolitis in infants? What are other common causes?

Back 51

RSV- respiratory syncitial virus. Other common causes are Influenza, Parainfluenza, and Adenovirus.

Front 52

Describe the pathophysiology of bronchiolitis.

Back 52

In bronchiolitis there is necrosis of epithelium, accumulation of cellular debris in bronchioles, and OBSTRUCTION which lead to higher lung volumes. This leads to abnormal lung mechanics with increased work of breathing (W.O.B) and hypoxemia from V/Q mismatch due to obstructed small airways.

Front 53

Name the five causes of hypoxemia.

Back 53

V/Q mismatch, shunt, diffusion abnormality, hypoventillation, abnormal hemoglobin

Front 54

Explain what leads to the pathology of Respiratory Distress Syndrome in infants.

Back 54

Lack of alveoli, Collapsed airspaces due to decreased surfactant, and increased epithelial permeability which allows protein and other fluid into airspaces. Thus there is a V/Q mismatch that produces hypoxia and hypercarbia. Because the alveoli cannot open due to lack of surfactant the lungs are rendered poorly compliant and this is seen as a "restrictive" physiology.

Front 55

What is the definition of Bronchopulmonary dysplasia (chonic pulmonary disease of infancy)?

Back 55

If an infant with RDS is still on ventillation after six weeks of therapy.

Front 56

What is the histological picture of the bronchioles and alveoli in and infant with Broncho Pulmonary Dysplasia? Is the disease focal or diffuse in the lungs?

Back 56

The bronchioles may show mild metaplasia or complete obliteration. The alveoli can be dysplastic and fibrotic, or emphysematous. Generally the lesions are focal as opposed to diffuse in the lung.

Front 57

Is Broncho pulmonary dysplasia (BPD) treatable?

Back 57

Yes, this disease is very treatable and often has favorable outcomes over 2-5 years.

Front 58

Is BPD an obstructive or restrictive disease? What is the main treatment?

Back 58

BPD is an obstructive disease. The main treatment is prolonged supplemental oxygen. Prognosis is good and with adequate nutrition you will see growth and without significant respiratory infections.

Front 59

Explain what a pulmonary sequestration is.

Back 59

This is non-functioning mass of pulmonary tissue that has no connection to the bronchiole tree.

Front 60

Can swallowing items and having them pass into the lung cause collapse of lobes?

Back 60

Yes, lobar collapse can happen as a result of swallowing and item, impacting the airways of the lung and lead to the collapse of lobes.

Front 61

Describe the problem associated with Congenital Central Hypoventilation Syndrome (CCHS). What is the treatment?

Back 61

This is when an infant, often normal term is breathing fine and has near normal blood gases while awake, but has abnormal sleep studies. During sleep there is hypercarbia, hypoxia, and prolonged apneas. These babies must be put on ventilators for long-term care.

Front 62

Describe the symptoms seen in association with Guillain-Bare syndrome. Explain the lethal compnent of this disease.

Back 62

Guillain-Barre syndrome is characterized by ascending symmetric paralysis. The most lethal component of this disease is when the respiratory system gets involved and becomes paralyzed. Difficulty coughing, difficulty swallowing, and decreased ability to generate Negative Inspiratory Force are all signs that the respiratory system is becoming involved.

Front 63

Name two types of Congenital Diaphragmatic Hernias found in children that affect lung function.

Back 63

Bochdalek and Morgagni hernias.

Front 64

Explain what a Bochdalek hernia is. What type of patient is it found in? Describe it frequency and its presentation.

Back 64

A Bochdalek hernia is a posteriolateral hernia found in 1/2200-3500 live births. This hernia presents on the left side 85-90% of the time. The Bochdalek hernia will often present <24hrs with tachypnea, cyanosis, and retractions. There is a high morbidity and mortality associated with this hernia. The main cause of this is pulmonary hypertension due to under-developed lungs from teh hernia.

Front 65

Explain what a Morgagni hernia is. What type of patient is it found in? Describe it frequency and its presentation.

Back 65

A Morgagni hernia is an anterior hernia that makes up in 1/300 hernias. This hernia presents on the right side more commonly than the left side. In contrast to the Bochdalek hernia, this congenital hernia is often asymptomatic and found only incidentally on CXR.

Front 66

What is the most likely cause of croup in children 0-5 yrs? Describe the onset, clinical presentation, and X-ray findings.

Back 66

The cause of Croup is most likely Parainfluenza virus. The onset is insidious and presents with a low fever, nontoxic infection, and subglottic narrowing.

Front 67

What is the most likely cause of Bacterial Tracheitis in children 1m-6y? Describe the onset, clinical presentation, and X-ray findings.

Back 67

The most likely cause of Bacterial Tracheitis in this setting is S.aureus or H.influenzae. The onset of this slow, but has sudden deterioration. There is a high fever associated with a toxic bacterial infection. Subglottic narrowing is also observed on X-ray.

Front 68

What is the most likely cause of Epiglottitis in children 2-6 yrs? Describe the onset, clinical presentation, and X-ray findings.

Back 68

The most common cause of Epiglottitis is H.influenzae and Grp A Strep. Its onset is sudden and presents with a high fever and toxic infection. A large Epiglottis is seen on X-ray.

Front 69

What are three conditions that can cause orthopnea?

Back 69

COPD, CHF, and Apical lung disease.

Front 70

In COPD are the upper lungs more damaged or the lower lungs?

Back 70

The upper lungs.

Front 71

What is hepatopulmonary syndrome? Describe its cause and its associated breathing condition.

Back 71

Heptopulmonary syndrome occurs in liver failure. There are analogous lesions in the capillaries of the lungs to the spider angiomas and ectasias seen on the surface of the chest. These dilated capillaries in the lungs happen mostly in the lower areas where blood flow is greatest and do not exchange O2 well. Thus the patient has more trouble breathing than when lying down = platypnea.

Front 72

What is the diagnosis of somebody exhibiting purse lipped breathing? Which body position might they be sitting and why?

Back 72

Obstructive airway disease. They may be sitting in a tripod position because this helps them use accessory muscle of respiration such as scalene and sternomastoid.

Front 73

Describe three conditions that can cause crackles in the lungs.

Back 73

Microorganisms, Fluid, Mucus. Crackles is the sound of alveoli snapping OPEN and overcoming the surface tension once they have collapsed.

Front 74

What do Ronchi sound like? Is this an expiratory or inspiratory phenomenon? What is causing it?

Back 74

Wheezes. This is an exporatory phenomenon and is usually caused by obstruction or fluid.

Front 75

Explain Stridor. Does it occur upon inspiration or expiration? What causes it?

Back 75

Stridor is wheezing upon inspiration. Obstructive diseases or diseases that narrow the airway because of excess fluid can cause this.

Front 76

Explain what might cause the finding of absent breath sounds upon ascultation of the lungs.

Back 76

There could be fluid outside of the lung, or the lung is solid.

Front 77

Describe the common symptoms of typical pneumonia.

Back 77

Fever, productive cough, dyspnea, malaise, myalgia.

Front 78

What does a non-productive, chronic cough make you think of?

Back 78

Interstitial lung disease.

Front 79

What are four positive Tier I findings that you may observe upon ascultation during a physical exam?

Back 79

Dullness, Crackles, Wheezes, and Tympany.

Front 80

What are the three tests that are used to differentiate consolidation versus effusion?

Back 80

Egophony, Whisper pectoriloquy, Tactile Fremitus.

Front 81

Explain the physical finding behind egophony. When does this happen in the patient? When do you hear this?

Back 81

Egophony is when you have someone say the letter "E" and you hear the sound on their chest as "Aaaa". This is called an E to A change. There can also be a B to Bahhh change. This happens in a patient when you find that there is consolidation in the lungs.

Front 82

Describe the principle behind the Whispered Pectoriloquy test. What is the phrase that is whispered? If there is no whispered pectoriloqy present then what is likely to be the problem?

Back 82

The principle here is similar for that of egophony: sound travels better through solids than air or liquid. The phrase that is whispered is "Sixty six whiskies please". If you here no whispered pectoriloqy then there is probably an effusion instead of a consolidation

Front 83

Where do you listen on the patient's body during the Whispered Pectoriloqy test? Describe what you are listening for.

Back 83

You listen over the trachea and over the lung fields. Here you are listening to see if you can find anything that sounds like what you heard over the trachea. You are listening for "clearer than normal" sounds, not "louder". The lungs would normally blunt this sound.

Front 84

Describe Tactile Fremitus and the principle behind this lung exam.

Back 84

The principle behind this technique is that you can feel asymmetry between one side of the chest/back versus the other due to a difference in lung involvement in disease.

Front 85

How does one execute the Tactile Fremitus technique.

Back 85

Stand behind the patient and place the palmar aspect of hands firmly on both sides of the chest and feel for asymmetry. Have them speak sounds that resonate in their chest such as toy boat and define the abnormal side. If there is decreased vibration = pleural effusion. If there is increased vibration = solid connection from bronchus to chest wall.

Front 86

Given these findings: Focal absent breath sounds. CXR shows consolidation, not effusion, but Tier II findings (egophony, whisper, pectoiloqy, fremitus) are all negative.

Make your diagnosis and explain your findings.

Back 86

The diagnose should be one that suspects bronchial obstruction. The explanation is the an open bronchus is required for sound to transmit from the larynx.

Front 87

Why does obstruction of an airway cause everything downstream of that airway to collapse? What is this phenomenon called?

Back 87

This happens because all the air that is trapped in the alveoli gets absorbed and the airways close on themselves. This is called Atelectasis.

Front 88

Define Atelectasis and its three main causes.

Back 88

Atelectasis is when there is no pnuemonia in the lung, but there is a collapse or consolidation. Airway obstruction, Pressure coming from the pleura squeezing the lung closed, or fibrosis that is not allowing the lung to open properly can all be causes of Atelectasis.

Front 89

What percent of the predicted normal FEV1 must be gone before a person becomes symptomatic?

Back 89

~50%

Front 90

Explain Dahl's sign. What causes it?

Back 90

Dahl's sign is a hyperpigmentation of the knees that occurs when someone is continually leaning on them in order to increase their ability to respire. This often happens when someone is suffering from COPD, or asthma (obstructive lung disease).

Front 91

What are some physical diagnosis signs that someone is suffering from obstructive lung disease?

Back 91

Pursed-lip breathing, Dahl's sign, Paradoxical abdominal movements (stomach moves in upon inspration) accessory muscle use, sternocleidomastoid hypertrophy (if thumb is larger than SCM), rapid shallow breathing.

Front 92

What are some of the pulmonary causes for Pulsus Paradoxus?

Back 92

Tension pneumothorax, Asthma, Chronic obstructive pulmonary disease

Front 93

How common is Primary Pulmonary Hypertension? What is the most common cause?

Back 93

Primary disease is rare. Pulmonary hypertension is usually due to severe left heart failure

Front 94

What findings are there in pulmonary hypertension with regard to heart sounds?

Back 94

In pulmonary hypertension there will be an increased P2 sound/physiological splitting because it will take longer for the pulmonary valve to close.

Front 95

Describe some of the main causes of pleural friction rubs.

Back 95

TB, cancer, asbestos exposure.

Front 96

A lung infection with what organism and patients with what condition have an association with spontaneous pneumothorax after being place on a ventilator?

Back 96

Pneumocystis jirovecii and patients with COPD.

Front 97

What is the predicted median survival of a Cystic Fibrosis patient as of 2007?

Back 97

~37 years.

Front 98

Which chromosome was the first CF mutation found on?

Back 98

Chromosome 7

Front 99

Describe the different classes of mutations (I-VI) capable of causing Cystic Fibrosis.

Back 99

Class I = No protein synthesis

Class II = Increased protein degredation

Class III = Defective regulation

Class IV = Defective conduction

Class V = abnormal mRNA splicing with reduced synthesis

Class VI = increased recycling of CFTR

Front 100

Which Class of mutation does deltaF508 (the most common mutation) found in Cystic Fibrosis fall into?

Back 100

Class II- Increased protein degradation.

Front 101

Which are the most common bacteria to cause infection in the CF patient?

Back 101

P.aerugenosa, S.aureus, H.influenza. (80% of patients have chronic pseudomonas respiratory infection by age 18.

Front 102

What are some complications that can be found to occur in patients suffering from Cystic Fibrosis?

Back 102

Hemoptysis, Pneumothorax, Cor pulmonale, and End-Stage lung disease.

Front 103

What are some associated problems in other organ systems that can be found to occur in patients suffering from Cystic Fibrosis?

Back 103

Exocrine and Endocrine pancreatic insufficiency, Focal biliary cirrhosis (leads to liver failure in 2-3% of pts), Meconium ileus, Infertility

Front 104

Briefly describe the new and future treatments that exist for Cystic FIbrosis.

Back 104

Gene therapy, Protein chaperones, ion transport modulators, new antibiotics, anti-inflammatory agents.

Front 105

Which inflammatory cells are seen to be at work in asthma?

Back 105

Mast cells, eosinophils, T cells, neutrophils, and epithelial cells.

Front 106

Describe some of the symptoms associated with Asthma.

Back 106

There are recurrent episodes of wheezing, breathlessness, chest tightness, and cough. There is reversible airflow obstruction either spontaneously or with treatment. Additionally there is increased bronchial hyperresponsiveness to a variety of stimuli.

Front 107

What is the most common chronic pulmonary condition?

Back 107

Asthma.

Front 108

Describe the Immediate IgE dependent inflammatory mediators that contribute to the obstructive airway disease seen in asthma. Describe the symptoms that correlate.

Back 108

IgE binding to mast cells causes immediate release of Granulation contents: TNF-alpha, Histamine, Proteases, and Heparin

Front 109

Describe the IgE-dependent inflammatory mediators that contribute to the obstructive airway disease seen in asthma minutes after mast cell activation. Describe the symptoms that correlate.

Back 109

After some minutes of IgE mediated mast cell stimulation we find that Lipid mediators, Prostaglandins, and Leukotrienes start to contribute to asthma and produce symptoms such as wheezing and bronchoconstriction.

Front 110

Describe the IgE-dependent inflammatory mediators that contribute to the obstructive airway disease seen in asthma hours after mast cell activation. Describe the symptoms that correlate.

Back 110

Over the course of hours after IgE-dependent release of inflammatory mediators we see specific cytokin production of TNF-alpha, IL-4, and IL-13. This leads to mucus production and eosinophil recruitment.

Front 111

What are some of the morphologic changes in the lung tissue that are seen in asthma over time?

Back 111

Vascular dilation, edema, inflammatory cell infiltration, epithelial damage, smooth muscle hypertrophy, mucous gland hypertrophy and hyper secretion, basement membrane thickening and fibrosis.

Front 112

Explain how the spirometry test helps to diagnose asthma.

Back 112

The spirometry test measures FEV1. If a patient has a change >/= 20% of their FEV1 upon spirometry after the administration of a bronchodilator, this patient is likely to have asthma.

Front 113

If you think that a patient might have asthma, but they present with normal PEFs and FEV1s, then what test should you do next? What can you interpret from the results of this test?

Back 113

Methacholine challenge. If this test is positive, this person may or may not have asthma. If this test is negative, the patient definitely does not have asthma.

Front 114

Who responds more quickly to a Methacholine challenge test: Asthma patients or COPD patients?

Back 114

Asthma patients. They respond to doses that are ~1000x less potent.

Front 115

If no other medication could be administered for PERSISTENT severe asthma, what is the one medication that should be?

Back 115

Inhaled Corticosteroids.

Front 116

What important, non-pharmacologic, interventions should be used at each step of asthmatic control?

Back 116

Patient education, environmental control, and management of comorbidities.

Front 117

Name five factors that can contribute to asthma severity.

Back 117

Allergen exposure, Rhinitis, Sinusitis, Viral infections, GERD.

Front 118

Which asthma drugs fall under the Relievers category?

Back 118

Inhaled fast-acting B2 agonists, and Inhaled anticholinergics.

Front 119

Which asthma drugs fall under the Controllers category?

Back 119

Inhaled corticosteroids, LABAs, ihaled cromones, oral ant-leukotrienes, oral theophyllines, oral coticosteroids, Anti-histamines

Front 120

Which asthma drugs fall under the Preventer category?

Back 120

Omalizumab, Immunotherapy.

Front 121

What is the definition of COPD? Is there an acute onset or is this progressive? Explain the cause.

Back 121

Chronic obstruction to airflow that is not reversible. The airflow limitation is usually progressive. The cause is due to an abnormal inflammatory response of the lung to noxious particles of gases, most commonly smoking.

Front 122

What is the #1 risk factor for COPD?

Back 122

Smoking.

Front 123

What % of people who smoke, will develop COPD?

Back 123

15-20%.

Front 124

Describe some of the host factors that predispose someone to COPD.

Back 124

AAT-1 deficiency, male gender, lower socioeconomic status, bronchial hyperresponsiveness, atopy and asthma, childhood illnesses, Vitamin C and E deficiencies.

Front 125

Which type of lymphocytes are thought to be very involved in the inflammatory changes and pathogenesis of COPD?

Back 125

CD8+

Front 126

What are the two main important types of Emphysema?

Back 126

Panacinar and Centriacinar emphysema

Front 127

Describe the damage seen in Panacinar Emphysema. Where does it occur most often in the lung and what type of patients get it?

Back 127

Looking at the lung in panacinar emphysema will reveal alveolar damage and a predominance to occur in the lower lobe. Panacinar emphysema is most commonly found in patients with alpha-1-antitrypsin deficiency and smokers.

Front 128

Which parts of the lung are most often involved in Centriacinar emphysema? What patients present with this?

Back 128

Centriacinar emphysema is seen to affect the respiratory bronchioles and have an upper lobe predomninance. This type of emphysema is found only in smokers and is the most common type of emphysema.

Front 129

Which type of Emphysema does AAT-1 deficiency contribute to?

Back 129

Panacinar emphysema.

Front 130

Describe some of the mechanisms of abnormal gas exchange in the lungs.

Back 130

V/Q mismatch (hypoxemia), increased dead space (hypercapnia), diffusion defect, alveolat hypoventilation, increased CO2 production, altered response to CO2, respitatory muscle fatigue/dysfunction.

Front 131

What is the normal partial pressure of O2 and CO2 in the alveolar capillaries?

Back 131

O2 = 40 mmHg

CO2 = 45 mmHg

Front 132

What is the normal partial pressure of O2 and CO2 in the alveoli?

Back 132

O2 = 100 mmHg

CO2 = 40 mmHg

Front 133

If there is a ventilation problem, what will the partial pressures of O2 and CO2 in the alveoli start to look like? What will the values be close to?

Back 133

The partial pressures will start to look like the partial pressures found in the aterial blood of the alveolar capillaries.

O2 = 40 mmHg

CO2 = 45 mmHg

Front 134

If there is a blood flow problem, what will the partial pressures of O2 and CO2 in the alveoli be close to?

Back 134

O2 = 150 mmHg

CO2 = 0 mmHg

Front 135

What does a blue bloater mean?

Back 135

Chronic bronchitis.

Front 136

What does a pink puffer mean?

Back 136

Chronic emphysema.

Front 137

Define Chronic Bronchitis.

Back 137

A chronic productive cough for most days of 3 consecutive months for 2 consecutive years.

Front 138

Why do people with emphysema become so emaciated?

Back 138

Because they are expending a lot of energy just trying to breath.

Front 139

If you see clubbing of the fingers in a patient that presents with COPD, what should you think of?

Back 139

You should think of bronchiectasis, CF, Bronchiogenic carcinoma, Intrapulmonary vascular malformations, and Congenital heart disease (R to L shunt) because clubbing is NOT a feature of COPD itself.

Front 140

What will you see on a CXR of a patient with Emphysema?

Back 140

Hyperinflation, flat diaphragm, decreased vascular markings, a small vertical heart

Front 141

What findings on spirometry confirm the presence of airflow limitation and COPD?

Back 141

FEV1/FVC <70% and a FEV1 <80% predicted.

Front 142

What is a normal FEV1/FVC? Describe a normal FEV1 and FVC.

Back 142

80%. A normal FEV1 = 4L. A normal FVC = 5L.

Front 143

Characterize the diffusing capacity associated with Emphysema. Why is it this way? How does the diffusion capacity in Asthma or Chronic bronchitis compare?

Back 143

A low diffusing capacity suggests emphysema. There is a low diffusing capacity because there is much alveolar damage associated with emphysema. The diffusion capacities in Asthma and Chronic Bronchitis are relatively unaffected because in those diseases the problems are not associated with the alveoli.

Front 144

Which tests help you to distinguish between the different types of COPD? PFTs or diffusing capacity tests?

Back 144

The PFTs will all be similar for the COPDs. The diffusion tests, however, will be different because of the different pathogenic mechanisms underlying each disease. The diffusion test for emphysema will be low, whereas the diffusion tests for Asthma and Chronic Bronchitis will be mostly normal.

Front 145

What is the most common cause of exacerbation of COPD?

Back 145

Infection of the tracheobronchial tree and air pollution.

Front 146

List the five examples of Chronic Obstructive Pulmonary Disease.

Back 146

Emphysema, Chronic Obstructive Bronchitits, Bronchiectasis, Asthma, and Small Airways Disease.

Front 147

Describe the pathophysiology behind COPD.

Back 147

COPD is an increase in resistance to airflow during expiration due to intrinsic disease of the airways or loss of elastic recoil of the lungs

Front 148

Describe the three forms of Small Airways Disease.

Back 148

Respiratory Bronchiolitis, Bronchiolitis Obliterans, Constrictive Bronchiolitis

Front 149

What defines a medically significant A-a gradient?

Back 149

A gradient >/= 30 mm Hg

Front 150

Name four causes of hypoxemia that are associated with an increased A-a gradient.

Back 150

Ventilation defect, Perfusion defect, Diffusion defect, RIght to Left Cardiac Shunt.

Front 151

Are extrapulmonary causes of hypoxia going to present with an increased, normal, or decreased A-a gradient?

Back 151

A normal A-a gradient.

Front 152

Are pulmonary causes of hypoxia going to present with an increased, normal, or decreased A-a gradient?

Back 152

An increased A-a gradient.

Front 153

Name two drugs whose side-effects include cough. How does each work?

Back 153

ACE inhibitors- inhibits the degredation of bradykinin and causes mucosal swelling and irritation in tracheobronchial tree.

Aspirin- allows increase in Leukotriene synthesis (LT C-D-E4) which are bronchoconstrictor (aspirin-related asthma).

Front 154

Describe some of the causes of hypoxemia with a normal A-a gradient,

Back 154

Depression of the respiratory center in the medulla, Upper airway obstruction, Chest bellows dysfunction.

Front 155

Describe the lung volumes that are not directly measured by spirometry.

Back 155

Any of the lung volumes that contain RV(residual volume) will not be able to be fully measure directly by spirometry. So, FRC, TLC, and RV itself, cannot be measured directly by spirometry.

Front 156

Describe a normal FVC value.

Back 156

5L

Front 157

Describe a normal FEV1 value.

Back 157

4L

Front 158

What are the pulmonary function tests whose results will differ depending on whether a patient as Restrictive or obstructive disease? Explain what the results will be for both.

Back 158

Total lung capacity, Residual volume, and FEV1/FVC ratio.

Obstructive
-total lung capacity is increased, residual volume is increased, ratio is decreased.

Restrictive
-total lung capacity is decreased, residual volume is decreased, ratio is increased

Front 159

Describe Choanal atresia. Who suffers from it and what causes it..

Back 159

Choanal atresia occurs when there is a unilateral or blateral bony septum between the nose and pharynx. This mostly affects newborns as they cannot breathe while they are breastfeeding

Front 160

Why do Nasal Polyps develop?

Back 160

Due to chronic inflammation.

Front 161

What is the most common type of Nasal polyp?

Back 161

Allergic polyps. These are often seen in adults with a history of IgE-mediated allergies.

Front 162

If you find a child with a Nasal Polyp, what is the first test you should order and why?

Back 162

If you find a child with a nasal polyp you should order a sweat test in order to rule out Cystic fibrosis.

Front 163

Which drug can be associated with producing allergic nasal polyps? Who does this most often occur in? What is the clinical triad associated?

Back 163

Aspirin and other NSAIDs can cause allergic pulmonary symptoms by allowing an increase in LT (C, D, E-4) production after blocking the COX pathway. These symptoms occur more commonly in women with chronic pain syndromes and the clinical triad that may be seen is NSAIDs, asthma, nasal polyps.

Front 164

What is the definition of obstructive sleep apnea? Describe its etiology.

Back 164

Excessive snoring with intervals of breath cessation (called apnea). Obesity is the most common cause of obstructive sleep apnea, where the pharyngeal muscles collapse due to the weight of tissue in the neck. Tonsillar hypertrophy and nasal septum deviation can also cause this.

Front 165

Explain the pathogenesis of Obstructive Sleep Apnea. What will blood gas findings show?

Back 165

Airway obstruction causes CO2 retention, leading to hypoxemia. There will be a decreased PO2 and O2 sat during apneic episodes, with an increased PCO2 (respiratory acidosis).

Front 166

What are some complications that may develop from Obstructive Sleep Apnea?

Back 166

Pulmonary hypertension leading to Cor pulmonale, and secondary polycythemia due to hypoxemic stimulus for erythropoeitin release.

Front 167

Which sinus is most commonly affected in sinusitis in adults?

Back 167

The Maxillary sinus.

Front 168

Which sinus is most commonly affected in sinusitis in children?

Back 168

The Ethmoid sinus.

Front 169

What is the most common cause of sinusitis? Describe its pathogenesis.

Back 169

Upper Respiratory infection. Its pathogenesis is related to the blockage of drainage into the nasal cavity.

Front 170

Which pathogen is most often responsible for causing Sinusitis?

Back 170

S.pnuemoniae

Front 171

Which fungi most often cause Sinusitis and which causes sinusitis most often in diabetic patients?

Back 171

Mucor or Aspergillus. Mucor is commonly responsible for fungal sinusitis in diabetics.

Front 172

Describe the most common malignant tumor of the nasopharynx. What demographics does it usually present in and what causal links are associated? Where is the most likely site of metastasis?

Back 172

The most commmon malignant tumor of the nasopharynx is Nasopharyngeal Carcinoma. There is an increased incidence in Chinese and African populations. There as been a causal relationship described with EBV, and a likely site of metastasis is the cervical lymphnodes.

Front 173

Describe the most common cause of Laryngeal Carcinoma. Which virus ca be associated with this? Where is the most common site?

Back 173

Cigarette smoking, then alcohol, are the two most common causes of Laryngeal Carcinoma. They also have a synergistic effect. Sometime HPV 6 and 11 have an association with Laryng. Carcin. The majority of these cancers are located in the True vocal cords.

Front 174

What is the most common cause of fever and dyspnea after surgery?

Back 174

Resorption atelectasis.

Front 175

What clinical findings will present in someone with Resorption Atelectasis?

Back 175

Fever and dyspnea usually within 24-36 hrs after collapse, absent breath sounds and tactile fremitus, ipsilateral elevation of diaphragm and tracheal deviation.

Front 176

Describe the etiology of Compression Atelectasis. What are some examples.

Back 176

Compression atelectasis occurs from air or fluid in the pleural cavity under increased pressure collapsing small airways beneath the pleura. Some examples of this are Tension pneumothorax and pleural effusion.

Front 177

Which cells in the lungs are responsible for making surfactant? What are the organelles that produce and store surfactant?

Back 177

Surfactant is synthesized by Type II Pneumocytes and stored in lamellar bodies.

Front 178

At what week of gestation does surfactant begin to be produced? What are factors that upregulate its synthesis? What are factors that decrease its synthesis?

Back 178

Surfactant begins to be produced at the 28th week of gestation. Its synthesis is increased by cortisol and thyroxine. Its synthesis is decreased by insulin.

Front 179

What are three factors that can contribute to decreased surfactant in the fetal lungs?

Back 179

Prematurity, Maternal diabetes (increased insulin), Cesarean section (increased cortisol).

Front 180

What is something that pregnant women who deliver prematurely receive in order to increase fetal surfactant synthesis?

Back 180

Corticosteroids.

Front 181

What are some of the complications that might be associated with RDS and lack of O2?

Back 181

Superoxide free radical damage from O2 therapy may result in blindness and and permanent damage to small airways (BPD), Patent ductus areteriosis (due to persistent hypoxemia), and Necrotizing enterocolitis from intestinal ischemia allowing entry of gut bacteria into the intestinal wall.

Front 182

What are the causes of Pulmonary edema?

Back 182

This can occur due to alterations of Starling forces (transudate) or because of cell and tissue injury (exudate).

Front 183

What is the most common cause of pulmonary edema?

Back 183

Left-sided heart failure.

Front 184

What are the risk factors for Acute Respiratory Distress Syndrome (ARDS)? Which is the most common cause?

Back 184

Gram (-) sepsis, Gastric aspiration, Severe trauma with shock, Diffuse pulmonary infections, heroine, smoke inhalation. Sepsis is the most common cause of ARDS

Front 185

Describe the etiology and pathogenesis behind ARDS.

Back 185

Acute damage to the alveolar walls and epithelial cells leads to recruitment of macrophage and others cells which release inflammatory cytokines. There is an increase of protein rich exudate which creates hyaline membranes. Decreases in surfactant production due to Type II pneumocyte damage. The inflammatory cells and changes cause further damage and thickening of membranes and eventual fibrosis if the patient lives through the episode (60% mortality).

Front 186

What pathogen is most often the cause of Community-acquired Typical pneumonia?

Back 186

S.pneumoniae.

Front 187

Explain the pathogenesis and lung involvement seen in bronchopneumonia? What does the lung histology look like?

Back 187

This infection begins as an acute bronchitis and spreads locally to the lungs. The lower lobes or the right middle lobes of the lungs are most often involved. The lung in Bronchopneumonia usually has patchy areas of consolidation, and microabscesses are present in the areas of consolidation.

Front 188

What areas of the lung are involved in Lobar Pneumonia? Describe the histological picture of the lung.

Back 188

In Lobar pneumonia there is a complete or almost complete consolidation of a lobe of the lung.

Front 189

Describe the clinical findings associated with Typical Community Acuired pneumonia.

Back 189

With Typical Community Acquired Pneumonia there is a sudden onset of high fever with a productive cough. There are signs of consolidation and and laboratory findings usually show a Positive Gram stain and Neutrophilic leukocytosis.

Front 190

What is the Gold standard test to diagnose pneumonia? What will the test show?

Back 190

The chest radiograph is the Gold standard test for diagnosing pneumonia. It will show patchy infiltrates (bronchopneumonia) or lobar consolidation.

Front 191

Describe the most common cause of Atypical Community Acquired pneumonia and how it presents.

Back 191

The most common cause of Atypical Community Acquired Pneumonia is Mycoplasma pneumoniae. Other causes include Chlamydia pneumoniae, viruses (RSV, Influenza, Adeno), and Chlamydia trachomatis. It usually has an insidious onset with a low-grade fever, non-productive cough, flu-like symptoms, and NO SIGNS of consolidation. Although there is interstitial mononuclear infiltrate, the alveolar spaces are free of exudate.

Front 192

Is atypical pneumonia usually found in the alveoli or the interstitium?

Back 192

Atypical pneumonia is an interstitial pneumonia.

Front 193

Which are the most common pathogens responsible for Nosocomial pneumonia?

Back 193

The most common Gram (-) pathogens responsible for Nosocomial pneumonia are Pseudomonas aeruginosa, and E.coli. The most common Gram (+) pathogens responsible for Nosocomial pneumonia is Staph aureus. P.aeruginosa is the most common overall and most associated with being put on a respirator.

Front 194

What treatment is usually responsible for Nosocomial pneumonia?

Back 194

Being put on a respirator.

Front 195

Describe the underlying risk factors that predispose somebody for acquiring Nosocomial pneumonia?

Back 195

Severe underlying disease, antibiotic therapy/immunosuppression, and respirators, which are the most common source of infection

Front 196

Which fungus should you associate with the description of septated hyphae?

Back 196

Aspergillus.

Front 197

What are three common infections causing pneumonia in immunocompromised hosts?

Back 197

CMV, Pneumocystis jiroveci, and Aspergillus fumigatus, with the most common of these being Peumocystis.

Front 198

HIV infected patients take Trimethaprim-Sulfamethoxazole prophylactically to prevent infection by which two microorganisms to prevent which two conditions.

Back 198

Bactrim prevents P.jiroveci pneumonia and cerebral Toxoplasmosis.

Front 199

What part of M.tuberculosis allows for acid staining? Is it an aerobe or an anaerobe?

Back 199

The mycolic acid in the cell wall is the component that holds on to the acid fast stain. M.tuberculosis is a strict aerobe.

Front 200

A Purified Protein Derivative test is used to screen for exposure to what organism? Does it tell u whether your infection is active or inactive?

Back 200

A PPD skin test is used to screen for exposure to TB. It does NOT distinguish between active and inactive infection.

Front 201

Where is the most common subpleural location for primary TB infection?

Back 201

The lower part of the upper lobes and the upper part of the lower lobes.

Front 202

Where is the most common location for Secondary (reactivation) TB infection? What is the cause of this? What specific types of lesions can this create?

Back 202

The most common location involved in a reactivated TB infection are the apices involving one or both of the upper lobes (this is because ventilation and oxygenation is greatest in the upper lobes). Cavitary lesions are a characteristic lesion that occur in a secondary reactivated TB infection, and are due to the release of cytokines from memory T cells.

Front 203

How does TB spread in the lungs after initial infection? How does it spread to extrapulmonary sites? Which extrapulmonary site is the most common, or first involved?

Back 203

TB spreads around the lungs due to invasion into the bronchus or lymphatics. It spreads to extrapulmonary sites from invasion of pulmonary vein tributaries. The kidney is the most common extrapulmonary site, but there can also be liver (granulomatous hepatitis), spleen, and spine (Pott's disease) involvment.

Front 204

What is the most common TB infection found in AIDS patients? What CD4 count is associated with this infection?

Back 204

MAC is the most common TB infection in AIDS and is occurs when the CD4+ count falls below 50. This infection often disseminates to other sites.

Front 205

Describe the most common cause of lung abscesses. What kind of bacteria can be responsible? When does it usually occur?

Back 205

The most common cause of lung abscesses is due to aspiration of oropharyngeal material (e.g. tonsillar material).Primary formation with Staph, Prevotella and Fusobacterium are causes, but complications of bacteria pneumonia with Staph, Kebsiella, etc. can also occur. Lung abscesses can commonly occur in patients with depressed cough relfexes (e.g. after anesthesia)

Front 206

What is the most common cause of the common cold and how is it transmitted?

Back 206

Rhinovirus.

Front 207

This is the most common cause of atypical pneumonia and bronchiolitis (wheezing) in children.

Back 207

Respiratory Syncytial Virus (RSV).

Front 208

Parainfluenza virus is the most common cause of what type of upper airway infection in infants? What is the sound produced? What is the characteristic sign seen on anterior X-ray of the neck?

Back 208

Parainfluenza is the mos common cause of Croup (laryngotracheobronchitis) in infants. Inspiratory stridor, from upper airway obstruction due to submucosal edema in the trachea is that sound that is commonly heard with Croup. The "steeple sign" is commonly seen on X-ray, indicating mucosal edema in the trachea.

Front 209

What is a common pneumonia found in immunocompromised transplant patients (e.g. bone transplant patients)?

Back 209

CMV.

Front 210

What other infection may be superimposed on Influenza pneumonia?

Back 210

Bacterial pneumonia, most commonly Staph aureus.

Front 211

What type of symptoms does Rubeola cause?

Back 211

Fever, cough, conjunctivitis, and excessive nasal mucus production. Koplik spots in the mouth precede the onset of rash.

Front 212

What virus is thought to have first infected humans through contact with the Chinese masked-palm civet? This virus infects the lower respiratory tract and then spreads systemically to produce severe respiratory infection.

Back 212

This is the SARS virus. it is diagnosed with viral detection by PCR or detection of antibodies.

Front 213

Which Chlamydia is the second most common cause of atypical pneumonia?

Back 213

C.pneumoniae.

Front 214

Which Chalmydia is responsible for pneumonia of the newborn? What are the characteristic eye signs, and cough?

Back 214

C.trachomatis is responsible for pneumonia of the newborn and is acquired from an infected mother as the infant passes through the birth canal. This infected eye displays conjunctivitis, and there is a characteristic staccato cough that can be associated.

Front 215

Which organism can cause atypical pneumonia, myocarditis, granulomatous hepatitis, and is most commonly contracted by dairy farmers and veterinarians through dealing with sheep, cattle and goats?

Back 215

Coxiella burnetii. This also represents the only rickettsia transmitted without a vector.

Front 216

What is the most common cause of atypical pneumonia that is common in adolescents and military recruits (closed crowded spaces)?

Back 216

Mycoplasma. Some complications of infection with mycoplasma include bullous myringitis, and cold autoimmune hemolytic anemia due to anti-I-IgM antibodies.

Front 217

Which lancet-shaped diplococcus is most likely to cause a pneumonia with rapid onset, productive cough, and signs of consolidation?

Back 217

Streptococcus pnemoniae.

Front 218

This Gram (+) coccus is a major cause of pneumonia in Cystic Fibrosis patients and I.V. drug abusers. It can cause hemorrhagic pulmonary edema, abscess formation, and tension pneumocysts (intrapleural blebs) that can rupture and produce a tension pneumothorax.

Back 218

Staph aureus. Infection with Staph is commonly superimposed on influenza pneumonia and measles pneumonia.

Front 219

Describe the mechanism of action of Corynebacterium diptheriae toxin. (Gram (+) rod)

Back 219

The diptheriae toxin inhibits protein synthesis by ADP-ribosylation of EF2 involved in protein synthesis; the toxin also impairs B-oxidation of fatty acids in the heart and produces a pseudomembrane in the oropharynx and trachea.

Front 220

Which bacteria is most commonly responsible for acute epiglottis, acute exacerbation of COPD, otitis media, and conjunctivitis? (Gram (-) rod)

Back 220

Haemophilus influenza.

Front 221

What Gram (-) diplococcus causes typical pneumonia is the second most common cause of exacerbation of COPD, causes chronic bronchitis, sinusitis, and otitis media?

Back 221

Moraxella catarrhalis.

Front 222

Which Gram (-) water-loving rod causes pneumonia often associated with infarction due to vessel invasion and causes green sputum?

Back 222

P.aeruginosa.

Front 223

This is a Gram (-) rod is surrounded by a mucoid capsule and is a common cause of pneumonia in elderly patients in nursing homes, alcoholics and can produce blood-tinged, thick, mucoid sputum. Lobar consolidation and abscess formation are also common.

Back 223

Klebsiella pneumoniae.

Front 224

This is a water loving Gram (-) rod that causes pneumonia associated with high fever, dry cough, flu-like symptoms. Infection with this organism may also produce tubulointerstitial disease leading to hyporeninemic hypoaldosteronism.

Back 224

Legionella pneumophilia.

Front 225

This is the most common opportunistic fungal infection. You find narrow-based buds surrounded by a thick capsule. They are often found in pigeon excreta (around buildings, outside office windows, under bridges); causes primary lung disease.

Back 225

Cryptococcus neoformans.

Front 226

Which fungal infection shows branching septate hyphae and is found to develop fungus balls in preexisting cavities in the lungs?

Back 226

Aspergillus.

Front 227

Which hypersensitivity reactions are associated with Allergic Bronchopulmonary Aspergillosis?

Back 227

Type I and Type III hypersensitivity reactions.

Front 228

What are Mucor species of fungus known for?

Back 228

This species of fungus is known for causing rhinocerebral mucormycosis in diabetic patients with ketoacidosis, and also for infecting immunocompromised patients.

Front 229

Which fungus presents as with spherules that contain endospores in the tissues and is also known to be found in arid desert areas in the southwesten U.S. ("valley fever", earthquakes and dust).

Back 229

This is Coccidioides immitis. There are flu-like symptoms and erythema nodosum associated with Coccidioides infection.

Front 230

What is the most common systemic fungal infection seen in the Ohio and Central Mississippi river valleys? This organism is known to be present in bat, stariling and chicken droppings.

Back 230

This is Histoplasma capsulatum. Infection with this fungus can simulate TB lung disease and produce coin lesions and the yeast forms are seen in macrophages.

Front 231

Which fungus has broad based budding yeast and occurs in the Great Lakes region and central and southeastern United States. This produces lung disease, but also produces skin disease that simulates squamous cell carcinoma.

Back 231

Blastomyces dermatiditis.

Front 232

This fungal infection is the most common AIDS defining lesion (occurs when CD4 <200)and has a cyst and trophozoite phase. We see diffuse alveolar foamy exudates with cup-shaped cysts.

Back 232

Pneumocystis jiroveci.

Front 233

Where do pulmonary thromboemboli originate?

Back 233

The Femoral veins.

Front 234

Describe potential complications of pulmonary artery occlusion.

Back 234

Increased pulmonary artery pressure, and decreased flow to the pulmonary parenchyma, which may lead to hemorrhagic infarction in the presence of existing disease.

Front 235

Where do the majority pulmonary embolisms occur in the lungs?

Back 235

The Lower Lobes of the lungs.

Front 236

Why does a saddle embolus in the the lungs produce sudden death?

Back 236

Because there is a sudden increase in pulmonary artery pressure and it produces acute right ventricular strain.

Front 237

Describe the most common symptom and sign of Pulmonary Infarction.

Back 237

Dyspnea and Tachypnea. There may also be fever, pleuritic chest pain (pain with inspiration), friction rub, and effusion.

Front 238

Describe the laboratory findings associated with pulmonary infarction.

Back 238

There is respiratory alkalosis, a PaO2 <80 mm Hg, increased A-a gradient, and a normal Ventillation scan, but abnormal perfusion scan.

Front 239

What setting needs to be present in a patient order for pulmonary infarction to occur?

Back 239

Decreased bronchial artery blood flow (e.g. decreased cardiac output) or previously underventilated lung (e.g. obstructive lung disease), then occlusion of the pulmonary vessel will likely result in a hemorrhagic infarction, which significantly increases risk of morbidity and death.

Front 240

What are the causes of Primary Pulmonary Hypertension? Is this more common in women or men?

Back 240

Vascular hyperreactivity with proliferation of smooth muscle; primary PH is more common in women.

Front 241

Describe some of the causes of Secondary Pulmonary Hypertension.

Back 241

Chronic hypoxemia(chronic lung disease), chronic respiratory acidosis (chronic bronchitis), loss of pulmonary vasculature (emphysema), left to right cardiac shunts, mitral stenosis, and endothelial cell dysfunction with loss of vasodilators (e.g. NO), and an increase in vasoconstrictors (e.g. Endothelin)

Front 242

What is a heart sound finding that will be accentuated in a patient that has Pulmonary Hypertension?

Back 242

The P2 sound in the physiological split.

Front 243

Define Cor Pulmonale.

Back 243

Its a combination of Pulmonary hypertension and Right ventricular hypertrophy leading to Right-sided heart failure.

Front 244

In Goodpasture syndrome, what often precedes renal failure?

Back 244

Pulmonary hemorrhage with hemoptysis.

Front 245

What is the main characteristic of Restrictive lung disease with regard to lung capacity and expiratory flow rate?

Back 245

Restrictive lung diseases are characterized by reduced total lung capacity in the presence of a normal or reduced expiratory flow rate.

Front 246

What categories do restrictive lung diseases fall into?

Back 246

Chest wall disorders in the presence of normal lungs (e.g. kyphoscoliosis, pleural disease, obesity), and acute or chronic interstitial lung diseases (e.g. ARDS, pneumoconiosis, sarcoidosis).

Front 247

Describe the most common cause of Secondary pulmonary hypertension.

Back 247

Respiratory acidosis and/or hypoxemia.

Front 248

How does interstitial fibrosis develop? What are the effects of interstitial fibrosis on the cells and mechanics of the lung?

Back 248

The earliest manifestation of interstitial fibrosis is alveolitis and leukocytes release cytokines, which stimulate fibrosis. This fibrotic proliferation induced by chronic inflammation leads to decreased lung compliance and increased elasticity. Damage to Type I/II pneumocytes and to endothelial cells results in the functional loss of alveolar and capillary units.

Front 249

Describe some clinical findings that are shared/common to all restrictive lung diseases.

Back 249

Dry cough and exertional dyspnea, late inspiratory crackles in the lower lung fields, the potential for Cor pulmonale, diffuse bilateral reticulonodular infiltrates.

Front 250

What does the FEV1/FVC ratio look like in restrictive lung diseases? Why?

Back 250

Decreased total lung volumes and capacities due to increased elasticity, produce FEV1/FVC ratios that are normal to increased (3L/3L vs. 4L/5L) from the expected ~80%

Front 251

What causes the broad category of the diseases known as Pneumoconioses?

Back 251

Inhalation of mineral dust into the lungs that leads to interstitial fibrosis.

Front 252

What are the mineral dusts that are most commonly inhaled leading to Pnemoconiosis? Which are the most fibrogenic and which are the least fibrogenic?

Back 252

Coal dust, Silica, Asbestos, and Beryllium. Coal dust is the least fibrogenic material, but Silica, Asbestos and Beryllium are very fibrogenic.

Front 253

Name the two types of Coal Workers Pneumoconiosis (CWP). Compare and contrast the two.

Back 253

The two types are Simple CWP and Complicated CWP. Simple CWP is due to coal deposits adjacent to respiratory bronchioles that produce centrilobar emphysema with small opacities in the upper lobes and upper portions of the lower lobes. Complicated CWP (progressive massive fibrosis) has larger opacities and can lead to crippling black lung disease.

Front 254

What is Pulmonary anthracosis? What are the symptoms usually associated? Describe the sources of anthracotic pigment.

Back 254

Anthrocosis is usually asymptomatic, but upon examination of the lung tissue anthracotic pigment in interstitial tissue and hilar nodes can be seen. Alveolar macrophages with anthracotic pigment are called "dust cells" Sources of anthracotic pigment (coal dust) may come from coal mines, large urban centers, and tobacco smoke.

Front 255

What two conditions may be associated with Complicated CWP/ Black lung disease?

Back 255

Cor pulmonale and Caplan syndrome (CWP plus large cavitating rheumatoid nodules in the lungs). There is NO INCREASED INCIDENCE of TB or primary lung cancer associated with Complicated CWP.

Front 256

Inhaling what mineral dust causes Silicosis? What are the most common sources? Describe the contents of the opacities found in Silicosis.

Back 256

Inhaling Silica quartz (crystalline silicone dioxide) is most often implicated. Sources of this type of mineral dust include foundries (casting metal), sandblasting, and working in mines. In Silicosis the opacities are often found to contain collagen and quartz.

Front 257

Explain the pathogenesis behind Silicosis and inhaling Silica.

Back 257

Quartz activates and is cytolytic to alveolar macrophages. The macrophages release cytokines that stimulate fibrogenesis.

Front 258

What type of histologic changes do we observe in someone who has had chronic Silica exposure? What are complications associated with Silicosis?

Back 258

We see nodular opacities in the lungs. There are concentric layers of collagen with or without central cavitation and the presence of quartz which polarizes in the nodule. We may also see "egg shell calcifications" in the hilar nodes. Complications include Cor pulmonale, and Caplan syndrome.

Front 259

There is an increased risk in acquiring what diseases in Silicosis, that there is NOT a risk of acquiring in chronic coal dust exposure.

Back 259

There is an increased risk for developing lung cancer and TB when someone has Silicosis.

Front 260

What are the geometric forms seen in histology sections of lungs with Asbestosis

Back 260

Serpintine -curly and flexible fibers that produce interstitial fibrosis and lung cancer.

Amphibole- straight and rigid, produces interstitial fibrosis, lung cancer, and mesothelioma.

Front 261

Describe the most common deposition sites of asbestos and the most common sources.

Back 261

The most common sites for deposition of asbestos is the Respiratory unit = the respiratory bronchioles, alveolar ducts, and alveoli. Common sources include insulation around old pipes in old naval ships, roofing material used over 20 years ago, demolition of old buildings.

Front 262

Describe what coats asbestos fibers in tissue. What do we see in sputum of someone with asbestosis?

Back 262

Fibers are coated by iron and protein. Macrophages phagocytose and coat the fibers with ferritin. There is a golden beaded appearance in the sputum of patients with asbestosis.

Front 263

What are some of the diseases you are likely to find in someone with asbestosis?

Back 263

Benign pleural plaques, Diffuse interstitial fibrosis with or without pleural effusions, Primary bronchogenic carcinoma, and malignant mesothelioma. There is NO increased risk for TB.

Front 264

What increases the risk (50-90%) of someone with asbestosis for developing Primary bronchogenic lung cancer. What are some complications in asbestosis that are shared with other Pneumoconioses?

Back 264

Smoking; Cor pulmonale and Caplan syndrome.

Front 265

Does malignant mesothelioma have an etiologic relationship with smoking? What part of the lung does this arise in? How long after first exposure does this occur?

Back 265

Malignant mesothelioma has no etiologic relationship with smoking. It arises from the serosa lining the pleura and encases and locally invades the subpleural lung tissue. It occurs 24-40 years after first exposure.

Front 266

What are the lesions associated with Berylliosis? How is someone put at risk of exposure? What diseases are you more likely to acquire?

Back 266

Diffuse interstitial fibrosis with noncaseating granulomas is seen in the lung tissue. Exposure most often occurs in the nuclear and aerospace industry. Patients with Berylliosis are at increased risk for developing Cor pulmonale and primary lung cancer.

Front 267

Describe what is thought to be the etiology of Sarcoidosis.

Back 267

It is thought that Sarcoidosis is a disorder of immune regulation with CD4 T-helper cells interacting with an unknown antigen. They release cytokines and cause the formation of noncaseating granulomas.

Front 268

Who is sarcoidosis common in?

Back 268

Blacks and non-smokers.

Front 269

Describe the primary target organ of Sarcoidosis, as well as the other organs that can be affected.

Back 269

Lungs are the primary target organ of Sarcoidosis, but skin lesions, eye lesions, and liver lesions can all be found.

Front 270

What is the most common, non-infectious granulomatous disease of the lungs?

Back 270

Sarcoidosis.

Front 271

How does Sarcoidosis affect the lungs? Describe the characteristic cells and inclusion bodies found.

Back 271

Sarcoidosis promotes granuloma formation in the interstitium and mediastinal and hilar nodes. The granulomas contain multinucleated Giant cells with laminated calcium concretions called Schaumann bodies and stellate inclusions called asteroid bodies.

Front 272

What is the most common non-infectious granulomatous disease of the liver?

Back 272

Sarcoidosis.

Front 273

Describe the three most characteristic findings of skin involvement in sarcoidosis.

Back 273

Nodular lesions containing granulomas, Violaceous rash occurs on the nose and cheeks (called Lupus pernio), and Erythema nodosum with painful nodules on the lower extremities and inflammation of subcutaneous fat.

Front 274

What type of Diabetes can be sometimes associated with Sarcoidosis?

Back 274

Diabetes insipidus.

Front 275

Describe the laboratory findings that might be associated with a patient with Sarcoidosis.

Back 275

Increase ACE enzyme (good marker), Hypercalcemia due to increased synthesis of 1-alpha-hydroxylase in granulomas (hypervitaminosis D), Polyclonal gammopathy, and cutaneous anergy to skin antigens due to consumption of CD4 T-helper cells in granulomas.

Front 276

What disease causes enlarged hilar and mediastinal lymph nodes called "potato nodes" as well as reticulonodular densities throughout the lung parenchyma?

Back 276

Sarcoidosis.

Front 277

Is Idiopathic Pulmonary fibrosis more common in women or men? Describe the pathogenesis. Does this fibrosis stenose or dilate airways? What is the characteristic appearance of the lungs due to this disease?

Back 277

Men. Repeated cycles of unexplained alveolitis involves cytokine release and produces interstitial fibrosis. Alveolar fibrosis leads to proximal dialtion of the small airways of the lung which leads to the characteristic. honeycomb appearance.

Front 278

What are the common collagen vascular diseases that can lead to interstitial fibrosis in the lung?

Back 278

Systemic Sclerosis, SLE, and Rheumatoid Arthritis.

Front 279

What is considered to be the cause of an unexplained pleural effusion in a young woman, until proven otherwise?

Back 279

SLE.

Front 280

What is the most common cause of death associated with Systemic Sclerosis?

Back 280

Pulmonary involvment; lung disease.

Front 281

Name the organism most likely responsible for Farmer's lung, which occurs when farmers are working with moldy hay.

Back 281

Saccharopolyspora rectivirgula, which is a thermophilic actinomycetes bacteria found in moldy hay.

Front 282

Explain the pathogenesis of Farmer's lung. Which type of antibodies are involved? Which type of hypersensitivity reactions are involved?

Back 282

Farmer's lung comes from exposure to actinomycetes found in moldy hay. Upon the first exposure the patient develops precipitating IgG antibodies. Upon the second exposure these antibodies combine with the inhaled allergens to form immune complexes (Type III hypersensitivity!), and these complexes produce inflammation in the lung. Chronic exposure produces granulomatous inflammation (Type IV hypersensitivity!)

Front 283

Describe the pathogenesis in Silo filler's disease.

Back 283

Here the culprit is the inhalation of gases (oxides of nitrogen) from plant material, which causes an immediate hyper sensitivity reaction associated with dyspnea.

Front 284

What causes the allergic reaction in Byssinosis? Describe the associated symptoms.

Back 284

Contact with cotton, linen, and hemp products cause dyspnea from exposure to antigens.

Front 285

Which drugs are associated with interstitial fibrosis?

Back 285

Amiodarone, Bleomycin and Busulfan, Cyclophosphamide, Methotraxate and Methysergide, Nitrosurea and Nitrofurantoin.

Front 286

Patients undergoing a certain type of cancer therapy exhibit this type of lung problem.

Back 286

Radiation for cancer can cause acute pneumonitits and chronic pnuemonitis.

Front 287

Emphysema targets which part of the lung in particular?

Back 287

Emphysema targets the respiratory unit.

Front 288

What are the two main causes of emphysema?

Back 288

Smoking and AAT deficiency.

Front 289

Describe the pathogenesis of emphysema in general terms of compliance and elasticity.

Back 289

Emphysema exhibits increased compliance and decreased elasticity.

Front 290

Describe how cigarette smoke exerts a pathogenic effect and leads to the development of emphysema.

Back 290

Cigarette smoke is chemotactic to neutrophils and macrophages. They accumulate in the respiratory unit and release free radicals and elastases. The free radicals in cigarette smoke actually inactivate AAT and antioxidants and produce functional AAT deficiency!!!

Front 291

Destruction of elastic tissue in the lung in the presence of emphysema causes the loss of what type of traction on the lung tissue?

Back 291

Radial traction.

Front 292

Which is the most common emphysema in smokers: Panacinar or Centriacinar?

Back 292

Centriacinar.

Front 293

Which parts of the lungs are most involved in Centriacinar emphysema? What are parts of the bronchial tree are targeted for elastic tissue destruction?

Back 293

The apical segments of the upper lobe are involved in Centriacinar emphysema. The distal terminal bronchioles and the respiratory bronchioles are the sites of elastic tissue destruction.

Front 294

Behind what level of the bronchial tree does air get trapped in Centriacinar emphysema? Which lung volumes are increased as a result?

Back 294

Air gets trapped behind the collapsed distal terminal bronchioles and distends the Respiratory bronchioles. The RV and TLC are increased as a result.

Front 295

What disease is Panacinar emphysema associated with? Is it an autosomal dominant or recessive disorder? What is the phenotype that leads to disease?

Back 295

Panacinar emphysema is associated with AAT deficiency. It is an autosomal dominant disorder. MM is a normal phenotype. ZZ has decreased synthesis of AAT by the liver.

Front 296

In Panacinar emphysema what parts of the lung are most affected? Which parts of the bronchiole tree? Where does air get trapped in the bronchiole tree?

Back 296

Panacinar emphysema primarily affects the lower lobes. Distal terminal bronchioles and all parts of the respiratory units are sites of elastic tissue destruction. Air gets trapped behind the terminal bronchioles and distends the entire respiratory unit.

Front 297

Why are breath sounds diminished in Emphysema?

Back 297

Breath sounds are diminished due to hyperinflation.

Front 298

Describe what you can expect to see on a Chest radiograph in a patient with emphysema.

Back 298

Hyperlucent lung fields, increased anteroposterior diameter, vertically oriented heart, depressed diaphragm due to hyperinflated lungs.

Front 299

What parts of the bronchiole tree does Paraseptal Emphysema affect? Does it produce COPD? What does it increase the risk of?

Back 299

Paraseptal emphysema primarily targets the alveolar ducts and alveoli. It does NOT produce COPD. It does, however, increase the incidence of spontaneous pneumothorax due to rupture of subpleural blebs.

Front 300

Describe Irregular Empysema. Does it produce COPD?

Back 300

Irregular Emphysema is a localized disease associated with scar tissue. It does NOT produce obstructive airway disease.

Front 301

Define Chronic Bronchitis.

Back 301

To have Chronic Bronchitis there must be the presence of a productive cough for at least 3 months for 2 consecutive years.

Front 302

What are the two most common causes of Chronic Bronchitis? Describe the pathogenesis.

Back 302

Smoking and Cystic Fibrosis. The pathogenesis occurs through hypersecretion of mucus in bronchi and subsequent obstruction to airflow in the terminal bronchioles (this obstruction is proximal to that seen in emphysema)

Front 303

What are the three best studied pathways that we know of to manipulate blood vessel in the lungs?

Back 303

Endothelin (constriciton), NO (dilation), Prostcyclin (dilation).

Front 304

What are the endothelial cell derived vasoconstrictors in the lungs? What channels do these pathways work through?

Back 304

Endothelin and serotonin; Voltage gated K+ channels.

Front 305

Why is there a build up of CO2 in patients with Chonic Bronchitis?

Back 305

Mucus plugs located in a proximal terminal bronchiole orevent the exodus of a large amount of CO2 arising from the distally located airways producing respiratory acidosis.

Front 306

Describe the changes in the bronchi that occur in Chronic bronchitis.

Back 306

Hypersecretion of submucosal mucus-secreting glands in trachea and bronchi, acute inflammation (neutrophils) often superimposed on chronic inflammation, loss of ciliated epithelium and presence of squamous metaplasia

Front 307

Describe the chest radiograph findings of Chronic bronchitis.

Back 307

Large, horizontally oriented heart, and increased bronchial markings.

Front 308

Are early dyspnea and later hypoxemia symptoms associated more with Emphysema or Chronic Bronchitis?

Back 308

Emphysema.

Front 309

Is late dyspnea and early hypoxemia more associated with Emphysema or Chronic Bronchitis?

Back 309

Chronic Bronchitis.

Front 310

Is an elevated blood pH and the absence of Cor pulmonale until the very advanced stages more associated with Emphysema or Chronic bronchitis?

Back 310

Emphysema.

Front 311

What are some potential reasons to think about why hypoxemia occurs early in patients with Asthma and Chronic Bronchitis versus, Emphysema?

Back 311

Because with Asthma and Chronic bronchitis air has trouble getting out, but it also has some trouble just getting in. With Emphysema air has a problem mostly with getting out which leads to problems with it getting in. Also, there is less V/Q mismatch occurring in Emphysema than there is in Chronic broncihitis or Asthma.

Front 312

Why are Cor pulmonale and pulmonary hypertension more of a problem in Chronic Bronchitis than in Emphysema?

Back 312

This is because there is greater levels of hypoxemia in Chronic bronchitis, which leads to greater amounts of vasoconstriction and resistance.

Front 313

What areas of the lungs does Asthma target?

Back 313

Bronchi and terminal bronchioles, where there is smooth muscle.

Front 314

What two types of Asthma exist?

Back 314

Extrinsic and Intrinsic.

Front 315

Describe the pathogenesis of Extrinsic Asthma.

Back 315

The pathogenesis of extrinsic asthma includes a Type 1 hypersensitivity reaction with exposure to extrinsic allergens. There is an initial sensitization to an inhaled allergen, and upon reexposure that inhaled allergen crosslinks IgE antibodies on mast cells on mucosal surfaces and causes the release of inflammatory cytokines. There is also a late phase reaction component that occurs 4-8 hours later.

Front 316

Explain the most important components of what takes place in the sensitization of a patient in Extrinsic Asthma, in terms of CD4 helper cells and Interleukins.

Back 316

In the initial sensitization to an inhaled allergen that will eventually produce Extrinsic asthma, there is induction of TH2 CD4+ cells that release IL-4 and IL-5. IL-4 is responsible for isotype switching to IgE production. IL-5 stimulates the production and activation of eosinophils.

Front 317

What chemotactic chemicals are produced during the Late Phase Reaction (4-8hrs) of Extrinsic Asthma and which inflammatory cells are called in?

Back 317

Eotaxin is produced and is chemotactic for, and activates, eosinophils. The Eosinophils are recruited to the site of allergen encounter and release major basic protein and cationic protein. This damages epithelial cells and produces airway constriction.

Front 318

Describe some of the histologic changes that occur in the bronchi of patients with Extrinsic Asthma.

Back 318

Upon inspection of the bronchial tissue there are observations of thickening of the basement membrane, edema and mixed inflammatory infiltrate, hypertrophy of submucosal glands, and hypertrophy/hyperplasia of smooth muscle cells.

Front 319

Describe some of the histological changes that occur in the terminal bronchioles of a person suffering from Extrinsic Asthma.

Back 319

The formation of spiral-shaped mucus plugs (Curschmann spirals due to desquamated epithelial cells), Charcot-Leyden crystals in eosinophils, patchy loss of epithelial cells, goblet cell metaplasia, thick basement membrane, smooth muscle hypertrophy and hyperplasia.

Front 320

How does asthma initially effect the blood pH.

Back 320

Asthma initially presents with alkalosis, later it can convert to acidosis if bronchospasm is not relieved.

Front 321

Describe some of the causes of Intrinsic (Nonimmune) Asthma.

Back 321

Virus-induced respiratory infection (rhino, parainflu, RSV), Air polluntants, NSAIDs, stress, exercise, cigarette smoke.

Front 322

Describe what happens to the lung tissue in Bronchiectasis.

Back 322

Permanent dilation of the bronchi and bronchioles due to destruction of cartilage and elastic tissue by chronic necrotizing infections. This most commonly occurs in the lower lobes and the dilated bronchi and bronchioles are filled with pus.

Front 323

What are some of the causes of Bronchiectasis?

Back 323

1) Cystic fibrosis (most common in the U.S.)
2) Infections (TB most common world-wide, but also Adeno, Staph, H.influenza)
3) Bronchial obstruction (proximally located bronchogenic carcinoma)
4) Primary ciliary dyskinesia (absent dynein in arm in cilia, which contains ATPase for movement of cilia
5) Allergic bronchopulmonary Aspergillosis

Front 324

Is there sputum production in Brochiectasis?

Back 324

Yes, cupfuls.

Front 325

Describe the most common gene mutation for CF and its mechanism of pathogenesis.

Back 325

There is a three nucleotide deletion mutation coding for a phenylalanine on chromosome 7 called DF508. This leads to the degredation of CFTR channel by the Golgi apparatus due to defective protein folding.

Front 326

What is the most common cause of death in CF patients?

Back 326

Death by infections.

Front 327

What secretions are dehydrated in CF patients?

Back 327

Secretions in bronchioles, pancreatic ducts, bile ducts, meconium, and seminal fluid.

Front 328

What are the 3 most common infections in CF patients?

Back 328

Pseudomonas, Staph aureus, H.influenza.

Front 329

What are some complications of CF that can occur due to the dehydrated secretions?

Back 329

Malabsorption (pancreatic exocrine deficiency), Type 1 Diabetes mellitus (due to chronic pancreatitis), Infertility in males, Meconium ileus, Secondary biliary cirrhosis.

Front 330

What is the most common cancer killer in both men and women?

Back 330

Primary Lung Cancer.

Front 331

What is the most common cause of lung cancer?

Back 331

Cigarette smoking.

Front 332

Name the top 5 most common Primary lung cancers in order of decreasing incidence.

Back 332

1) Adenocarcinoma
2) Squamous cell carcinoma
3) Small cell lung carcinoma
4) Large cell carcinoma
5) Bronchial carcinoid

Front 333

Which lung cancers have the greatest association with smoking? Where are they most commonly located in the lung?

Back 333

Squamous and small cell lung carcinomas. They are most commonly located centrally i.e. the main stem bronchus.

Front 334

Do adenocarcinomas have an association with smoking? Where do they generally occur in the lung?

Back 334

Adenocarcinomas have the weakest association to smoking of the top 5 lung cancers. The generally occur in the lung periphery.

Front 335

Describe what a "coin lesion" in the lung is. What is the most common cause of coin lesions?

Back 335

A solitary pulmonary nodule or coin lesion is the term applied to a peripheral lung nodule smaller than 5cm. Causes of a pulmonary nodule in descending order include granulomas (e.g. TB, histoplasmosis), malignancy (usually primary cancer), and a bronchial (chondroid) hamartoma.

Front 336

Describe the most common type of lung cancer.

Back 336

Metastatic cancer from the breast, then colon, then renal cell.

Front 337

What is the most common symptom in metastatic lung cancer? What is the most common symptom of primary lung cancer?

Back 337

Dyspnea; Cough

Front 338

Do Bronchial hamartomas more often occur peripherally or centrally in the lung?

Back 338

Peripherally

Front 339

Define which is more common in women and which is more common in men: 1) Adenocarcinoma 2) Squamous and small cell carcinoma

Back 339

Adenocarcinoma- women

Squamous and small cell- men

Front 340

Describe what a Pancoast tumor of the lung is? What syndrome can it cause if it starts to affect the superior cervical sympathetic ganglion?

Back 340

A pancoast tumor of the lungs is usually a primary squamous cancer located at the extreme apex of the lung. Destruction of the ganglion can produce Horner's syndrome = Ptosis, Miosis, Anhydrosis.

Front 341

What are some of the paraneoplastic syndromes found to be associated with lung tumors?

Back 341

Digital clubbing, Muscel weakness (Eaton-Lambert syndrome), Ectopic hormone secretion.

Front 342

Describe the most common site for primary tumor metastasis from the lung.

Back 342

The Hilar lymph nodes are the most common site. After that comes the adrenal glands, liver, brain, then bone.

Front 343

Which primary cancer of the lung have a worse prognosis: small cell or non-small cell?

Back 343

Small cell cancers have a worse prognosis than non-small cell cancers.

Front 344

If you find a malignant mediastinal mass in an older individual is the mass more likely to be primary or metastatic?

Back 344

Metastatic.

Front 345

If you find a malignant mediastinal mass in a younger individual is the mass more likely to be primary or metastatic?

Back 345

Primary.

Front 346

What compartment is the most common site for a mediastinal mass?

Back 346

The anterior compartment.

Front 347

Describe the most common primary mediastinal masses.

Back 347

In descending order: Neurogenic tumors (usually malignant in children and benign in adults), Thymomas, Primary Cysts, Malignant lymphomas (usually nodular sclerosing Hodgkin's lymphoma in a woman), Teratoma.

Front 348

What is a Thymoma? Is it usually benign or malignant? Does it consist of epithelial or lymphoid tissue?

Back 348

A thymoma is a tumor of the Thymus. They are normally benign (70%) and consist of epithelium and not lymphoid tissue. They may have a follicular B cell hyperplasia component (contributing to symptoms of myasthenia gravis) or may be associated with hypogammaglobulinemia.

Front 349

What syndrome involving the neuromusclar junctions is most commonly associated with Thymomas? Describe the pathogenesis of how the thymoma leads to this syndrome

Back 349

Myasthenia Gravis. This occurs when there is a follicular B-cell hyperplasia in the thymus and it becomes a site for synthesis of antiacetylcholine receptor antibodies.

Front 350

Describe the most common movement of fluid into the lungs from a pleural effusion. What are some of the most common causes of pleural effusion?

Back 350

The most common movement of pleural fluid comes from the parietal pleura into the pleural space and into the lungs. Common causes include increased hydrostatic pressure in the visceral pleura, decreased oncotic pressure, obstruction of lymphatic drainage from the visceral pleura, increased permeability of visceral pleural capillaries, metastasis to the pleura.

Front 351

What is the most common cause of Spontaneous pneumothrorax?

Back 351

The most common cause is Idiopathic, but other causes include Paraseptal emphysema and Marfan syndrome.

Front 352

Describe the pathogenesis of Spontaneous pneumothorax.

Back 352

An intrapleural bleb ruptures and the pleural cavity pressure rises to the same as atmospheric pressure. The negative intrathoracic pressure is lost and this causes a portion of the lung or the entire lung to collapse.

Front 353

What are the symptoms and clinical findings associated with Spontaneous pneumothorax?

Back 353

Sudden onset of dyspnea with pleuritic type of chest pain; Tympanitic percussion not, absent breath sounds, trachea deviated to the side of collapse.

Front 354

What type of atelectasis does Tension pneumothroax produce? When is there compromised venous return to the heart? What is the treatment?

Back 354

Compression atelectasis. There is compromised venous return to the heart if the left lung is invovled. The treatment is to stick a needle into the pleural cavity to relieve pressure.

Front 355

Which organism responsible for lung infection has the appearance of crushed ping pong balls?

Back 355

P.jiroveci

Front 356

Describe Bronchioloalveolar carcinomas. Where are they located? What type of cells are they? How do they grow?

Back 356

Bronchioloalveolar Carcinomas are peripheral (but intraparenchymal) masses with atypical epithelial cell growing along the framework of the lung.

Front 357

What tissue of the lung does a Hamartoma arise from? What tissue component is usually present?

Back 357

A Hamartoma is a peripheral intraparenchymal mass with a significant component of fibrous connective tissue and usually with cartilage present.

Front 358

What pleural sign is often associated with a metastatic malignancy?

Back 358

Bloody pleural effusion.

Front 359

Describe the type of pleural mass a malignant mesothelioma would form.What cytologic marker is commonly present with it?

Back 359

A malignant mesothelioma forms a pleural mass that is not well circumscribed. The cells are atypical and cytokeratin positive.

Front 360

What do the Charcot-Leyden crystals seen in sputum samples from persons suffering from Extrinsic asthmatic attacks represent? What about Curschmann spirals?

Back 360

These crystals represent the breakdown of products in eosinophilic granules. The Cruschmann spirals represent the whorls of sloughed off epithelium in the mucin.

Front 361

Why does smoking lead to emphysema? Describe the mechanism of pathogenesis.

Back 361

The inflammation that can accompany smoking leads to increased neutrophil elaboration of elastase, as well as the elaboration of macrophage elastase that is not inhibited by the antiprotease action of Alpha1-antitrypsin due to protein denaturing from smoking.

Front 362

What is Kartagener syndrome?

Back 362

When Dynein arms normally present in respiratory cilia are absent or abnormal.

Front 363

What type of inflammatory cells are pesent in Pneumoconioses? What do the T-cells release that activate the cells from the question above??

Back 363

Macrophage recruitment and activation by Interferon-Gamma released from T-cells is a feature of the chronic inflammatory conditions and pneumoconioses.

Front 364

When are Calcifications and Cavitations most commonly seen to be associated with TB infection?

Back 364

Calcification and cavitations are most commonly seen after reinfection or reactivation of tuberculosis infections in adults.

Front 365

What are clinical findings associated with primary TB infection?

Back 365

Lymphadenopathy or subpleural granuloma formation is more frequent in primary tuberculosis.

Front 366

Observations of a diffuse reticulonodular pattern suggests what type of TB?

Back 366

Miliary spreading TB.

Front 367

What is Acquired Pulmonary Alveolar Proteinosis? What autoantibody is characteristic this disease? Describe the etiology of the congenital form of this disease.

Back 367

Acquired Pulmonary Alveolar Proteinosis is an uncommon condition of unknown etiology characterized by autoantibodies against GM-CSF(Granulodcyte macrophage colony stimulating factor). Ten percent of PAP cases are congenital due to mutations in the granulocyte macrophage colony stimulating factor gene. Both forms of PAP have impaired surfactant clearance by alveolar macrophages.

Front 368

Anti-topoisomerase I antibodies indicate what disease that produces fibrosis of the lungs?

Back 368

Systemic Scleroderma.

Front 369

What autoantibodies are seen to be present in Goodpasture syndrome?

Back 369

Anti-glomerular basement membrane antibody is present in Goodpasture syndrome with extensive alveolar damage.

Front 370

What disease presents with anti-neutrophilic myeloperoxidase antibodies?

Back 370

Anti-neutrophil myeloperoxidase is a type of anti-neutrophil autoantibody seen in Wegener's granulomatosis.

Front 371

What type of paraneoplastic involving the level of a mineral in the blood might you see with Squamous cell carcinoma of the lung?

Back 371

Hypercalcemia.

Front 372

What paraneoplastic syndrome that may be associated with Small cell carcinoma of the lung produces symptoms of truncal obesity, backpain, easy bruisability and high blood pressure?

Back 372

Cushing syndrome, resulting from ectopic corticotropin production (most commonly from a pulmonary small cell carcinoma, but could also be a renal cell carcinoma), which drives the adrenal cortices to produce excess cortisol.

Front 373

Are Small cell carcinomas of the lung aggressive or treatable?

Back 373

Small cell carcinomas are aggressive tumors that tend to metastasize early. Even when they appear to be small and localized, they are not or will not remain so. Surgery is not an option for these patients and they are treated as if they have systemic disease (offers maybe an extra year). Cure is uncommon.

Front 374

Describe the type of inflammatory cells that can be expected to be found in adult ARDs. What type of inlfammatory processes and damage are taking place?

Back 374

ARDs is characterized by diffuse alveolar damage, initiated in most cases by injury to capillary endothelium by neutrophils and macrophage. Leukocytes aggregate in alveolar capillaries and realease toxic O2 metabolites, cytokines, and eicosinoids. Damage to the capilllary endothelium alows leakage of protein-rich fluids and eventually the overlying epithelium is also damaged.

Front 375

Describe the etiology and pathogenesis of Goodpasture syndrome.

Back 375

In Good Pasture syndrome pulmonary and renal lesions are produced by an antibody directed against an antigen common to the basement membrane in glomerulus and alveolus. This leads to a TYPE II HYPERSENSITIVITY reaction.

Front 376

Which ANCA is seen in Wegener's syndrome?

Back 376

C-ANCA.

Front 377

What disease exhibits the Gohn complex? What is it?

Back 377

The Ghon complex is a feature of Primary Tuberculosis which is most often a subclinical dsease of younger persons. The Ghon complex consists of a small subpleural granuloma with extensive hilar nodal caseating granulomas.

Front 378

Name two bacterial infections of the lungs that are particularly prevelant in patients with CF.

Back 378

Pseudomonas and Burkholderia

Front 379

What fungus may lead to vascular invasion and thrombosis, and cause pulmonary infarction as a result?

Back 379

Aspergillus.

Front 380

What type of lung injuries show hyaline membranes?

Back 380

Acute lung injuries can produce Hyaline membranes due to diffuse alveolar damage.

Front 381

What type of cancer are most paraneoplastic syndromes associated with in the lungs? Which paraneoplasic syndrome is an exception to this rule above?

Back 381

Small cell anaplastic (oat cell) carcinomas. Hypercalcemia is an exception to that rule- this is most commonly cause by Squamous cell carcinoma.

Front 382

What do fluffy infiltrates in the lung suggest?

Back 382

An infectious process.

Front 383

What are upper lobe lung cavitations associated with?

Back 383

A secondary tuberculosis infection.

Front 384

Daphragmatic pleural plaques can be a feature of what restrictive lung disease?

Back 384

Pneumoconioses, in particular asbestos.

Front 385

A subpleural nodule with hilar adenopathy is classic for what disease?

Back 385

The Ghon complex and primary TB.

Front 386

What does an air-fluid level suggest in the lung?

Back 386

This suggests liquefaction in an abscess.

Front 387

What are two large cell carcinomas in the lung that are generally found peripherally and are not generally associated with paraneoplastic syndromes?

Back 387

Adenocarcinoma and bronchioalveolar carcinoma.

Front 388

Describe the fundamental abnormality in Intrinsic Asthma.

Back 388

The fundamental abnormality is bronchial hyperresponsiveness (i.e. the threshold of bronchial spasm is intrinsically low).

Front 389

In hypersensitive pneumonitis, what type of hypersensitivity reactions do we see?

Back 389

Type III hypersensitivity reaction followed by a Type IV hypersensitivity reaction.

Front 390

When a lung infection is suspected what is GMS stain good for identifying?

Back 390

Pneumocystis jiroveci and fungi.

Front 391

What doe Asbestos fibers become encrusted with in the lung tissue?

Back 391

Iron and calcium.

Front 392

What causes the lung characteristic described as "Honeycomb lung"?

Back 392

The progressive pulmonary interstitial fibrosis of a restrictive lung disease such as pneumoconiosis can eventually lead to dilation of remaining airspaces, giving a "honeycomb" appearance. After the diffuse alveolar damage associated with ARDs, if patients survive for weeks, the diffuse alveolar damage may resolve to honeycomb change.

Front 393

In talking about lung disease what are the terms Honeycomb lung and velcro rales/dry crackles essentially synonymous with?

Back 393

Fibrosis.

Front 394

If Scleroderma is causing lung disease what other ogran system will also likely be involved?

Back 394

The Skin.

Front 395

With Goodpasture syndrome, is the onset of hemoptysis slow and progressive or acute and sudden?

Back 395

Acute and sudden.

Front 396

What condtion do the acronyms BOOP and COP refer to? Describe its histological picture.

Back 396

Bronichiolitis Obliterans with Organizing Pneumonia (or Cryptogenic Organizing Pneumonia) is an uncommon, non-specific reaction to a lung injury such as an infection or toxic exposure. A chest radiograph may show bilateral patchy, small alveolar opacities and a chest CT may show small scattered ground glass nodular opacities. A transbronchial biopsy may display polypoid plugs of loose fibrous tissue and granulation tissue filling bronchioles, along with a surrounding interstitial infiltrate of mononuclear cells. The condition may be relieved by corticosteroids.

Front 397

What is DIP and what is it related to? What kind of inflammatory cells are involved?

Back 397

DIP stands for desquamative interstitial pneumonitis. It is an uncommon smoking related interstitial disease in which monocytes gather together to form intra-alveolar macrophages.

Front 398

Describe some characteristic features of Bronchoalveolar carcinoma and distinguish it from Adenocarcinoma and Large cell carcinoma of the lungs.

Back 398

Bronchoalveolar carcinoma is a peripheral tumor that can mimic atypical pneumonia. Most of these tumors are well differentiated and tend to procduce a localized mass. Whereas, Adenocarcinomas and Large cell carcinomas of the lungs are also peripheral, but tend to be large and pleomorphic and form sheets.

Front 399

Give a brief description of adenocarcinoma of the lung and how it is treated.

Back 399

Primary adenocarcinomas in the lung tend to be small peripheral masses that are amenable to surgical excision and have a better overall prognosis than other forms of lung cancer.

Front 400

Describe the appearance and growth pattern of Bronchioalveolar carcinoma.

Back 400

Bronchioalveolar carcinomas are peripheral masses with a distinctive appearance of neoplastic cells proliferating along the alveolar and bronchiolar framework.

Front 401

Are localized mesotheliomas related to asbestos exposure?

Back 401

No, localized mesotheliomas are not related to asbestos exposure and are pedunculated masses attached to the pleura.

Front 402

What are key clinical findings that point to a diagnosis of Sarcoidosis? Describe the inflammatory process that underlies this disease.

Back 402

Sarcoidosis will often present with prominent hilar lymphadenopathy, reticulonodular infiltrates bylaterally, and microscopic findings will include interstitial fibrosis and small, non-caseating granulomas (asteroid bodies can be a buzz-word). This granulomatous diseasae has an unknown cause, but the presence of granulomas and activated T-cells in the lungs indicates a delayed hypersensitivity response to some inhaled antigen.

Front 403

Describe the most common gene mutation and pathophysiology behind Idopathic Pulmonary Hypertension.

Back 403

Gene mutation often occurs in BMPR2. Bone Morphogenic Receptor 2 (BMPR2), is a surface protein belonging to the TGF-B receptor superfamily and normally stops proliferation of vascular smooth muscle and favors apoptosis. In the absence of BMPR2 smooth muscle proliferation occurs and hypertension ensues.

Front 404

Are hamartomas of the lung generally central or peripheral?

Back 404

Peripheral.

Front 405

What stain can we use to visualize Legionella?

Back 405

Dieterle Silver Stain.

Front 406

The pathogenesis of emphysema may be thought of in terms of a balance problem between what two types of proteins? Where does the prototypical example of each type come from?

Back 406

It is thought to be an imbalance between elastases and antiproteases. Neutrophil elastase and AAT(antiprotease) from the liver.

Front 407

Why can cigarette smoking cause a functional AAT deficency?

Back 407

Because smoking stimulates Macrophage to release IL-8 and recruit Neutrophils, which release O2 radicals that inhibit AAT. Oxidants in cigarette smoke also inhibit AAT.

Front 408

Cigarette smoke activates macrophage and recruits neutrophils. How does AAT work differently on the elastases from each?

Back 408

AAT does not work on Macrophage elastases, whereas it does on Neutrophil elastases.

Front 409

Describe the histological findings in Chronic bronchitis that explain the excessive mucus production.

Back 409

There is hypersecretion of mucus due to hypertrophy and hyperplasia of submucosal glands and increases in goblet cells

Front 410

Which is more likely to lead to Cor pulmonale: Emphysema or Chronic bronchitis?

Back 410

Chronic bronchitis.

Front 411

Compare and contrast the destruction of lung structures in Centriacinar vs. Panacinar emphysema.

Back 411

In Centrilobular emphysema destruction is confined to the terminal bronchioles and the respiratory bronchioles. In Panacinar emphysema the peripheral alveoli are also involved.

Front 412

Describe the acute reaction mediator molecules in extrinsic asthma.

Back 412

Histamine, Leukotrienes B4 (chemotactic for neuts. and esoins.) Leukotriene C4, D4, E4, Prostaglandin D2, and PAF.

Front 413

Describe the late phase (4-8hrs.) reaction mediator molecules in extrinsic asthma.

Back 413

Major basic protein, eotaxin.

Front 414

What two features will be present in a patient who has Aspirin induced asthma?

Back 414

Recurrent rhinitis, and nasal polyps.

Front 415

Describe the features are conditions of the lung associated with Kartagener's syndrome.

Back 415

Structural ciliary abnormalities with the absence of dynein arms, bronchiectasis, sinusitis, situs inversus, females can be infertile.

Front 416

Which two primary cancers of the lung are most closely associated with smoking?

Back 416

Squamous cell carcinoma and small cell carcinoma.

Front 417

What type of cells are small cell carcinomas of the lung usually derived from? How big are they? Are they easily detectable early?

Back 417

Small cell carcinomas of the lung are derived from bronchial neuroendocrine cells. The tumor is comprised of small cells about 2-3x the size of a lymphocyte, with very little cytoplasm and numerous mitotic figures. These tumors are centrally located and are very aggressive, usually having metastasized widely at the time of presentation.

Front 418

Which lung tumor is most often associated with paraneoplastic syndromes?

Back 418

Small (oat) cell carcinoma.

Front 419

What two conditions can a lung tumor that obstructs an airway cause?

Back 419

Post-obstructive pneumonia and bronchiectasis.

Front 420

What is superior vena cava syndrome and what causes it?

Back 420

A tumor may compress the vena cava resulting in venous congestion with resultant edema of the head and arams with ultimate circulatory compromise.

Front 421

What are two paraneooplastic syndromes commonly cause by small cell carcinoma of the lungs?

Back 421

Hyponatremia (ADH secretion), and Cushing's syndrome (ACTH secretion)

Front 422

What paraneoplastic syndrome is mostly produced from squamous cell tumors of the lung?

Back 422

Hypercalcemia.

Front 423

Describe Eaton-Lambert syndrome.

Back 423

Eaton-Lambert syndrome is Myasthenia Gravis produced by tumor production of neuronal antibodies. This is seen primarily with Small cell carcinomas.

Front 424

What are the similarities and differences of Carcinoid and Small cell tumors of the lung?

Back 424

They both arise from bronchial neuroendocrine cell lines, but the Carcinoid tumors are much more indolent than Small cell tumors. They also are the most common lung tumor in young patients and are not associated with smoking.

Front 425

Where in the lung do metastatic cancers often show up? Do they show up as singular or multiple lesions?

Back 425

They often show up in the periphery and present as multiple nodules. This is in contrast to the single, frequently central presentation of a primary lung tumor.

Front 426

Describe some of the nerves that can be effected by nerve entrapment syndrome associated with lung tumors.

Back 426

Recurrent laryngeal nerve (hoarseness), Phrenic nerve (diaphragmatic paralysis), sympathetic system (horner syndrome), brachial plexus (brachial plexopathy from "superior sulcus" tumors)

Front 427

Describe some of the nerves that can be effected by nerve entrapment syndrome associated with lung tumors.

Back 427

Recurrent laryngeal nerve (hoarseness), Phrenic nerve (diaphragmatic paralysis), sympathetic system (horner syndrome), brachial plexus (brachial plexopathy from "superior sulcus" tumors)

Front 428

What are the most common causes of Aspiration pneumonia? This type of pneumonia lends itself to formation of what in the lungs?

Back 428

Bacteriodies, Prevotella, Fusobacterium, and Peptostreptococcus. This type of pneumonia is prone to ABSCESS formation in the lungs.

Front 429

What are the most common causes of Chronic pneumonia?

Back 429

TB, atypical mycobacteria, Hitsoplasma, Coccidiodies, Blastomyces dermatiditis, Actinomyces, Nocardia.

Front 430

What microbial pathogens must be considered in the cause of pneumonia of immunocompromised patients in addition to all those that would be causes in immunocompetent patients?

Back 430

Cytomegalovirus, Pneumocystis jiroveci, MAC, Invasive Apsergillosis, Invasive Candidiasis, Pesudomonas, Legionella, HSV, LIsteria, Cryptococcus.

Front 431

Name the two most common bacterial infections to complicate COPD.

Back 431

H.influenzae and Morexella

Front 432

What organ might Legionella affect in addition to the lungs?

Back 432

The Kidneys (hyponatremia)

Front 433

What are factors that contribute to bronchopneumonia?

Back 433

Loss of cough reflex, injury to mucociliary escalator, congestion and pulmonary edema, accumulation of secretions distal to obstruction, interference with function of alveolar macrophages

Front 434

What are the most common isolates found in bronchopneumonia?

Back 434

Staphylococcus and Gram (-) rods.

Front 435

Klebsiella can cause lobar pneumonia like Strep pneumoniae. What sputum characteristic will Klebsiella present with that Strep will not?

Back 435

Mucoid sputum, because Klebsiella has produces a thick mucoid capsule.

Front 436

Describe the four stages of pneumonia development.

Back 436

1. Congestion
2. Red hepatization
3. Grey hepatization
4. Resolution

Front 437

Name three bacteria that are not from the oral cavity that tend to form abscesses in lung infections.

Back 437

Pneumococcus type 3, Staph, and Klebsiella.

Front 438

Describe some complications of lung abscesses.

Back 438

Brain abscesses, clubbing of the fingers, and secondary amyloidosis.

Front 439

How does Legionella infection stain with Gram stain when you are biopsying lung tissue?

Back 439

Legionella stains poorly with Gram stain and is best identified by Silver Stain.

Front 440

What are two water-loving bacteria that we know about that can cause lung infections?

Back 440

Pesudomonas and Legionella.

Front 441

What type of lung infection can present with increased serum cold agglutination titers?

Back 441

Atypical Pneumonias.

Front 442

Pneumocystis pneumonia often occurs in immunocompromised patients and has frequent concurrent infection with what other microbe?

Back 442

CMV.

Front 443

Most often Histoplasmosis infection of the lungs looks a lot like the work up for that of TB, but infection can also spread to the whole body. How does Disseminated histoplasmosis occur, what type of patients are usually affected, and what or systems are prefered?

Back 443

Disseminated histoplasmosis normally occurs in immunocompromised patients. Granulomas are not formed, but instead numerous macrophages packed with yeast organisms are disseminated throughout the body. Organs of the reticuloendothelial system are preferentially involved such as lymph nodes, bone marrow, and spleen.

Front 444

What type of immunity is important in Tuberculosis infection?

Back 444

Cell mediated immunity.

Front 445

What does a positive Purified Protein Derivative (PPD) test indicate?

Back 445

It indicates infection, but not necessarily disease.

Front 446

What type of hypersensitivity reaction gives rise to the granuloma formation seen in TB?

Back 446

Type IV hypersensitivity.

Front 447

What type of T-cell pathway is involved in pathogenesis of TB infection? Explain the process of granuloma formation.

Back 447

TH1, CD4+. The APC presents antigen to the CD4+ TH1 cell in the context of Class II MHC. The APC also releases IL-12 which activates the TH1 cell. The TH1 cell releases IL-2 which acts back on itself and TNF & IFN-y which recruit and activate monocytes respectively. The activated monocytes lead to walling off of the infection and granuloma formation.

Front 448

What cells are present in the TB granuloma?

Back 448

Giant cell, epitheliod cells,monocytes, fibroblasts, lymphocytes, and macrophages.

Front 449

Is primary TB infection more likely to occur in the middle or upper part of the lung? What about reactivation/reinfection/secondary TB

Back 449

The middle part of the lung. Reactivation TB happens in the upper part of the lung.

Front 450

What puts a person at risk for progressing to Active Tuberculosis if they get infected?

Back 450

Conditions that put the lung in a compromised state (e.g. Silicosis, Diabetes), and conditions that compromise the immune system (e.g. Heme malignancies, anatomically proximal Carcinomas, corticosteroids, malabsorption syndromes)

Front 451

The Ghon complex is an indication of what type of TB infection?

Back 451

Primary infection. It happens when the bacteria spread to the regional draining lymphnodes form a primary complex that heals with calcification and fibrosis. This healed lesion is the Ghon complex.

Front 452

Name some of the sites that Miliary Tuberculosis infection can spread to.

Back 452

Meninges, Vertebrae, Lymphnodes, Lungs, Liver, Spleen, Adrenals, Joints and long bones.

Front 453

What are some complications of Tuberculosis?

Back 453

Fungus ball, secondary amyloidosis, Addison's disease, Hyphosis, Basal fibrosing meningitis, Mononarticular arthritis, Tuberculomas of the CNS.

Front 454

What are some of the factor that put someone at risk for Pulmonary Embolism?

Back 454

Hypercoagulable states, recent surgery, cancer, pregnancy, obesity, indweling venous lines.

Front 455

How are pulmonary emboli detected?

Back 455

Perfusion lung scan.

Front 456

What are the three main causes of ARDS?

Back 456

Pulmonary infections, sepsis, and following major trauma.

Front 457

What are the proinflammatory cytokines that Macrophage use to recruit neutrophils to areas of injury in the lung?

Back 457

IL-8, IL-1, and TNF.

Front 458

What are the factors released by neutrophils that cause lung damage in ARDS?

Back 458

Leukotrienes, oxidants, proteases, and platelet activating factor (PAF) contribute to local tissue damage, accumulation of edema fluid in the airspaces, surfactant inactivation and hyaline membrane formation.;

Front 459

What are the macrophage derived growth factors that sustain their own activation? What factors are fibrogenic?

Back 459

Macrophage inhibitory factor (MIF) sustains the pro-inflammatory response. TGF-B and PDGF stimulate fibroblast growth and collagen deposition.

Front 460

What is the definition of organizing pneumonia?

Back 460

When loose plugs of fibroelastic tissue fill alveolar spaces.

Front 461

What is the treatment and prognosis for BOOP/COP?

Back 461

The treatment is corticosteroid therapy and the outcome is excellent.

Front 462

Describe the most common causes of interstitial lung diseases.

Back 462

Environmental agents (e.g. pneumonconioses), Sarcoidosis, Idiopathic Pulmonary Fibrosis, and those associated with Collagen Vascular Diseases.

Front 463

What clinical (not histological) signs and symptoms might a patient present with who is suffering from progressive Sarcoidosis? What is the demographic most affected?

Back 463

Patients typically present with fever, night sweats, (fatigue and weight loss may occur), CXRay shows pulmonary infiltrates and BILATERAL HILAR LYMPHADENOPATHY, and sometimes an elevated ACE level. Black women from the Southeastern U.S. have the highest incidence of this disease.

Front 464

What kind of diagnosis is Sarcoidosis?

Back 464

Sarcoidosis is a diagnosis of exclusion.

Front 465

Which fibrotic lung disease exhibits Temporal Heterogeneity (i.e. the fibrosis is patchy and is of varying ages) with variable fibrosis?

Back 465

Idiopathic interstitial fibrosis. Temporal heterogeneity is maniffested by areas of dense collagen (OLD) appearing adjacent to areas of fibroblastic tissue (NEW). The fibroblastic foci represent areas of active injury. Inflammatory cells are generally not prominent.

Front 466

What is the name for the histologic pattern seen on lung biopsy corresponding to a clinical diagnosis of IPF?

Back 466

Usual Interstitial Pneumonia (UIP).

Front 467

Describe the treatment and prognosis for patients with Idiopathic Interstitial Fibrosis (IPF).

Back 467

Treatment with corticosteroids is attempted and people often respond poorly. The disease is ultimately fatal with a median survival of 4-5 years.

Front 468

Name the signaling pathway that has a vague association with IPF and the progression of fibrosis.

Back 468

The Wnt-B-Catenin pathway in the mesenchymal cells of the fibro-proliferative lesions.

Front 469

What is Desquamative Interstitial Pneumonia (DIP)? Describe the histological picture of the lung. What is the treatment and prognosis for this disease?

Back 469

DIP is a disease of thought to be a disease of smokers as over 90% of those who acquire this disease are smokers. Histologically we see diffuse filling of airspaces with alveolar macrophages accompanied by interstitial fibrosis. Outcome is excellent and nearly all cases respond to steroid therapy and cessation of smoking.

Front 470

Who gets Lymphocytic Interstitial Pneumonia (LIP)?

Back 470

LIP is seen primarily in children with HIV or in adults with HIV or Sjogren's syndrome.

Front 471

What interstitial pneumonia shows diffuse interstitial expansion by lymphocytes and plasma cells, massive alveolar wall expansion, variable amounts of fibrosis, and presents mostly in children with HIV or adults with HIV or Sjogren's syndrome?

Back 471

Lymphocytic Interstitial Pneumonia.

Front 472

Describe the classic Triad of Chronic Hypersensitivity Pneumonitis. What does the hypersensitivity result from?

Back 472

Bronchocentric chronic inflammation/fibrosis, organizing pneumonia, and poorly formed granulomas. Hypersensitivity results from the inhalation of organinc dusts containing thermophilic bacteria, true fungi, animal proteins or bacterial products.

Front 473

How do Bleomycin, Methotrexate, and Amiodarone cause problems in the lungs? Briefly describe each of their mechanisms

Back 473

Bleomycin- results in interstitial inflammation and fibrosis due to direct toxicity.

Methotrexate- produces a similar reaction although typically provokes a mild granulomatous response

Amiodarone- also causes pulmonary fibrosis and is often associated with an accumulation of peculiar foamy appearing macrophages.

Front 474

Which collagen vascular disease presents with lung involvement in the form of BOOP, an interstitial fibrosis with UIP, and Caplan's syndrome?

Back 474

Rheumatoid athritis; there are also commonly rheumatoid nodules and pleuritis present.

Front 475

This collagen vascular disease presents with DAD and intra-alveolar hemorrhage with interstitial fibrosis.

Back 475

Systemic Lupus Erythematosus.

Front 476

This is a collagen vascular disease that has lung involvement most similar to IPF with UIP.

Back 476

Scleroderma.

Front 477

Sjogren's syndrome presets with what type of characterized lung invovlment?

Back 477

Pleuritis, Lymphocytic Interstitial Pneumonia (LIP), and lymphoma. These lung findings can also present in children with HIV and adults with HIV.

Front 478

What is the antigen associated with Goodpasture syndrome? Depostition of what can be seen along the alveolar walls?

Back 478

Goodpasture antigen is a peptide in the non-collagenous portion of the alpha chain of Type IV collagen. In Goodpasture's linear deposits of immunoglobulins can be seen along the alveolar walls.

Front 479

What histological feature do both Goodpasture's syndrome and Idiopathic Pulmonary Hemosiderosis share?

Back 479

Findings include filling of alveoli with hemosiderin-ladden macrophages and variable degrees of pulmonary fibrosis.

Front 480

How do you treat Goodpasture's syndrome?

Back 480

Plasma exchange and steroid therapy.

Front 481

Describe the classic triad for Wegener's sndrome.

Back 481

1. Acute necrotizing granulomas of the upper respiratory tract (usually sinuses) and lung.

2. Necrotizing/granulomatous vasculitis

3. Renal disease usually in the form of crescentic glomerulonephritis.

Front 482

Churg-Strauss Syndrome looks like what other condition? How does it differ?

Back 482

Wegener's syndrome. Chrug-Strauss is similar to Wegener's syndrome in the presence of necrotizing granulomas and vasculitis histoogically, however Churg-Strauss also demonstrates EOSINOPHILIA!. Heart, skin, spleen, and peripheral nerves are often involved. Renal disease is UNCOMMON, and it is associated with p-ANCA instead.

Front 483

What is secondary PAP (Pulmonary Alveolar Proteinosis) associated with? Which antibody?

Back 483

Acute silicosis, immunodeficiency, malignancies, and hematopoetic disorders. It is also associated with anti-GM-CSF antiobodies.

Front 484

Explain how the Quantiferon-TB Gold Test works.

Back 484

This detects release of Interferon-Gamma when it is incubated with mixtures of synthetic in M.tuberculosis: ESAT-6 and CFP-10. These proteins are absent from all Bacille Calmette Guerin (BCG) vaccine strains and this test is more specific than the tuberculin test. This test can detect either latent or active infection.

Front 485

What are some of the etiologies of Anterior Superior Mediastinal tumors?

Back 485

Thymomas or thymic cysts, Thyroid lesions, teratomas, germ cells tumors, malignant lymphomas, and parathyroid lesions.

Front 486

What are some of the etiologies of MIddle Mediastinal tumors?

Back 486

Malignant lymphoma, pericardial cysts, bronchogenic and foregut cysts.

Front 487

What are some of the etiologies of Posterior Mediastinal tumors?

Back 487

Neurogenic tumors; and gastro enteric cysts

Front 488

What are the conditions that might cause an inflammatory pleural effusion?

Back 488

Inflammatory lung disease, lung infarct, connective tissue disease, uremia, and metastatic carcinoma.

Front 489

Define empyema.

Back 489

Empyema is purulent pleural exudate.

Front 490

What conditions might cause hemorrhagic pleural effusions?

Back 490

Tuberculous disease, neoplastic involvement of the pleura, or trauma, bleeding diathesis.`

Front 491

What injuries might cause Hemothorax?

Back 491

Hemothorax may be secondary to trauma, or ruptured aortic aneurysm.

Front 492

Describe the type of injuries that could cause Chylothorax.

Back 492

Chylothorax is milky fluid of lymphatic origin. This is often secondary to thoracic duct trauma or obstruction by tumor

Front 493

Describe the types of diseases/conditions that may increase the risk of spontaneous pneumothorax.

Back 493

Any form of disease that causes rupture of the alveolus may increase the risk of spontaneous pneumothorax. Thus, spontaneous pneumothorax may be secondary to interstitial emphysema, bullous emphysema, asthma, tuberculosis, abscess, and trauma.

Front 494

Which asbestos fibers are more pathogenic for mesotheliomas, serpentine (chrysotile), or amphibole (crocidolite)? Which is more fibrogenic?

Back 494

Amphibole (Crocidolite) are more pathogenic for mesotheliomas. Both are fibrogenic, with a dose-respose correlation for fibrogenesis.

Front 495

What stain is used to visualize AAT bodies in liver tissue with AAT deficiency?

Back 495

PAS.

Front 496

Describe the most common type of laryngeal carcinoma.

Back 496

Glottic Squamous Cell Carcinoma

Front 497

What are likely precancerous lesions seen preceding Gotting Squamous Cell Carcinoma?

Back 497

Squamous cell hyperplasia with dyplasia and hyperkeratosis.

Front 498

Do patients with subglottic laryngeal carcinomas present with hoarseness? Describe their symptomatology. Are lymph nodes often invovled?

Back 498

Patients usually do not present with hoarseness. Symptomatology may be late with acute onset of laryngeal obstruction requiring emergency tracheostomy. Approximetly 50% of cases have positive paratracheal lymph nodes which are not clinically apparent prior to resection.

Front 499

Do patients with supraglottic tumors present with changes in their voice? What functional complaints might they have? How do they grow?

Back 499

Presenting complaints are related to change in quality of voice. Dysphagia and odynophagia are additional common presenting complaints. They rarely grow inferior but instead typically grow upward or superior

Front 500

What is the overall 5 year survival of glottic tumors ? Subglottic tumors ?

Back 500

80%, 40%

Front 501

Which type of laryngeal carcinoma is a well differentiated squamous cell carcinoma with prominent keratinization , has wart-like features, and is locally aggressive without significant metastatic potential ?

Back 501

Papillary (exophytic) squamous cell carcinoma.

Front 502

What type of laryngeal growth has been associated with Epstein-Barr virus?

Back 502

Lymphoepithelioma.

Front 503

Can laryngeal papilomas become malignant?

Back 503

Squamous cell carcinoma arising in laryngeal papillomas occurs but is a rare event.

Front 504

Do solitary papillomas respond well to surgical excision or do they respond agressively? What is the prognosis after surgical excision? In adults, who gets papillomas more frequently, men or women?

Back 504

Solitary adult and solitary juvenile forms are less aggressive and are usually cured after single surgical excision. Juvenile and adults with multiple papillomas have guarded prognoses due to unpredictable multiple recurrences. The adult form is seen predominently in males.

Front 505

Describe Laryngeal papillomas. Who gets them and what does their histology look lilke? Is there a difference between those that occur in adults and children?

Back 505

Though it occurs and is a medical emergency, only a minority of patients develop acute respiratory distress secondary to laryngeal obstruction. The juvenile form is seen equally among males and females. The majority of patients with the multiple form of papillomas develop dysplasia leading to squamous cell carcinoma. The majority of cases of juvenile papillomatosis present at less than 7 years of age. Retrograde extension done the tracheobronchial tree into alveoli rarely occurs. The histological features of the juvenile form and adult form are indistinguishable. Delicate fibrovascular stalks are lined by stratified maturing squamous epithelium. Dysplasia and/or koilocytotic squamous atypia may be observed

Front 506

What three bacterial pathogens in particular can be responsible for consolidating lobar pneumonia?

Back 506

s.pneumo, Klebsiella, and Legionella.

Front 507

What organism tends to "cuff" blood vessels in the lung and produce a hemorrhagic necrotizing pneumonia?

Back 507

Pseudomonas aeruginosa.

Front 508

What are the two pseudos associated with Candida?

Back 508

Pseudohyphae and Pseudomembranes.

Front 509

Where dose Langerhans histiocytosis typically evolve in the lung?

Back 509

Centrilobular areas. This is a celluar fibrotic process. This destroys airways and produces airtrapped cysts distal to the areas off involvement and patients are prone to recurrent pneumothorax.