Pulmonary: Obstructive Lung Diseases

Front 1

All Obstructive lung diseases regardless of cause, are characterized by:

2-3) In ALL obstructive lung disease the _____2______ a ratio is below its normal value of ____3____%.

Back 1

1)decreased expiratory airflow
2) FEV1/FVC

Front 2

Lung Compliance changes:
1) Emphysema
2) Chronic Bronchitis
3) Asthma

Back 2

1) Increased
2) Normal
3) Normal

Front 3

In Obstructive Lung Disease, how does the
1) FRC change?
2) Residual capacity change?
3) Why does this happen in chronic bronchitis and asthma?
4) Why does this happen in Emphysema
5) Provide another mechanism of change in RC and FRC common to all three disorders.

Back 3

1) Increase
2) Increase
3) Narrowing of the larger airway lumen
4) Decrease of tethering of the small airways by alveoli
5) SOB causes tachypnea which decreased amount of expiratory time.

Front 4

Air trapped in the lungs by Obstructive diseases has both positive and negative consequenced.
1) Name one positive consequence
2-4) name three negative consequences

Back 4

1) Enlarged resting volume (FRC) distedns airways decreasing resistnace to flow and decreasing burden on muscles respiration
2) Inspiring at high FRC requires more inspiratory forcef due to the non-linear characteristics of the lung P-V curve.
3) Increased distension of the chest wall signal dyspnea
4) Flattened diaphragm loses leverage on the chest wall .

Front 5

1) Which of the three obstructive diseases shows increased TLC.
2) WHat property of this disease makes this possible?

Back 5

1) Emphysema
2) Increased compliance shifts balance of lung volume towards the recoil pressure of the chest wall

Front 6

1) How does the RV/TLC ratio change in Obstructive Lung disease?

Back 6

Increases because Air has trouble being pushed out. Especially true in Emphysema because along with V going up, TLC is also larger.

Front 7

1) What is the normal change in FEV1 per year?
3) What is this number in obstructive lung disease?

Back 7

1) Decrease 30ml/year
2) Decrease about 60 ml/year

Front 8

1) Chronic airway obstruction in larger airways is?
2) Chronic airway obstruction in the smaller airways is?

Back 8

1) Chronic Bronchitis (or asthma i guess)
2) Emphysema

Front 9

In terms of emphysema vs chronic bronchitis, most patients have...

Back 9

a mix

Front 10

Define Chronic Bronchitis

Back 10

Hypersecretion of mucus sufficient to cause cough and expectoration on most days for at least three months of the year over two successive years.

Front 11

Obstruction in chronic bronchitis is due to narrowing of the airways by___1___ and ___2___

Back 11

1) mucous
2) Inflammation

Front 12

1) Define The Reid Index
2) In what disease is it increased?
3) What functional process does it define and where does this occur?

Back 12

1) Ratio of bronchial gland thickness to bronchial wall thickness
2) Chronic bronchitis
3) Mucous gland hypertrophy and hyperplasia in the cartilaginous bronchioles.

Front 13

in Chronic bronchitis, describe the pathology seen in the small airways

Back 13

mucous plugging
mural fibrosis
narrowing
goblet cell hyperplasia
inflammatory cell infiltrates
(neutrophil, mac, lymphocytes)

Front 14

Emphysema is characterized by enlargement of the airways distal to the ____1___ and destruction of __2__.
(two synonymous terms)

Back 14

1) non-respiratory bronchioles
Terminal bronchioles
2) alvoelar walls

Front 15

An obstructive disease where involving the lung parenchyma and not the bronchioles.

Back 15

Emphysema

Front 16

1) Why do small airways collapse in emphysema?
2) Why are the bronchioles unaffected?

Back 16

1) Reduced tethering by alveolar walls
2) They contain rigid cartilage

Front 17

1) The PRIMARY cause of COPD is?
2) Other causes include (3)

Back 17

1)Cigarette smoking
2) air pollution, inadequately treated asthma, AAT deficiency

Front 18

Alpha-1 antitrypsin deficiency:
1) Is associated with what allele?
2) What is the normal allele
3) Which enzyme is inhibited by AAT normally?
4) What specific disease is caused by AAT deficiency
5) What additional risk factors contribute to development of this disease in the AAT deficient person

Back 18

1) Z
2) M
3) Neutrophil elastase.
4) Panacinar Emphysema
5) Cigarettes, dusty occupational exsposure, parental Hx of COPD

Front 19

1) Pink puffer is?
2) Blue bloater is?

Back 19

1) emphysema
2) Chronic Bronchitis

Front 20

1) What is the V/Q relationship in emphysema?
2) Why?

Back 20

1) Normal
2) Loss of vessels in alveolar septae causes concurrent loss of airways and ccapillaries.

Front 21

1) In a pt. with pure emphysema, what will arterial oxygenation usually be?
2) If it is changed (only in some cases) how will it change and why?

Back 21

1) Normal due to normal V/Q
2) It will go downdue to hypoxemia caused by loss of ventilation (due to airway collapse) to areas where perfusion is maintained.

Front 22

1) What obstructive lung disease most predisposed to CO2 retention?
2) Why do people retain CO2 anyways?

Back 22

Chronic Bronchitis due to chronically increased large workload of respiration, making muscles succeptible to fatigue.
2) Higher venous CO2 is more efficiency at unloading CO2 to the lungs, and can thus CO2 load can be excreted in a fewer number of breaths. In other words high aterial PCO2 decreases the amount of ventilation required to maintain a constant arterial CO2.

Front 23

1) What happens to pulmonary vascular resistance in obstructive lung disease?
2) Why does this change occur?
3) How does this manifest in the RIght heart? (2 ways)

Back 23

1) Increases
2) Alveolar distension due to high intrathoracic pressure and high lung volumes cause capillary atteuation
3) Right ventricular hypertrophy and right axis deviation (the later in acute asthma) due to high right ventricular afterload.

Front 24

1) Explain why right ventricular distension is seen upon inspiration in patients with extrememly obstructed airways.
2) How does this effect Blood pressure?

Back 24

1) Upon inspiration they have to generate alot of negative intrathoracic pressure to pull air in. This causes the RA to distend and suck in blood from the Vena Cava. This causes a high preload in the RV which pushes the intraventricular septum over,taking up space in the LV.
2) This smaller LV volume leads to reduced preload, which leads to an inspiratory drop in BP called. This when combined with the increased negative pressure on the LV decreasing its contraction causes PULSUS PARADOXUS.

Front 25

If a pt. has a pulsus paradoxus with bad airway obstruction, why might it go away when the pt...
1) Improves
2) Worsens

Back 25

1) Less obstruction leads to less generation of negatice intrathoracic pressure, and hence less RV preload. LV will not be impinged upon.
2) Fatigue of inpiratory muscles causes less negative pressure generation, and thus less RV preload. LV will not be impinged upon.

Front 26

1) Why do patients with obstructive lung disease have trouble exercising?
2) Which obstructive lung disease causes the most drop in Arterial oxygen tension with oxygenation?
3-4) Why does it cause more of a problem? (2 reasons)

Back 26

1) Cannot increase minute ventilation
2) Emphysema
3) Loss of capillaries in obliterated alveolar septae decrease blood transit time i remianing capillaries. In exercise, increased CO may further increase the transit time, leaving insuffiecient time for pulmonary blood flow to equilibrate with the alveolar air.
4) Additionally, loss of pulmonary vascular beds in emphysema cause an inability to decreae pulmonary resistance during exercise. This impedes and increase in C.O.- leading to an increase in tissue oxygen extraction and causes a drop in mized venous oxygen tension.

Front 27

Why do obstructive patiens often not present with dyspnea until they have advanced disease

Back 27

Activities of daily living require very little lung fucntion. Therefore they dont become symptomatic til things are very bad!!

Front 28

Describe two reasons why obstructive lung disease causes dyspnea

Back 28

1) V/Q mismatch, causing them to breath at a higher percentage of they maximum lung volume.
2) Lung muscle dysfunction causes smaller change in chest wall position than expected. This is experienced as dyspnea.

Front 29

1) Why do patients with chronic bronchitis or emphysema get SOB when they use arms to carry a package?
2) Why do some patients report relief from dyspnea when leaning forward?

Back 29

1) They are now using accessory muscles of respiration to hold weight.
2) Causes diaphragm to assume more domes shape, increasing its ability to move chest wall.

Front 30

1) Patients with obstructive lung disease should avoid...
2) What vaccine is indicated in these patients.
3) What other vaccine is indicated if the pt. is also elderly?

Back 30

1) Cigarettes
2) Flu
3) Pneumococcus

Front 31

1) What is the only therapy for obstructive lung disease shown to increase life expectancy?
2) When is it indicated?
3) What other therapy should be offered because it increases exercise capacity, Quality of life, and reduces dyspnea and hospitalizations?

Back 31

1) Supplemental oxygen up to 90% sat.
2) PaO2 < 55 mmHg
3) Pulmonary rehab with exercise.

Front 32

Surgical Tx for Obstrutive Lung Disease:
1) What specific condition calls for lung volume reduction.
2-5) Who is a candidate for transplant?
Patients with severe ___2___ complicated by ___3-5___ without coexisiting medical disease.

Back 32

1) Severe upper lobe emphysema
2) Severe emphysema
3) Pulmonary HTN
4) Hypoxia
5) Hypercapnea

Front 33

Even when asthma is not active, patients show hyperreactivity characteried by a ......

Back 33

eosinophilic desquamative bronchitis

Front 34

Five Hallmarks of Asthma

Back 34

1) Hyperreactive tracheobrinchial tree
2) paroxysms of couging, wheezing, dyspnea
3) Obstructive disease with obstruction varying widely in the trachobronchial tree.
4) Pathologic changes and scarring are present even when asymptomatic
5) Many kinds of triggers

Front 35

Airway involved:
1) asthma
2) CB
3) Emphysema

Back 35

1) All
2) Central
3) Peripheral

Front 36

Parechymal involvement:
1) asthma
2) Chronic Bronchitis

Back 36

1) Not involved
2) destruction

Front 37

Airway Hyperresponsiveness:
1) asthma
2) Chronic Bronchitis

Back 37

1) Present
2) may or may not be present

Front 38

Bronchial smooth muscle:
1) asthma
2) Chronic Bronchitis

Back 38

1) Enlarged mass in large airways
2) Enlarged mass in small airways

Front 39

Epithelium:
1) asthma
2) Chronic Bronchitis

Back 39

1) Shedding
2) Metaplasia

Front 40

Basement membrane:
1) asthma
2) Chronic Bronchitis

Back 40

1) Thickened with hyaline deposition
2) May or not be affected

Front 41

Mucous cells:
1) asthma
2) Chronic Bronchitis

Back 41

1) Metaplasia debated
2) Present

Front 42

Name the Inflammatory cells involved in
1) Asthma
2) COPD

Back 42

1) Degranulated Eosinophils
TH2
Mast Cells
Macrophages
2) Eosinophils (not degranulated)
Macrophages
FEW T-helper cells

Front 43

Name the Inflammatory mediators Present in:
1) Asthma
2) COPD

Back 43

1) Histamine
IL-4, IL-5, IL-13
LTB4
Exotaxin
RANTES
2)IL-8, IL-4
TNF- alpha
LTB4
GM-CSF

Front 44

1) How does Acute Bronchoconstriction evolve to contribute to airway obstruction in asthma?

Back 44

1) Allergen induced IgE dependant release of mast cell mediators including trypatase, hitstamine, LTs, and PGs All of these directly contract sirway smooth muscle.
This can also be caused by cold, nebulized water, dust, and is contributed to by stress.

Front 45

How is apsirin pro-asthma?

Back 45

Causes Arachidonic acid to be shunted to the lipoxygenase pathway where it is converted to LTC4 and LTB4 which are potent bronchoconstictors

Front 46

What causes the airway edema which obstructs the airways in asthma?

Back 46

Swelling due to increased vascular permeability caused by mediator release. This can also stiffen the airway.

Front 47

What can cause asthma to become intractable and persistent?

Back 47

Mucus plug formation

Front 48

Are the airway changes in asthma reversible?

Back 48

Only partially. There may be long term structural changes in the airway matrix

Front 49

What is the rationale in intervening early in asthma with anti-inflammatory therapy?

Back 49

Airway modeling can be permanent due to airway matrix remodeling.

Front 50

Two basic modalities of asthma therapy?

Back 50

Bronchodilators and anti-inflammatory

Front 51

Name the three types of bronchodilators?

Back 51

Beta agonists
Anti-cholinergics
Theophylline

Front 52

1) Do bronchodilators have any effect on the underlying airway pathology i asthma?
2) Do anti-inflammatory drugs for asthma have any acute effect to relieve an attack?

Back 52

1) No
2) No

Front 53

1) Describe the distribution of Beta-2 receptors in the lung.
2) What two tissuesdo beta agonists they act on on and what effects do they give?
3) What other cell do they act on and what effect do they have?

Back 53

1)Bronchi to terminal bronchioles (this is all of the smooth muscle containing walls)
2) Airway smooth muscle relaxation
Airway epithelial cells- influence ion and fluid transport

3) Stabilization of mast cell membrane by stimulating an adenylate cyclase.

Front 54

1) most common route of beta agonist adminitration in asthma
2)why?
3) what limits this?

Back 54

1) inhalation
2) minimze side effects
3) need to perfrom correct sequence of inhalation/puffing

Front 55

1) Predominant innervtion to airways which gives basic bronchomotor tone?
2) WHere the ganglia lay.
3) describe post-ganglionic projections
4) What does ACh release cause?

Back 55

1) Cholinergic from the vagus
2) in large and medium sized airways
3) short projections to smooth muscle and mucosal glands
4) smooth muscle contraction and secretion of mucous

Front 56

1) Albuterol, metaproteranol, terbutaline, pirbuterol and salmetrol are all examples of?
2) Which one is long acting?

Back 56

1)Inhalational Beta-2 agonists for asthma
2) Salmetrol

Front 57

What is the name for irritat receptors in the airways that can cause reflex constriction by the cholinergic system?

Back 57

J-receptors

Front 58

1) Anticholinergic agents which block cholinergic input to the airways are given in which disease?
2) Name the most common 2
3) What is unique about their atomic makeup?
4) What pharmacokinetic property does this cause?

Back 58

1) Asthma
2) Ipratropium Bromide, Tiotropium
3) Pentavalent Nitro
4) non-absorbtion because insoluble in lipids-- no side effects

Front 59

1) Peak effect of anti-cholinergic in asthma is how long after administration?
2) Route of administration?

Back 59

1) 30-90 mins
2) inhalational

Front 60

1) Which most commonly gives the best bronchidilation in asthma--- B2 agonists or anti-cholinergics
2) How about in Chronic Bronchitis?

Back 60

1) B2
2) anti-cholinergics

Front 61

We dont know how theophylline works to make asthma better. We do however know that in non-pharmacological levels (much higher) it increases ___1___ by inhibiting ____2___
3) Why, besides the dose problem, do we think this is not the mechanism of action in vivo?
4) What do we think theophylline inhibits in helping asthma
5) What is one step downstream from this action?
6) evidence against this mechanism of action?

Back 61

1) cAMP
2) PDE
3) more potent inhibitors of PDE dont help asthma
4) Adenosine receptor
5) Adenosine usually inhibits NE release, so loss of adenosine action may cause NE release on B2.
6) Other methylxanthines with more potent bronchodilator effects do not bind adenosine receptors

Front 62

Why do we not give thephylline as a first line agent for COPD or asthma??

Back 62

Narrow therapeutic index and relatively weak bronchodilation

Front 63

Recruitment of what things potentiat mast cell degranulation in asthma?

Back 63

eosinophils, platelets, and neutrophils

Front 64

What phenomenon may underlie both
1) the fact that a local asthmatic phenomenon can be amplified to the whole tracheobronchial tree?
2) Non-allergic initiation of asthma attacks

Back 64

chronic effects of inflammatory mediator release include epithelial damage and nerve endings.

Front 65

1) These cells are markedly increased at sites of chronic bronchitis, and can cause all the damage seen on the pathology.
2) What other cells play a role

Back 65

1) Macrophages
2) CD8 and neutrophils

Front 66

1) Define a primary mediator of inflammation
2) Define a secondary mediator of inflammation

Back 66

1) released directly from a mast cell
2) PRoduced as a consequence of pirmary immune events

Front 67

Tell me whether the mediator is primary or secondary
1) Histamine
2)LT
3)Thromboxanes
4) Neutrophil chemotactic factor
5) Platelt activating factor (PAF)
6) Eosinophil factor of anaphylaxis
7) PGs
8) Serotonin
9) Basophil Kallikrein
10)Bradykinin

Back 67

1) primary
2)secondary
3)secondary
4) primary
5) primary
6) Primary
7) Secondary
8) secondary
9) primary
10)secondary

Front 68

1) prostaglandin E2 causes?
2) Prostaglandin F2 causes?
3) Which leukotriene is a potent chemoattractant for leukocytes

Back 68

1) bronchial smooth muscle constriction
2) bronchial smooth muscle relaxation
2) LTB4

Front 69

1) AA is usually in the __1___
2-4) name three events that can cause its release

Back 69

1) Cell membrane
2) membrane perturbation
Ca++ influx
Phospholipase A2

Front 70

1)In asthma, orticosteroids decrease synthesis of ___1____ and ____2___
2) they also appear to potentiate B2 agonist effects by reducing___3___ nd increasing ____4____

Back 70

1) AA
2) PG
3) Catecholamine uptake and deactivation
4) B2 receptor density

Front 71

Studies have found that asthmatics who do not respond to bronchodilator therapy may respond to _____1_____ which _____2_____.

Back 71

1) corticosteroids
2) reduce airway hyperreactivity

Front 72

Inhaled corticosteroids are now recommended for any asthmatic requiring ___1___

Back 72

regular use of inhaled bronchodilators

Front 73

1) Inhaled corticosteroids are effective in __1___% of emphysema and CB as oppsed to most cases of asthma

2) What may account for this difference?

Back 73

1) 20-30%
2) Different inflammatory cell populations

Front 74

INTRINSIC bronchodilating or anti-inflammatory activity?
1) Corticosteroids
2) Cromolyn

Back 74

1) nope
2) nope

Front 75

1) Cromolyn helps asthma how?
2) In order to be beneficial Cromolyn must be adminsitered when?
3) for how long?
4) works better in kids or adults?

Back 75

1) stabilizes mast cell membranes
2) At a time when the airway is being esposed to repetitive or chronic stimuli
3) 2 weeks
4) kids

Front 76

4 ways that leukotrienes contrbute to asthma

Back 76

1) impair mucociliary clearance
2) Enhance mucous secretion
3) Atrtact leukocytes
4) Increase pulmonary vascular permeability increasing edema

(These things make the airway hyper-responsive to irritants_

Front 77

1-2) ____1____ and ___2____ are 1000x more potent than histamie at causing airflow obstruction
3-4) ____3_____ airways are 100-1000x more sensitive to these than ___4___ airways

Back 77

1) LTB4
2) LTC4
3) Asthmatic
4) normal

Front 78

_______ have been identified in the urine, sputum, nasal secetions, an bronchoalveolar lavage fluid of asthmatic patients

Back 78

Leukotrienes

Front 79

Two ways to block LTs in asthma: name them

Back 79

1) block synthesis
2) block receptor binding

Front 80

Two ways to block LTs in asthma:
1) block synthesis: what are the two targets of this strategy?
2) What drug is used?
3) block receptor binding- what receptors is blocked?
4) 2 drugs that do this

Back 80

1) Target 5-lipoxgenase enzyme or 5-lipoxygenase activating protein
2) Zileuton
3) Competitive antagonism of LTD4
4) afirleukast and Monteleukast

Front 81

3 mechanisms explaining why CO2 retention can INCREASE in a pt.(who has chronic bronchitis for example) when he is given supplemental oxygen.

Back 81

1) He is now getting fully oxygenated and has lost his hypoxic vasoonstriction due to low ventilation. The oxygen allows vasodilation and perfusion to these still under-ventilated alveoli. This is shunted away from exchanging airways to these places where 2) CO2 cannot exchange.

2) Loss of hypoxic respiratory drive causes a decrease in RR and hence a rise in ArtPCO2

3)Haldane effect- More O2 makes hemoglobin less avid for CO2. This allows CO2 to fall off of hemoglobin and go into dissolved cO2.