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Pulmonary Disease
Examination and
Board Review
NO ICE
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Pulmonary Disease
Examination and
Board Review
Edited by
Ronaldo Collo Go, MD
F ly
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Pulmonary Disease Examination and Board Review
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T is book is dedicated to:
Cont r ibu t or s x
Pr efa ce xv
vii
viii Co n t e n t s
xi
xii Co n t r ib u t o r s
Patricia Walker, MD
Co-director of Adult Cystic Fibrosis Center
Acting Chief
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M S B hI l
N w Y k, N w Y k
Preface
xv
1
he Cell and Immunology
Ronaldo Collo Go MD
G0
CASE 2
G1 S Human immune system consists o two parts: innate
immunity which recognizes pathogen receptor moti s in
many microbes and adaptive immunity which involves
Mitos is G2 generation o speci c antigen receptors on and B cells.
1
2 Pu l m o n a r y Dis e a s e e x a m in a t io n a n D Bo a r D r e v ie w
paracrine, or endocrine. Which cytokine is responsi- Question 6: What type o hypersensitivity involves
ble or the release o eosinophils? arthus reaction?
A. IL-5 A. ype I hypersensitivity reaction
B. IL-1, IL-6, NF-alpha B. ype II hypersensitivity reaction
C. IL-2 C. ype III hypersensitivity reaction
D. Il-17 D. ype IV hypersensitivity reaction
E. IL-10 E. ype V hypersensitivity reaction
Question 4: Adaptive immunity requires an initial con- Question 7: Which inter eron is prominent in granu-
tact with the antigen ollowed by a more vigorous loma ormation in sarcoidosis?
in ammatory response af er re-exposure to the antigen. A. Inter eron alpha
Bone marrow is the major site or B cells and thymus is B. Inter eron beta
the major site or cells. In the lymph nodes, the cells C. Inter eron gamma
are in the deep paracortical areas around B-cell germi- D. Inter eron alpha and beta
nal centers. wo important subsets o cells include E. All o the above
the cytotoxic CD8+ /MHC Class I and helper CD4+ /
MHC Class II. Which o the ollowing is not true Question 8: Which oll-like receptor proteins are
regarding the -cell recognition o an antigen? associated with gram-negative septic shock?
A. It is a heterodimer with CD3 subunits. A. LR1
B. It closely resembles the immunoglobulin heavy and B. LR3
light chains. C. LR4
C. Diversity is determined by rearrangements o V D. LR5
(variable), D (diversity), and J (joining) regions. E. LR6
D. CR recognizes protein antigen peptides which have
been “processed” by antigen presenting cells. Question 9: Anti-IgE therapy in asthma involves which
E. None o the above. type o antibody?
A. IgG
Question 5: B cells express immunoglobulins on their B. IgA
sur ace which can recognize unprocessed native anti- C. IgM
gens, and components o activated complement. D. IgD
Which immunoglobulin is ound as either a monomer E. IgE
or dimer, with J chain, and has secretory properties?
A. IgG Question 10: Which o the ollowing is pro brotic?
B. IgA A. GF-beta
C. IgM B. Plate-derived growth actor
D. IgD C. Insulin-derived growth actor
E. IgE D. Connective tissue growth actor
E. All o the above
Answers
3
4 Pu l m o n a r y Dis e a s e e x a m in a t io n a n D Bo a r D r e v ie w
CELL MEMBRANE CELL MEMBRANE CELL MEMBRANE CELL MEMBRANE CELL MEMBRANE CELL MEMBRANE CELL MEMBRANE CELL MEMBRANE
Pro-cas pas e 8
Cas pas e 8
P53
Cytochrome C
Cas pas e 9
Cas pas e 3
APOPTOSIS
Figure 1–1 T ere are two pathways leading to apoptosis. T e intrinsic pathway involves the P53 system which detects stress signals
via DNA damage, oncogene, and hypoxia. T is activates the BAX to proceed to increased permeability and release o cytochrome
C. T e extrinsic pathway involves binding o Fas Ligand and entering the apoptosis pathway via Caspase 3.
E ector Cells
P53
Macrophages First line o de ense o innate immunity
Binding LPS
APC to lymphocytes
Secretions o IL-1, NF-a, IL-12, IL-6
Dendritic cells APC
P16
P21 P27 INK CD83, MHC II, multiple thin membrane
projectile
Most potent producers o IFN-alpha
Natural killer Sur ace receptors or Fc o IgG, NCAM-I
cells (CD56), CD8
Dual role: Antibody-dependent cytotoxicity
CDK2 and nonimmune killing o target cells
Cyclin E2 Killing ability is inversely related to levels
o MHC I
Rb Rb
Granulocytes:
CDK2 Neutrophils Fc receptors or IgG (CD16) and or com-
Cyclin D1
E2F E2F plement components (C3b and CD35)
Secretes azurophilic granules into the sur-
Figure 1–2 RB Pathway. T e retinoblastoma pathway is the ace generating superoxide radicals a er
downstream pathway or P53 and disrupts G1 entry to S phase. stimulation rom immune complexes or
T is is highlighted by phosphorylation o RB/E2 F product, opsonized bacteria
causing dissociation o E2 F rom RB. (Reproduced with per- Eosinophils Fc receptors o IgG (CD32)
mission o Brambilla E, Gazdar A. Pathogenesis o lung cancer Cytotoxic to parasitic in ections
signalling pathways: roadmap or therapies. Eur Respir J. 2009; Contents include major basic protein,
33(6):1485–1497.) eosinophilic cationic protein, neurotoxin
and Anti-in ammatory enzymes such as
histaminase, arylsul ase, phospholipase D
T e ve phases o host de ense include: (1) migration o Basophils IL-4
leukocytes to antigen; (2) antigen recognition by innate High af nity or IgE (FCRI)
immunity; (3) antigen recognition by adaptive immu- Release histaminine, eosinophlic chemo-
nity; (4) in ammatory response; and (5) destruction and tactic actor, neutral protease
removal o particles. Expresses C3a and C5b receptors
**
Migration o the leukocyte, such as a neutrophil, involves pathway. C4a, C3a, and C5a release histamine rom
interaction with endothelial cells and con ormational basophils and mast cells.4 C3b and C3bi participate in
change with their adhesion molecules. T e rst stage, the phagocytosis by neutrophils and macrophages and
called attachment and rolling, involves leukocyte leav- participate in the ormation o immune complex. C5–9
ing the blood stream through the post-capillary venule, is the membrane attack complex.
mediated by L-selectin molecule. T e second stage, rm
adhesion with activation-dependent stable arrest, is Question 3: A. IL-5
attachment o leukocyte to high endothelial venules via Recognition interleukins and their roles might have
cytokines. T e third stage is the migration o leukocyte to therapeutic implications such as in asthma. T e normal
endothelial cells and release o matrix metalloprotenases airway is rich with T 1 cells. In an asthmatic airway, they
which digest the subendothelial basement membrane. are rich in T 2 cells.8 Below is a table that lists selected
interleukins, their mechanisms, and associated drugs.8
Question 2: E. C5–9
T e complement system is a cascading series o reactions Question 4: E. None o the above
which results in cell lysis. T ere are three pathways which MHC-peptide- CR is the initiation o an antigen
include classic activation pathway via immune com- driven immune response. T e major histocompatibility
plex, mannose-binding lectin pathway, and alternative complex (MHC), also called human leukocyte antigen
6 Pu l m o n a r y Dis e a s e e x a m in a t io n a n D Bo a r D r e v ie w
IL-10 • Anti-in ammatory and inhibits release o IL-1,IL-6,IL-12, and NF-alpha • Corticosteroids
• Deactivates macrophages, mast cells, and eosinophils • Vitamin D
(HLA) complex, is located on chromosome 6 and has a Other groups o HLA are organ speci c such as: HLA-
role on antigen speci city and presentation. T ey have DRB1*12 and HLA-DRB1*14 are associated with lung
roles in pathogen resistance and autoimmune disease. involvement, HLA-DRB1*04-BQB1*0301 are associated
T ere are two classes. Class I, HLA-A,-B, and -C, appear with uveitis, and HLA-DQB1*0601 are associated with
to have particular characteristics such as polymorphism cardiac involvement.13–18
and linkage disequilibrium. Recognized by CD8 cells,
class I allele has a heavy chain and a nonpolymorphic **
B2-microglobulin light chain. Recognized by CD4 cells, CD4 helper cells produce cytokines. T 1 CD4+ aide
class II consists o a heterodimer with amino-terminal in cellular killing and help generate opsonizing antibod-
domains representing antigen-binding regions. ies that lead to a delayed hypersensitivity response. T ey
secrete IL-2, IFN-gamma, IL-3, NF-alpha, GM-CSF, and
**
NF-beta. T 2 CD4+ produce IL3-6, IL-10, and IL-13
T e association o HLA and sarcoidosis has been well
regulate humoral immunity and isotype switching.
documented, initially with Class I HLA-B8 but more
so with Class II HLA, with variable implications.13
**
HLA-DQB1*0201 and HLA-DRB1-301 are associated
with good prognosis in British and Dutch and in Swish CD4 and CD8 regulatory cells are produced by den-
respectively.14,15 HLA-DRB1*01 and HLA-DQB1*0501 dritic cells and suppress immune response, particularly
have been shown to be protective against sarcoidosis.14 those rom sel -antigens.
c h a Pt e r 1 t h e c e l l a n D im m u n o l o g y 7
Fibrocytes • Bone marrow derived, they produce collagen and express CD45 (leukocytes) and CD34
(stem cells)
• Di erentiate to myo broblasts and contribute to ECM or di erentiate into mesenchy-
mal cells
• Recruitment dependent on CXCL12, CCL2, CCL3, and IL-10
CD40–CD40 L • Co-stimulators in the activation o CD4+ cells via CD40L and antigen presenting cell
(APC) via CD40
• With IL-4, promotes broblasts
Integrins • Cell sur ace molecules involve in adhesion between cell to cell and cell to ECM
• Roles in cell migration, growth, and survival
REFERENCES 10. odd NW, Lyzina IG, Atamas SP. Molecular and cellular
mechanisms o pulmonary brosis. Fibrogenesis Tissue
1. Rom WN, Hay JG, Lee C, et al. Molecular and genetic
Repair. 2012;5(11):1–24.
aspects o lung cancer. Am J Respir Crit Care Med. 2000;
11. Strunk RC, Bloomberg GR. Omalizumab or asthma.
161:1355–1367.
N Engl J Med. 2006;354:2689–2695.
2. Brambilla E, Gazdar A. Pathogenesis o lung cancer signal-
12. Abbas AK, Lichtman AH. Basic Immunology. New York,
ing pathways: roadway to therapies. Eur Respir J. 2009;33(6):
NY: Saunders; 2010.
1485–1497.
13. Inannuzzi MC, Rybicki BA, eirstein AS. Sarcoidoisis. N
3. Armanios, M. elomerase and idiopathic pulmonary
Engl J Med. 2007;357:2153–2165.
brosis. Mutat Res. 2012;730:52–58.
14. Grunewald J, Eklund A. Lo gren’s Syndrome. Human Leu-
4. Stone KD, Prussin C, Metcal e DD. IgE, mast cells, basophils
kocyte Antigen Strongly In uences the Disease. Course.
and eosinophils. J Allergic Clin Immunol. 2010;125:S73–S80.
Am J Respir Crit Care Med. 2009;179:307–312.
5. Marzouk K, Saleh S, Kannass M, et al. Inter eron-induced
15. Sato H, Grutters JC, Pantelidis P, et al. HLA-DQB1*0201.
granulomatous lung disease. Curr Opin Pulm Med. 2004;
Am J Respir Cell Mol Biol. 2002;27:406–412.
10(5):435–440.
16. Sato H, Woodhead FA, Ahmad , et al. Sarcoidosis HLA
6. Petousi N, T omas EC. Inter eron-B-induced pulmonary
Class II genotype distinguishes di erences o clinical phe-
sarcoidosis in a 30-year-old woman treated or multiple
notype across ethnic groups. Hum Mol Gen. 2012;19:
sclerosis. J Med Case Reports. 2012;6:344.
4100–4111.
7. Morris DG, Jasmer RM, Huang L, et al. Sarcoidosis
17. Iannuzzi MC, Maliarik MJ, Poisson LM, et al. Sarcoidosis
ollowing HIV In ection: Evidence or CD4+ lymphocyte
susceptibility and resistance HLA-DQB1 alleles in A rican
dependence. Chest. 2003;124:929–935.
Americans. Am J Respir Crit Care Med. 2003;167:1225–
8. Garcia G, aille C, Pierantonio L, et al. Anti-interleukin-5
1231.
therapy in severe asthma. Eur Respir Rev. 2013;22:251–257.
18. Ayyala US, Nair AP, Padilla ML. Cardiac Sarcoidosis. Clin
9. Gibeon D, Menzies-Gow AN. argeting interleukins to treat
Chest Med. 2008;29:493–508.
severe asthma. Expert Rev Respir Med. 2012;6(4):423–429.
2
Pulmon ry Func ion ss
Ronald Evans DO, Ronaldo Collo Go MD, Andrew Matragrano MD, and
Paul Simonelli MD, PhD
0 1 2 3 4 5 6
IRV
Time (s econds ) IC
IVC
4 VT
)
TLC
d
3
n
o
ERV
c
e
2
S
(
FRC
w
1
o
l
F
RV
0 1 2 3 4 5 6
R pro uc wi h p rmission rom W ng r J, Cl us n JL, Co s
Time (s econds ) A, l. S n r is ion o h m sur m n o lung volum s.
Eur Respir J. 2005;26(3):511–522.
Question 1: What kind o arti act do you see?
A. Cough Question 1: Which o the ollowing are increased
B. H si ion during the third trimester o pregnancy?
C. E rly rmin ion A. V n IC
D. Air l k B. VC
E. Glo is closur C. FRC, ER, RV
9
10 Pu l m o n a r y Dis e a s e e x a m in a t io n a n D Bo a r D r e v ie w
2
D. LC
N
f
o
E. FRC III
%
II
CASE 3 I
**
Spirom ry p r orm by his prim ry c r physici n
prior o sp ci l y consul ion is s ollows:
12 Re f P re P re P o s t Pos t Pos t
Me a s % Re f Me a s % Re f % Chg
8
FVC Liters 5.09 5.40 106 5.38 106 - 0
4 FEV1 Liters 4.39 3.80 87 3.87 88 2
FEV1/FVC % 85 70 72
0 FEF25–75% L/s ec 4.92 2.82 57 2.86 58 1
PEF L/s ec 9.39 7.90 84 7.70 82 - 2
- 4 FET100% Sec 10.46 9.62 - 8
FIVC Liters 5.09 5.28 104 5.40 106 2
- 8 FIF50% Liters 5.13 4.70 - 8
MVV L/min 179
- 12
- 2 0 2 4 6 8
Volume
**
H is s n or m h cholin ch ll ng s s h r is
s rong n o cl ri y i h ruly h s i gnosis o
s hm . R sul s o h m h cholin ch ll ng s r
s ollows:
12 12
12 10 10
10 8 8
8 6 6
6
4 4
4
2 2
2
0 0 0
- 2 2 4 6 - 2 1 2 3 4 5 6
- 2 1 2 3 4 5 6
- 4 - 4 - 4
- 6 - 6 - 6
- 8 - 8 - 8
- 10 - 10 - 10
- 12 - 12 - 12
Pred Pred
Pred Pre Pre
Pre Chlg Pos t
12 Pu l m o n a r y Dis e a s e e x a m in a t io n a n D Bo a r D r e v ie w
Question 1: What can be said about this patient having C. T p i n r nk cup o r gul r co on h w y
a diagnosis o asthma? o his m h cholin s
A. T p i n bsolu ly h s s hm s vi nc by D. T p i n ook 1,000 mg c minoph n on h
h > 20% cr s in FEV1 uring m h cholin morning o his m h cholin s
s ing E. H lso k s lisinopril or hyp r nsion
B. T p i n bsolu ly o s no h v i gnosis o
s hm s his FEV1 i no ll b low 20% un il CASE 5
conc n r ion on 8 mg/mL m h cholin
C. T prob bili y o h p i n h ving s hm is bor r- A 73-y r-ol m n h s r c n ly b n i gnos wi h
lin u o h m h cholin conc n r ion n o COPD n h s smok 1 p ck p r y or 50 y rs. H
in uc 20% or gr r cr s in FEV1, bu his l ck no s his shor n ss o br h is no limi ing his ily
o s hm ic symp oms giv him low pr - s prob - c ivi i s n h con inu s oing s r nuous m nu l
bili y or i gnosis o s hm l bor roun his hom ily. H no s ily symp oms o
D. PF s prior o m h cholin s ing show 2% cough pro uc iv o y llow-brown spu um n s s h
improv m n in FEV1 ollowing broncho il or. T is h s on o wo bou s o “bronchi is” p r y r, or which
lon shows bronchi l r sponsiv n ss n prov s h s s his prim ry c r physici n n is ypic lly r
nough vi nc or h i gnosis o s hm in his wi h cours o or l n ibio ics n or l cor icos roi s.
p i n
**
E. H h s s hm s vi nc by h i gnosis h c r-
ri s rom chil hoo His physic l x min ion is o h rwis unr m rk bl
xc p or BMI 32 n occ sion l xpir ory wh z .
Question 2: Which o the ollowing may have inter-
ered with the methacholine challenge testing? **
Pulmon ry unc ion s s r shown b low:
A. T p i n us lbu rol inh l r 1 y prior o
m h cholin s ing
B. T p i n c m o clinic r ing milk n o
c r l or br k s prior o m h cholin s ing
Pre-Bronch Post-Bronch
Actual Pred %Pred SD LLN Actual %Chng
— SPIROME RY —
FVC (L) 2.86 3.97 72 0.54 3.08
FEV1 (L) 1.42 2.88 49 0.45 2.14
FEV1/FVC (%) 50 73 67 6 63
FEF 25% (L/s c) 1.61
FEF 75% (L/s c) 0.27
FEF 25–75% (L/s c) 0.58 2.12 27 0.92 0.60
FEF m x (L/s c) 3.75 7.56 49 1.33 5.37
FIVC (L) 2.22
FIF m x (L/s c) 2.71
(continued)
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Yours most affectionately in our common Lord,
G. W.
LETTER MXXIV.
To Mr. ――.
Dear Sir,
B Y your writing, I guess you are a brand plucked out of the fire of
the polite and gay world.—Happy deliverance! I intreat you to
rejoice, give thanks, and sing,
G. W.
LETTER MXXV.
To Lady H――n.
Honoured Madam,
G. W.
LETTER MXXVI.
To Mrs. G――.
London, February 15, 1754.
Dear Madam,
W ITH this I send you the promised pamphlet, which was written
with a single eye to prevent fraud and superstition, and to
promote the Mediator’s glory. Notwithstanding, I would advise you,
dear Madam, not to let other people’s foibles drive you from the
cross of Christ: he is altogether lovely.—And if persons were more
taken up in contemplation of his loveliness, and their own
deformities, they would not have so much time to talk of others, nor
take so much pains to gain proselytes to any particular party under
heaven. Such a practice is beneath the dignity of a free-born child of
God.—His spirit breathes another kind of language, and teaches us
to be all eye within. O that your heart may be filled with that wisdom
which is from above, which is first pure, then peaceable, gentle, easy
to be intreated, without partiality, without hypocrisy, and full of faith,
self-denial, zeal, disinterestedness, and good works! That Jesus,
whom I believe you love, is able, dear Madam, to fill you with this
wisdom. He hath promised, “if we ask, it shall be given.” Nay, he
hath said, “that he giveth liberally and upbraideth not.” May you be
enabled to lay hold on him in the omnipotence of prayer, and find
grace to help in every time of need! Have you not found him faithful,
in your intended visit to your friend? May you be made wise as an
angel of God, to win her and others over to the ever-loving, ever-
lovely Jesus! Pray, dear Madam, have you heard from Bath? There
is a copy you may safely write after; but a perfect one is no where to
be found but in our common Lord, the God-man Christ Jesus. To
his tender and never-failing mercy do I most humbly recommend
you, and, for his great name’s sake, most heartily subscribe myself,
dear Madam,
G. W.
LETTER MXXVII.
To Mr. S――
Yours, &c.
G. W.
LETTER MXXVIII.
To Mr. B――.
G. W.
LETTER MXXIX.
To Mr. R. K――n.
G. W.
LETTER MXXX.
To Mr. C――.
My dear Friend,
G. W.
LETTER MXXXI.
To Mr. A――.
I NDEED you have lost the seeing and hearing of many strange, but
to a truly enlightened soul, instructive things. I thank God for
sending me here; I know your heart hath been here also; but all is
well.—What is, is best. I hope you go on comfortably at home, whilst
I, unworthy, ill and hell-deserving I, am travelling for the same Lord
Jesus abroad. He doth not leave me comfortless,—he doth not
leave me alone;
G. W.
LETTER MXXXII.
To the Rev. Mr. Z――.
G. W.
LETTER MXXXIII.
To Mr. C――.
T HIS leaves me pretty well satisfied (not to say surfeited) with the
ecclesiastical curiosities of Lisbon. This day fortnight we
arrived; and the country being in want of rain, and it being Lent
season, we have been savoured with frequent processions, and
several extraordinary pieces of scenery. Alas! to what lengths will
superstition run! And how expensive is the pageantry of a false
religion! Blessed be God for being born in England! Blessed be God
for being born again, and thereby being taught to worship the Father
in spirit and in truth! This, my dear Sir, I believe is your happy
portion; and therefore if it should be our lot never to meet here any
more, I am persuaded nothing can prevent our meeting in a blissful
country hereafter. O that we may be kept from flagging in the latter
stages of our road! I am confounded, when I think what a drone I
have been, and daily wonder why the Lord employs such a
worthless wretch.—Surely it must be, that in me he may shew all
long-suffering. Help me, my dear friend, to praise him. Lisbon air
seems healthy for the body; and what I have seen and heard I trust
will benefit my soul. Be pleased to remember me to Mrs. C――, your
son, and all enquiring friends. You will not forget to visit my widow
wife. Blessed be God, her Maker is her husband, and ere long we
shall all sit down together at the feast, the marriage supper of the
Lamb. In a believing prospect of this, I subscribe myself, very dear
Sir,
G. W.
LETTER MXXXIV.
To Mr. F――.
Dear Sir,
I OWE you much love.—I wish you and yours much ♦ happiness,
and earnestly pray that you may walk together many years as
heirs of the grace of life. Was I to be confined long in my present
situation, I should be in danger of envying my protestant friends, who
breathe in a free air, and are taught to worship the father of spirits in
spirit and in truth. This I fear is the lot but of few here; all is
pageantry and pomp. Particulars perhaps I may send by another
opportunity. Blessed be God that I have seen and heard for myself.
It surpasseth all description. This week we expect to sail: I beg the
continuance of both your prayers; it will be a very great act of charity;
for indeed I am a poor helpless worm, but notwithstanding, if I know
any thing of my heart, willing to spend and be spent for Jesus. He
doth not forsake me on the mighty waters.—My fatherless charge
are all well, and in due time I hope we shall safely arrive at our
desired port.—Ere long I hope to be, from whence I shall never put
to sea any more. O for a triumphant entrance into the blissful
harbour! Jesus is able to do this for us. To his never-failing mercy do
I earnestly commend you, your brother, and all enquiring friends, as
being, dear Sir,
G. W.
My dear Friend,
G. W.
LETTER MXXXVI.
To the Same.
My dear Friend,