- restrictive pulmonary diseases
- diaphragm weakness or paralysis
- interstitial lung diseases (ILD)
- pneumoniae
- lung cancers
- diseases of the pleura
- lung suppurations
- anomalies of pulmonary ventilation
Table of contents :
,
nontuberculous mycobacteria;
symptoms include coughing, spitting of blood, and gradual deterioration
of health
or Eisenmenger's
syndrome.,
sometimes with paralysis of one vocal cord)/patent
foramen ovale (PFO))
(cardiac asthma) but sometimes occurring
in patients with chronic pulmonary diseases. During sleeping blood volume
increases due to hydroelectrolyte retention, reabsorption of oedema and
decrease in oncotic pressure in lung interstitium; it lasts for 10'-30'.),
NO2)
increasing intercellular permeability and hence enhancing exposure to allergens
(with decreased PEF)
agonist which acts as bronchoconstrictor : Lofarma liophilized metacholine
required dilution in 3 mL water) : a type of bronchial challenge or inhalational
challenge used as a test for airway reactivity or atopic asthma; aerosolized
methacholine 0.2% (2 mg/mL for 0.8"; each puff erogates 20 mg
metacholine; first puff => second puff after 0.55" => 2 puffs after 0.55"
(total = 80 mg)) => 1% (10 mg/mL for 1"; each
puff erogates 100 mg metacholine; first puff
=> 2 puffs after 0.55" => 4 puffs after 0.55" => 8 puffs after 0.55" =>
8 puffs after 0.55" (total = 2380 mg)) is applied
to the airways and the patient is assessed for responsiveness or hyperresponsiveness.
In babies methacholine has to be replaced with 6' of outdoor running. Test
is positive when provocative dose that causes a 20% decrease in FEV1
(PD20) < 1.2 mg
phosphate challenge : a type of bronchial challenge done to assess
responsiveness of the mucosa: histamine is applied to the nose or mucous
membrane and mucosal swelling is monitored; allergic or otherwise susceptible
subjects have lowered thresholds of reactivity
agonists (2 puffs of salbutamol) / FEV1, before treatment
> 115%.
among patients with poorly controlled asthma, treatment with proton-pump
inhibitors does not improve asthma control. Asymptomatic gastroesophageal
reflux is not a likely cause of poorly controlled asthmaref
(acute chest syndrome)
or brain stem lesion; voluntary control remains intact but central
sleep apnea
occurs),
morphine,
sedatives,
ethanol)
(traumatic apnea)
therapy for reduces the rate of bronchopulmonary
dysplasia in infants with very low birth weightref.
The 2 primary types are :
(no chest movement; please consider newborn are obliged nasal breathers
(e.g. in choanal atresia a permanent oral cannula is required) and chest
movements are usually minimal)
for the purpose of limiting the motion of the apices of the lung
or hypoxemia
or both
,
progesterone
or hypoxemia
(low PO2, atm)
rebound
=> type II respiratory failure
(wet lung).
In chronic failures the respiratory centre becomes tolerant to hypercapnia.
It is usually reversed by 7-8 days of resting of respiratory muscles, but
up to 10% cannot be weaned (in a 2-3 days time). Treatment :
(in type II respiratory failures)
)
(if significant hypercapnia
still occurs))
: a manifestation of severe rosacea involving the lower half of the nose
and sometimes spreading to adjacent cheek areas, usually seen in men, and
characterized by thickened, lobulated overgrowth of the sebaceous glands
and epithelial connective tissue.
,
throat and ear pain, and productive cough suggest complications. Excessive
blowing of the nose, which forces bacteria into the sinuses and Eustachian
tube and traumatizes the sinus orifices, and severe coughing, which strips
the cilia from the bronchial lining, are the most common causes.
(31%)
(21%)
+ Haemophilus influenzae
(5%)
(2%)
(4%)
(2%),
aerosinusitis,
or barometric vertigo.,
environmental irritants
inhalation,
and marked by ulceration, caries of the nasal bone, and a fetid discharge.,
and attended with ulceration, caries of the nasal bone, and ozena
: fungal aetiology can not be proved with certainty. Attempts to culture
the fungus on various media have also been unsuccessful.
The new findings justify a change in the name "rhinosporidiosis" that had
been associated with the fungus Rhinosporidium seeberi
(usually 5th month) usually responds to no treatment except delivery
: amoxicillin + clavulanic acid + cefpodoxime or cefurioxime for 8-10 days
in the nose; through a cerebrospinal fluid fistula => infectious
meningitis
and encephalitis).
)
?)
in immunodeficient patients, Streptococcus
pneumoniae)
aspergilloma.,
often in mid-morning to late afternoon, tenderness to percussion over the
sinus, or pressure on the floor in the supraorbital region, swelling of
the upper eyelid
with inability to concentrate, fever,
malaise, and anorexia
from ethmoidofrontal sinusitis
from ethmoidofrontal sinusitis
and antifungal agents are the most common additives : an additive of interest
is xylitol, a naturally occurring sugar that lowers the salt concentration
of airway surface liquid and appears to upregulate antimicrobial factors.
Delivery of the nasal solution can be by positive-pressure squeeze, negative
pressure, or nebulizers. Of these, the nebulizer may be least effective,
as evidence suggests that this method does not deliver solution to the
sphenoidal or frontal sinuses.,
or retrobulbar pain. Usually, the oropharynx is somewhat inflamed, and
there is occasionally neck stiffness or edema of the uvula
.
It is estimated that the risk of rhinopharyngeal cancer is 20% in Chinese
with high levels of anti-VCA IgA.
,
tinnitus
or osteolysis of skull basis)
except VII and VIII
due to cervical plexus infiltration
due to muscular infiltration
due to orbit infiltration.
(to assess bone invasion)
(to assess soft tissue invasion)
(to assess bone
metastases)
: maximum dose of 45 Gy is given to the Clinical Target Volume which is
1 cm margin around the MRI-detected primary site and inferiorly down to
the clavicles to include the lymph nodes. Treatment is given in 2 phases:
105u/kg intravenously (i.v.) 3 times a week for 6 months
120 mg/m2 as a bolus on day 1, cisplatin
100mg/m2 over 6 hours on day 1 with standard hydration, mannitol
and electrolyte replacement, and folinic
acid
25mg/m2 every 6 hours for a total of 6 doses as well as 5-fluorouracil
1000mg/m2 per day from day 2 for 5 days as a continuous infusion.
They receive 3 courses of chemotherapy every 21 days or on full blood count
recovery followed by irradiation and IFN-b as
per low risk patients.)
speech
speech
after prolonged irritation, usually the result of chronic misuse of the
voice, smoking, or excessive exposure to dry air or dust).
Types range from a benign variety lasting a few days to a virulent form
with edema that obstructs the airway
in children
in adults
(diphtheritic laryngitis / laryngeal diphtheria)
(25%)
and normal voice,
continue inspiratory dyspnea at night when edema
worsens, cough, normal voice (differential diagnosis with layngeal diphtheria),
lip and nail cyanosis,
cutaneous cyanosis
and sudden inspiratory laryngeal dyspnea (both inspiratory
and expiratory), respiratory failure => shock, bronchopneumonia
(laryngotyphus),
i.v. GR agonists
for 5-6 days, elimination of irritants (especially tobacco and ethanol),
voice rest and humidification, tracheotomy.
(tuberculous laryngitis / laryngeal tuberculosis / laryngophthisis /
tuberculosis of larynx : ulceration of the vocal cords and elsewhere
on the mucosa, and commonly attended by hoarseness, cough, pain on swallowing,
and hemoptysis)
(syphilitic laryngitis)
=> cricoarytenoid ankylosis)ref
of the epiglottisref
of the larynx
(keratinized or nonkeratinized)
: may represent a reactive pseudosarcomatous stromal change, a spindled
or sarcomatous squamous cell carcinoma, or a true sarcoma arising with
a squamous cell carcinoma
=> inspiratory laryngeal dyspnea, metastatic cervical
lymphadenopathy.
in emergencies
(better functional results). Careful selection of patients with early-stage
glottic tumors that recur or progress after radiation allows patients to
be successfully treated by partial laryngectomy with excellent survival
outcome. However, despite an aggressive policy of performing partial laryngectomy
when feasible, up to 50% of patients will require a total laryngectomy
owing to progression of disease. These patients have poorer survival outcomes
manifested by local, regional, and distant disease progressionref.
: thyrotomy / median
laryngotomy.
Laser cordectomy provides excellent local control and laryngeal preservation.
Close follow-up of patients with positive or suspicious margins is an alternative
to further routine treatmentref
: lateral pharyngectomy. It causes dysphagia (lack of epiglottis closure
while swallowing).
(both false and true vocal cords and ventricle) : it requires a temporaneous
tracheostomy
as it causes massive edema
(70 Gy, given in 35 fractions of 2 Gy each over a 7-week period) with concurrent
administration of cisplatin
(100 mg/m2 i.v. on day 1) is superior to induction chemotherapy
followed by radiotherapy or radiotherapy alone for laryngeal preservation
and locoregional controlref
, but not always works. 5-yr OS 55%. The rates of acute toxic effects were
higher in both chemotherapy groups than in the group that received only
radiotherapy, but the rate of late toxic effects, including swallowing
dysfunction, was similar in all 3 groups. A striking finding is the higher
rate of swallowing dysfunction at one year in the group assigned to concurrent
chemotherapy and radiotherapy than in the group assigned to induction chemotherapy
followed by radiotherapy (26% vs. 9%). Multicenter randomized studies,
including one from the Radiation Therapy Oncology Group (RTOG), have shown
that significantly improved tumor control and voice preservation can be
achieved with altered fractionation schedulesref1,
ref2,
ref3.
This improvement is, it seems, at least the equal of that obtained by adding
concurrent chemotherapyref.
Only one had statistical power to determine the benefit for laryngeal cancer,
specifically early-stage glottic cancerref
for cancers of sinus pyriformis),
separating the airways and the digestive tract. The nasal, nasopharyngeal,
and oropharyngeal mucosae undergo atrophy (parosmia
may result), while the tracheal epithelium undergoes metaplasia into squamous
epithelium. Patients can speak with esophageal or erygmophonic voice
by replacing the glottis with the cricoid sphincter (phonation time is
shorter and speak is often interrupted)) : elderlies with hyposthenia may
use artificial larynx.
(also for lymph node staging),
respiratory dystress (an acute form is the most common cause of croup)
0.15 mg/kg. More severe cases of croup that require inpatient treatment
can be treated with glucocorticoids within 6 hours and lasts up to 12 hours
over the traditional treatment with nebulised racemic epinephrine,
based on shorter hospital stays and improved croup scores.
,
and usually accompanied by a barking cough and expiratory stridor or wheezing;
nearby organs such as the esophagus or aorta may compress the trachea and
cause apnea.
combined with a fixed completecartilaginous ring)
from the bronchi (see hemorrhagic bronchitis)
and a productive cough. Repeated attacks may indicate chronic
bronchitis
=> middle lobe syndrome
(usually dissecating)
=> upstream overdistension
or hepatic metastases
(liver increases its mass from 1.5 to 3 kg)
born before 28 weeks gestation, but only in 15-30% of those born between
32 and 36 weeks. About 25% of babies born at 30 weeks gestation develop
HMD severe enough to need a mechanical ventilator (breathing machine).
The more premature the baby, the higher the risk and the more severe the
HMD. Although most babies with HMD are premature, other factors can influence
the chances of developing the disease. These include the following:
(too much insulin in a baby's system due to maternal diabetes can delay
surfactant production)
gene including homozygous nonsense mutations in codons 106 and 1142, a
homozygous frameshift mutation, and heterozygous insertion mutations and
splice-site mutations (7 missense mutations in conserved amino acids are
not found in control subjects) => abnormal lamellar bodies
of lungs - often show a unique "ground glass" appearance called a reticulogranular
pattern (stages I-IV)
often show lowered PO2 and increased PCO2
sometimes used to rule out congenital
cyanotic cardiopathies
into the baby's windpipe,
ROS react with neuronal phospholipids due to poor antioxidant defenses,
chronicization of pneumopathy, complete alveolarization at age 8, volubarotrauma
=> cytokines => BPD)
with artificial surfactant - most effective if started in the first 6 hours
of birth. Surfactant replacement has been shown to reduce the severity
of HMD. Surfactant is given as prophylactic (preventive) treatment for
some babies at very high risk for HMD. For others it is used as a "rescue"
method. The drug comes as a powder to be mixed with sterile water and then
is given through the ET tube (breathing tube). Surfactant is usually given
in several doses.
(38%)
(30%)
up to physiological maturation of the fetal surfactant system (pregnancy
week 35)
between 24 and 34 weeks gestation has been shown to dramatically lower
the risk and severity of HMD in the baby
=> inspirated air distributes dyhomogeneously => alveolar rupture => pneumothorax
(usually first in right lung due to higher ventilation, then bilateral)
of insidious onset during the first month of life and often resulting in
death. Radiographically, there are multiple cystlike foci of hyperaeration
throughout the lung with coarse thickening of the interstitial supporting
structures. The disorder has been attributed to disparity of maturation
of parenchymal elements, especially of alveoli proliferation, and hence
has been called pulmonary dysmaturity.
(< 10%)
(< 4%)
(19.6%), Pseudomonas
aeruginosa
(16.8%) and Haemophilus
influenzae
(7.5%), followed by Acinetobacter
baumannii(6.9%),
Enterobacter
species
(6.1%) and Staphylococcus
aureus
(6.1%). The incidence of Streptococcus
pneumoniae
was 2.4%ref.
Moraxella
catarrhalis,
SO2, O3)
=> hypochloremia
,wheezes
(absent in complete bronchostenosis), right
heart failure,
Grancher's
sign : equality of pitch between expiratory and inspiratory murmurs;
a sign of obstruction to expiration.
=> sudden respiratory effort related arousals (RERAs)
(highly risky !), behaviour alterations, consciousness impairment, morning
headache,
night sweats, decreased libido, palpitations and/or chest pain, cough nicturia,
impaired sleep of the partner
(BMI > 27)
mask is used if 5 < RDI < 30 with severe symptoms or anyway if RDI
> 30
=CYPs=>
oxidizing metabolytes that inhibit a1-antitrypsin
& activate MMPs
of Clara cells
and often hypercapnia,
hypercapnia
and respiratory acidosis
=> pulmonary artery vasoconstriction => cor pulmonale => right
heart failure.
These patients are known as "blue bloaters".
,
bronchial gland thickness (Wright index).
=> lung vascular sclerosis => chronic
cor pulmonale
and relatively limited blood flow through a fairly well oxygenated lung
with normal blood gases and pressures in the lung. Alveolar cell apoptosis
is involved in the pathogenesis of emphysema, a prevalent disease primarily
caused by cigarette smoking. Ceramide, a second messenger lipid, is a crucial
mediator of alveolar destruction in emphysema. Inhibition of enzymes controlling
de novo ceramide synthesis prevented alveolar cell apoptosis, oxidative
stress and emphysema caused by blockade of the VEGFRs in both rats and
mice. Emphysema was reproduced with intratracheal instillation of ceramide
in naive mice. Excessive ceramide triggers a feed-forward mechanism
mediated by activation of secretory acid sphingomyelinase, as suggested
by experiments with neutralizing ceramide antibody in mice and with acid
sphingomyelinase-deficient fibroblasts. Concomitant augmentation of signaling
initiated by a prosurvival metabolite, sphingosine-1-phosphate,
prevented lung apoptosis, implying that a balance between ceramide and
sphingosine-1-phosphate is required for maintenance of alveolar septal
integrity. Finally, increased lung ceramides in individuals with smoking-induced
emphysema suggests that ceramide upregulation may be a crucial pathogenic
element and a promising target in this disease that currently lacks effective
therapiesref.
(cyanosis)
and pulmonary cachexia => muscle wasting and weight loss ("pink puffer"
when young => "blue boater" when elderly).
and cigarette smoking
(=> acquired a1-antitrypsin
deficiency and activation of elastase secretion by PMNs) and is most prominent
in the upper lobes and apical segments of lower lobes, following an infectious
bronchiolitis (adenoviruses)
(presence of inflammatory cells).
pathway —a protein involved in protecting against oxidative stress by transactivating
antioxidant enzymes (AOE) — is critical in the protection of the lungs
in mice against the inflammation and destruction and may act as a major
determinant of susceptibility to tobacco smoke–induced emphysemaref.
The Nrf2 nuclear transcription pathway regulates a number of critical antioxidant
pathways, including SOD3,
which is normally highly expressed in lung airways and is a primary defense
against inhaled oxidants
shows accentuation of vascular and bronchial visualization
equally. It usually involves the lung bases
equally.,
complication of acute miliary tuberculosis
=> apical dystrophies => apical supbleural emphysematous bullae
,
life expectancy < 1-2 years, satisfying physicomental conditions, not
further improvable pharmacotherapy, continuous O2-therapy.
if vascular compression occurs. Not practiced in patients with non-upper
lobe disease and high exercise capacity.)
)
=> HRCT
: increased retrosternal and retrocardiac air spaces, "drop heart", flattened
or concaved diaphragm due to endothoracic hypertension, lack of costophrenic
sinuses
and improves survival
)
: they are more common in right lower lobe due to inclination of tracheal
bifurcation
and grayish, tenacious sputum; often associated with (tracheo)bronchial
asthma.,
sometimes evolving to respiratory
bronchiolitis–associated interstitial lung disease),
chronic sinusitis, sterility
and bronchiectasis),
chest CT,
bronchoscopy,
bronchography
(may cause cough !)
,
hemorrhages)
(Pickwick syndrome).
(internal hemorrhages or pernicious anemia)
with contrast enhancement
and DCs : cholesterol serves as a docking site that facilitates interactions
between Mycobacteria molecules (e.g. LAM)
and surface receptors on AM (e.g. FcRs,
CD222
/ Man6P-R, CRs,
CD14
/ LPS-R,
SPR
and CD209 / DC-SIGN
> TLRs)
that mediate phagocytosis : DC-SIGN interaction prevents the maturation-inducing
interactions with TLRs and induces production of the antiinflammatory cytokine
IL-10.
Early-phagosome harbouring Mycobacteria characteristically retain
TACO,
which prevents further maturation of most phagosomes by inhibiting V-H+
ATPase-dependent acidification and fusion with the endosomal pathway (hypothetical
role for mycolic acids first and newly synthetized Glu then). Inside the
phagosome, mycobacteria undergo replication (average doubling time : 20
hrs) and up to 40 bacilli may accumulate in the macrophage before pressure
causes lysis of alveolar macrophages (within 72-96 hrs). Toxins
also cause necrosis of pulmonary parenchyma (on the contrary of
ischemic necrosis cytoarchitecture is lost and cell appears homogeneously
pink after H&E staining). The usual course of untreated disease (may
vary due to iatrogenic pathomorphism after initation of polychemotherapies)
is :
individuals there may be fibrinous angioflogosis as the only manifestation
(exudative tuberculosis / tuberculous pneumonia : the simplest form
of pulmonary tuberculosis, frequently the earliest reaction to infection,
in which the alveolar spaces and the smaller bronchi become filled with
a cellular exudate consisting mainly of large mononuclear cells), with
the primary complex consisting of a parenchymal pulmonary lesion and a
corresponding lymph node focus
and accumulate up to inhibition contact, becoming epitheloid cellsand
forming the elementary "soft tubercle" (Ø = 1-5 mm) within
96 hrs from infection (primary (non-immune) granulomatous response).
Killing effectiveness depends on genome, being favourited by the presence
of the H+/divalent cation (Fe2+, Zn2+,
Mn2+ and Cu2+, used for ROI and RNI production during
oxidative burst) antiporter NRAMP1 / SLC11A1 in late endosome/lysosome,
encoded by the Bcg/Lsh/Ity locus, present in Homo
sapiens,
Rattus
norvegicus
and Mus musculus,
but not in Macaca mulattaand
Cavia
porcellus
(in the latter case LD50 = 3 bacilli !). Monocytes infected
with live M. tuberculosis differentiate into CD1-80lo83+CCR7+MHC
class IIlo DCs that are defective in IL-12 production. The inner
granuloma region undergoes autolysis (cheese-like coagulative necrosis
(caseous necrosis) => colliquative necrosis (cold abscess)
=> draining through bronchus fistula => pleurisy,
productive cough, hemoptysis => cavities
(a.k.a. caverna / cavern). Fatty acids and hypoxiainhibit
mycobacteria growth. DCs activate different subset of T-cells :
(that recognize mycobacterial lipoproteins and glycolipids incorporation
into vesicles that are shuttled within the cell and after apoptosis also
travel to bystander cells)
(that recognize phospholigands)
cells (thanks to IL-12,
which can't be synthesized by macrophages due to IL-10)
and ATP
(acting on P2Y7 / BLR
receptors) : both enhance Rab7-dependent phagolysosome formation and allows
IL-12 synthesis by macrophages, too. Exposure to sunlight increase available
1,25-(OH)2-vitamin
D3,
that also activates macrophages through VDR:
seasonal variations in vitamin D levels has been suggested as the explanation
of the seasonal incidence pattern of tuberculosis.
(Ghon focus, primary lesion or tubercle : the primary parenchymal
lesion of primary pulmonary tuberculosis in children)
("hilitis" or tracheobronchial lymphadenopathy) with lymphnodal caseous
necrosis => fibrous encystment => calcification => ossification
(osteneogenesis => "bacilli buried alive"), viewable by schermography as
Simon's
foci : hematogenous areas in the apices of the lungs of children regarded
as precursors of apical tuberculosis in later life
detects interstitial striae joining parenchymal opacities to enlarged hili
is associated)
(< 10%) => exudative tuberculosis with draining of cavities => fibrotic
cavities : cavities of the lung composed of granulation tissue surrounded
by scar tissue, as in IPF or tuberculosis; in tuberculosis they may be
the source from which the disease spreads to other pulmonary segments.
in the caseating area may lead to hemoptysis
and death by suffocation. Once treated with collapse
therapy)
or drug-resistant mycobacteria; usually evolution of an exudative post-primary
PTB; it is characterized by relapsing-remitting course and dissemination
by contiguity through perifocal exudative halos. Routes of dissemination
:,
unfavourable prognosis in diabetes
mellitus,
often associated with silicosis
(silicotuberculosis / tuberculosilicosis) and anthracosis
(anthracotic tuberculosis). It is also associated with lung cancer
due to cicatricial healing (which prevents carcinogen clearance) and frequent
chest X-rays.
-associated
and interstitial fibrosis.
pneumoconiosis
pneumoconiosis
leaves
+ silicosis / pneumosilicosis /
grinders' disease,
caused by coal with a high silica content
+ silicosis / pneumosilicosis /
grinders' disease
+ silicosis / pneumosilicosis /
grinders' disease
+ pulmonary siderosis / pneumoconiosis
siderotica
+ pulmonary siderosis / pneumoconiosis
siderotica).
It begins with alveolitis and progresses to emphysema, often with pneumothorax
sequel-related
acute lung injury (TRALI) was not recognized as a distinct clinical
entity until the 1980s with the report of a series of 36 patientsref.
TRALI has since become recognized as a not uncommon clinical complication
of transfusion and over the past 2 reporting years has become the leading
cause of transfusion-related death in the USrefref.
A recent report implicated massive transfusion as a risk factor for TRALI
in patients receiving solid
organ transplantsref.
Moreover, follow-up information from the Mayo Clinic group in their series
of 36 TRALI patients revealed that all of these patients had had recent
surgeryref1,
ref2.
In addition, 2 other patient groups appear to be at risk for TRALI, patients
receiving fresh
frozen plasma
for coumadin reversal and patients with thrombotic
thrombocytopenic purpura (TTP)
who have widespread endothelial cell activation (personal communications
from Patricia M. Kopko, MD and Richard Benjamin, MD). In published series
of TRALI, plasma-containing blood components are most commonly implicated,
with whole blood–derived platelet concentrates (WB-PLTs) having caused
the largest number of these reactionsref1,
ref2
(Popovsky MA. Transfusion related acute lung injury. In: Popovsky MA, ed.
Transfusion Reactions. Bethesda, MD: AABB Press; 2001). Although
the plasma fraction of blood or blood components rather than the cellular
constituents appears to be etiologic in TRALI, 2 of the most frequently
implicated products (WB-PLTs and PRBCs) do not contain large amounts of
plasma. Blood products implicated in TRALI listed in the order of numbers
of published cases :
antibodies, and a complement sourceref.
In this ex vivo model pulmonary edema occurred 3–6 hours following
the infusion of the admixtureref.
However, if any one of the three components were deleted pulmonary edema
did not occurref.
Furthermore, if immunoglobulins with indeterminate antigen specificity
were infused together with complement and human PMNs, lung injury was not
observedref.
Recently, Bux et al have demonstrated that employing anti-granulocyte antibodies
and PMNs that have the cognate antigens may cause pulmonary edema without
the addition of a complement sourceref.
Although antibodies to HLA class I or granulocyte antigens explain many
TRALI cases, a number of problems with this mechanism remain. In the original
description, only 59% of the immunoglobulins identified demonstrated antigen
specificity and in published series of TRALI only about 50% of the implicated
antibodies demonstrate specificity for recipient antigensref
(Popovsky MA. Transfusion related acute lung injury. In: Popovsky MA, ed.
Transfusion Reactions. Bethesda, MD: AABB Press; 2001). Since such "non-specific
antibodies" did not cause TRALI in the ex vivo animal model, the
significance of these immunoglobulins, especially in the context of TRALI,
is undefinedref.
The precise mechanism for antibody-mediated TRALI is not known; moreover,
there are a number of cases of TRALI in which an antibody either in the
donor or in the recipient is not present, and recently a case of autologous
TRALI has been reportedref1,
ref2,
ref3,
ref4
(Popovsky MA. Transfusion related acute lung injury. In: Popovsky MA, ed.
Transfusion Reactions. Bethesda, MD: AABB Press; 2001). Antibodies to HNA-3a
are commonly implicated in TRALI. HNA-3a antibodies prime PMNs and cause
PMN-mediated cytotoxicity through a 2-event pathogenesis. Isolated HNA-3a+
or HNA-3a- PMNs were incubated with plasma containing HNA-3a
antibodies implicated in TRALI, and their ability to prime the oxidase
was measured. Human pulmonary microvascular endothelial cells (HMVECs)
were activated with endotoxin or buffer, HNA-3a+ or -
PMNs were added, and the co-culture was incubated with plasma ±
antibodies to HNA-3a. PMN-mediated damage was measured by counting viable
HMVECs/mm2. Plasma containing HNA-3a antibodies primed the fMLP-activated
respiratory burst of HNA-3a+, but not HNA-3a-, PMNs,
and elicited PMN-mediated damage of LPS-activated HMVECs, when HNA-3a+,
but not HNA-3a-, PMNs were used. Thus, antibodies to HNA-3a
primed PMNs and caused PMN-mediated HMVEC cytotoxicity in a 2-event model
identical to biologic response modifiers implicated in TRALIref.ref1,
ref2.
The PMNs then diapedese through the endothelial layer, chemotax to the
site of infection and phagocytize. If the orderly process of PMN transmigration
is altered by a stimulus coming from the intravascular space rather than
the tissues, these intravascular stimuli activate vascular endothelial
cells (ECs) and cause attraction, firm adhesion and priming of PMNs. As
shown the vascular endothelium is activated causing the release of chemokines
that attract PMNs to the endothelial surface followed by selectin-mediated
tethering and firm adhesion through the ICAM-1:ß2-integrin
interaction. However, since there are not signals to cause diapedesis and
PMN chemotaxis into the tissues, the PMNs become sequestered, and these
primed, hyper-reactive leukocytes may be activated by stimuli that normally
have no effect including antibodies directed against specific leukocyte
antigens or the lipids that accumulate during routine storage of cellular
blood components. Activation of these adherent PMNs causes endothelial
damage, capillary leak, and organ injuryref.
with the insidious onset of acute pulmonary distress temporally related
to transfusionref1,
ref2,
ref3.
The clinical findings of TRALI consist of the rapid onset of tachypnea,
cyanosis, dyspnea and fever (>= 1°C)ref
(Popovsky MA. Transfusion related acute lung injury. In: Popovsky MA, ed.
Transfusion Reactions. Bethesda, MD: AABB Press; 2001). Auscultation of
the lungs reveals diffuse crackles and decreased breath sounds, especially
in dependent areasref
(Popovsky MA. Transfusion related acute lung injury. In: Popovsky MA, ed.
Transfusion Reactions. Bethesda, MD: AABB Press; 2001). The physiologic
findings include acute hypoxemia, with PaO2/FiO2
< 300 mm Hg, and decreased pulmonary compliance despite normal cardiac
functionref1,
ref2,
ref3
(Popovsky MA. Transfusion related acute lung injury. In: Popovsky MA, ed.
Transfusion Reactions. Bethesda, MD: AABB Press; 2001). Radiographic examination
reveals diffuse, fluffy infiltrates consistent with pulmonary edemaref
(Popovsky MA. Transfusion related acute lung injury. In: Popovsky MA, ed.
Transfusion Reactions. Bethesda, MD: AABB Press; 2001)
ref1,
ref2
(Popovsky MA. Transfusion related acute lung injury. In: Popovsky MA, ed.
Transfusion Reactions. Bethesda, MD: AABB Press; 2001). Milder forms of
TRALI have been described that require prompt delivery of supplemental
oxygen aloneref1,
ref2,
ref3,
ref4.
As with acute lung injury (ALI) and ARDS, there is no role for treatment
with corticosteroids or diuretics, although one infant was successfully
treated with extracorporeal
membrane oxygenation (ECMO)
for a particularly severe clinical presentationref1,
ref2,
ref3
(Popovsky MA. Transfusion related acute lung injury. In: Popovsky MA, ed.
Transfusion Reactions. Bethesda, MD: AABB Press; 2001)
involve respiratory distress related to bronchospasm manifested by tachypnea,
wheezing, cyanosis, and severe hypotension. Facial and truncal erythema
and edema are common, with urticaria characteristically involving the head,
neck, and trunk. The respiratory distress from anaphylactic transfusion
reactions is related to laryngeal edema rather than pulmonary edema as
in TRALI. These reactions occur rapidly during the transfusion of any type
of protein containing blood component and may occur following the transfusion
of very small volumes of blood (Vamvakas EC. Allergic and anaphylactic
reactions. In: Popovsky MA, ed. Transfusion Reactions. Bethesda, MD: American
Assocaition of Blood Banks; 1996:81–124)
stimulation of SMCs => endothelial cell dysfunction
representing dilatations of the lung parenchyma; it is also seen with multiple
small cysts or cavities)
and azathioprine,
preserves vital capacity and DLCO in patients with IPF better
than does standard therapy aloneref,
characterized by patchy inflammation of bronchioles with filling of their
lumina as well as adjacent alveoli and alveolar ducts by pigmented macrophages,
resulting in dyspnea and a productive cough; it
is usually a benign condition that will clear up upon cessation of smoking.,
while working in recently filled silos; death may occur from acute
pulmonary edema
or heart-lung
transplant
of organizing pneumonia in several
important ways including fibroblast/myofibroblast phenotype, rates of fibroblast/myofibroblast
apoptosis, modulation of extracellular matrix deposition, and extent of
neovascularizationref.
Differences in the character and extent of reepithelialization may play
a pivotal role in determining why "fibroblast foci" of UIP/IPF resolve
into a scar while the Masson bodies of organizing pneumonia disappear without
a trace. Disordered reepithelialization in UIP/IPF has previously been
linked to upregulation of epithelial cell apoptosis and impaired adhesion
to damaged basement membranesref1,
ref2,
ref3.
(acute lupus pneumonitis : characteristics include rapid onset,
fever,
dyspnea,
and coughing.),
and the other causes abnormalities in the b
chain of GM-CSF-R
(most commonly hematologic) or in association with inhalational exposure
to silica,
aluminum
dust, titanium dioxide,
or other material
autoantibodies, which prevent the binding of GM-CSF to GM-CSF-Rs on alveolar
macrophages. GM-CSF–initiated signaling plays a unique, nonredundant role
in alveolar macrophage function and pulmonary homeostasis.
supplementation. Previously, therapy consisted of whole-lung lavage, which
results in numerous complications and does not address the pathogenetic
mechanisms. Administration of exogenous GM-CSF appears to help many patients,
and its potential as a subcutaneous or aerosolized therapy is being evaluated.
Whether patients with pulmonary alveolar proteinosis have defects in host
defense and innate immunity is not clear, nor is the effect of such defects.
GM-CSF–/– mice clearly have a defect in pulmonary defense against
pathogens, as well as extrapulmonary abnormalities and a decreased susceptibility
to experimentally induced autoimmune disorders. Patients with pulmonary
alveolar proteinosis do not have deficient expression of GM-CSF, but they
have neutralizing GM-CSF autoantibodies, which may account for differences
between host defense defects in such patients and defects in mice. Although
secondary infections have been described in these patients, our understanding
of host defense in this disorder is limited by its rarity, the variability
of its outcomes, and reporting biases. Patients may be at risk for secondary
infections, but bacteria that commonly cause respiratory infections are
not often the inciting agentsref.
Opportunistic pathogens — most commonly Nocardia, but occasionally
Cryptococcus,
Histoplasma,
Aspergillus,
or Mycobacterium tuberculosis — have been reported in about 13%
of patientsref,
with systemic infection documented in some cases. In a review of 65 cases
in which death was attributable to pulmonary alveolar proteinosis, respiratory
failure was the apparent cause of death in 47 cases (72%), whereas uncontrolled
infection was the cause in 12 (18%)ref.
These findings suggest that clinically important lung infections occur
in some patients and that systemic infections are less common. Few researchers
have investigated whether GM-CSF autoantibodies cause defects in cells,
other than alveolar macrophages, that express GM-CSF receptors. Uchida
et al. reportref
on the effects of GM-CSF autoantibodies on neutrophil functions. Their
observations show that neutrophils from patients with pulmonary alveolar
proteinosis have defects in both basal and GM-CSF–primed antimicrobial
functions. In particular, the phagocytic index and phagocytic capacity
of neutrophils isolated from these patients were approximately 90% and
30% lower, respectively, than those of neutrophils from healthy control
subjects. The basal capacity for adhesion to plastic, the oxidative burst
in whole blood, and the killing of Staphylococcus aureus were also
reduced. Furthermore, GM-CSF priming in vitro was impaired. Similar defects
in basal neutrophil functions were observed in GM-CSF–/– mice,
although no defect in GM-CSF priming was observed. The defect in affected
human neutrophils was mimicked by treating blood from healthy control subjects
with GM-CSF autoantibodies. Thus, neutrophils from patients with pulmonary
alveolar proteinosis have functional defects when tested in vitro.
How the signaling of GM-CSF through its receptor on neutrophils augments
neutrophil function remains an important questionref.
PU.1 is apparently critical in GM-CSF–initiated signaling in alveolar macrophages
but not in neutrophils, since Uchida et al. show that neutrophils from
patients with pulmonary alveolar proteinosis do not have lower PU.1 expression
than those from healthy control subjects. Furthermore, defects in neutrophil
function are apparent in vitro, but it is not clear how they contribute
to a defect in host defense in vivo. Humans and mutant mice with defects
in innate immunity, including abnormal neutrophil function, often have
increased blood levels of neutrophils, G-CSF, and cytokines; the failure
to destroy pathogens leads to the persistence of pathogen-induced stimuli.
In contrast, in the study by Uchida et al., patients with pulmonary alveolar
proteinosis who had defective neutrophil function in vitro did not have
increased neutrophil counts and serum G-CSF levels, suggesting that their
host defense and innate immunity were sufficient for managing daily exposures
to common pathogens and commensal organisms. Clinically apparent infections,
especially with opportunistic microbes, do occur in some patients; microbes
were identified at presentation in more than half the patients studied
by Uchida et al. Whether host defense mechanisms are able to compensate
for defects in neutrophil and macrophage function until the environment
delivers a particular pathogen or a large load of pathogens, or until a
combined assault is made on the immune system, remains to be elucidated.
The absence of repeated infections, particularly in the lungs, is surprising,
given the magnitude of the neutrophil defects seen in vitro; perhaps
products of surfactant degradation have important antimicrobial effects.
Clearly, the study by Uchida et al. raises important, provocative questions
that beg to be pursued.
recipients iatrogenic immunosuppression combined with defective clearance
of alveolar material by alveolar macrophages created a milieu conducive
to the accumulation of surfactant, lipoprotein, and fibrinous debris that
was morphologically identical to alveolar proteinosis.
for < 7 days, cough, hypoxemia => acute respiratory
failure => dyspnea, and eosinophilia
(Ascaris pneumonitis / pulmonary ascariasis),
one of the major components of the fungal cell wall, are elevated in the
BALFs (rather than blood) of patients with AEP and the same decreases with
clinical improvementref,
night sweats, weight loss, eosinophilia, and a chest film revealing nonsegmental,
nonmigratory infiltrates in the lung periphery. It affects 1% of patients
with (tracheo)bronchial asthma (chills, cough, anorexia)
in sputum
in the bronchioles and alveoli,
acrolein)
and maleic anhydride
:
(hydrocortisone 100 mg/3 hrs, prednisone 25 mg/3 hrs)
:,
hypercapnia,
mild, compensated respiratory
alkalosis,
normocapnia, respiratory
alkalosis,
hypercapnia
and respiratory acidosis
:
dust or fumes; it may be acute, in which form it is often fatal, or it
may be chronic and recurring,
caused by the inhalation of mercury fumes.
prior to or during delivery. Postterm
infants
and hypoxic or acidotic fetuses are at higher risk.
did not reduce the risk of moderate or severe meconium aspiration syndrome,
perinatal death, or other major maternal or neonatal disordersref
)
or oropharyngitis))
: per os anti-constipation
emulsions ingested before lying at bed
resulting from radiation
exposure, usually radiation therapy, with coughing, dyspnea,
and alveolar infiltration, leading to mild to severe or even fatal fibrosis
6 to 9 months after the exposure. It may extend to areas other than the
irradiation field when autoimmunity is triggered.
characterized by extensive pulmonary consolidation and rapidly progressive
functional deterioration and by alveolar exudate (with the presence of
Masson
bodies), interstitial infiltrates, and necrotizing arteritis.).
,
nephropathies,
systemic
arterial hypertension,
neurological
disorders,
immune
deficiencies.
Mortality : 1%.
(Frankel-Weichselbaum pneumococcal
pneumonia) (15-76% of all pneumonia, 90% of all bacterial pneumonia;
expecially by types 1, 2 (severe !), 3, 4, 5, 6, 7, 8, 9, 12, 14, 18 and
19 (often endogenous infection in nasopharyngeal carriers, whose frequency
relates to age and community life-style) : a type of lobar
pneumonia with fibrinous angioflogosis of one or more lobe(s)
of the lung, expecially in Winter and early Spring, usually following a
viral URT infection; characteristics include chills followed by sudden
fever,
dyspnea,
tachypnea,
pain in the side, and coughing with bloodstained sputum. It usually begins
in the lower lobe :,
crepitatio
indux
(streptococcal pneumonia : pleural effusion,
with or without pleural empyema, is particularly
common)
(4%; a common type of bacterial pneumonia, usually bronchopneumonia.
Since many strains of Staphylococcus are antibiotic-resistant, this
type is often seen in hospitals in patients on antibiotic therapy after
surgery (MSSA => early; MRSA => late); it also commonly infects debilitated
patients such as those suffering from other respiratory infections or viral
infections such as influenzaviruses.
Characteristics include fever,
dyspnea,
rales, pleural effusion, and pleural empyema)
(anthrax pneumonia / inhalational anthrax / woolsorter's pneumonia)
(meningococcal pneumonia : rare; many cases are subclinical, but
some infections become overwhelming, with fever,
pleural
effusion, and even death)
(tularemic pneumonia / pulmonary tularemia.)
and characterized by white fatty degeneration of the lungs, which appear
pale and virtually airless
(amebic pneumonia : pneumonia resulting from so-called amebic abscesses
in the lung)
(malarial pneumonitis : characterized by cough with bloody sputum
and coarse rales; in severe cases thromboses may result from the agglutination
of parasitized erythrocytes in small blood vessels of the lung)
treatment after 3 days is not inferior to discontinuing it after eight
days in adults admitted to hospital with mild to moderate-severe community
acquired pneumonia who substantially improved after an initial three days'
treatmentref
,
endotracheal
intubation
for > 3 days (preventable by oropharynx disinfection; nasogastric
tube
decreases pneumonia risk but increases sinusitis risk !), thoracic surgery
lasting > 4 hrs, hypoalbuminemia),
(22.6%) (late)
(14.1%)
(8.2%) (early)
(5.8%; it is often fatal to immunocompromised patients)
(debilitated or immunocompromised patients and is characterized by consolidation
with abscesses in the upper lobes)
(glanders pneumonia / pneumonia malleosa : caseous or calcified
granules and pulmonary consolidation)
(20.9%; a common type of bacterial pneumonia, usually bronchopneumonia.
Since many strains of Staphylococcus are antibiotic-resistant, this
type is often seen in hospitals in patients on antibiotic therapy after
surgery (MSSA => early; MRSA => late); it also commonly infects debilitated
patients such as those suffering from other respiratory infections or viral
infections such as influenzaviruses.
Characteristics include fever,
dyspnea,
rales, pleural effusion, and pleural empyema)
(early), ...) (13%)
(pulmonary blastomycosis
/ bronchoblastomycosis
: pneumonia with multifocal progression; it
often resolves with fibrosis or takes an indolent course, sometimes with
cavitation and eventual spread to other organs. In some patients there
is an acute onset of symptoms with ARDS
that can be fatal)
(a common type of bacterial pneumonia, usually bronchopneumonia.
Since many strains of Staphylococcus are antibiotic-resistant, this
type is often seen in hospitals in patients on antibiotic therapy after
surgery (MSSA => early; MRSA => late); it also commonly infects debilitated
patients such as those suffering from other respiratory infections or viral
infections such as influenzaviruses.
Characteristics include fever,
dyspnea,
rales, pleural effusion, and pleural empyema)
(often after contact with an infected animal; it is often subacute, with
consolidation and cavitation visible radiographically => pulmonary malacoplakiaref1,
ref2)
: a sometimes fatal type of bacterial pneumonia seen in immunocompromised
patients. It is usually bronchopneumonia,
and characteristics include acute onset of dyspnea
with fever,
productive cough, chest pain, and abscess formation or pleural
empyema.
(usually mild type, generally seen in patients with some other debilitating
condition, especially smokers with chronic obstructive pulmonary disease.
Symptoms include fever
and dyspnea)
(a rare type of bacterial pneumonia, usually in the bronchi or a lower
lobe, seen most often in debilitated patients or infants)
(a rare type usually seen in patients with chronic lung disease; characteristics
include fever,
cough, and dyspnea, sometimes with pleural
empyema)
(Pittsburgh pneumonia : a type
of pneumonia resembling legionnaires' disease, and occurring as a nosocomial
infection especially in immunocompromised patients)
(plague pneumonia / pneumonic plague)
(usually nosocomial, seen in young children and debilitated or immunocompromised
adults; characteristics include fever
and coughing with lung nodules that may be either firm or hemorrhagic and
may progress to necrosis of the alveoli with cavitation)
or Enterobactercloacae;
it is usually nosocomial and seen in debilitated patients.
(sporotrichoid)
(seen with severe pulmonary nocardiosis)(sometimes
seen in pulmonary aspergillosis; it colonizes pulmonary cavities
(bronchiectasis, cavities, and lung abscesses;
target
lesion : a small, sharply delineated focus of necrosis, seen in the
lungs in invasive aspergillosis, consisting of a rounded gray center surrounded
by a hemorrhagic border)
(pulmonary candidiasis : from inhalation of fungi in patients with
esophageal candidiasis)
: it branches by 90° angles
(respiratory sporotrichosis)
(coccidioidal pneumonia : pneumonia following primary coccidioidomycosis.
It varies from a slowly-developing disease with chronic cough, chest pain,
hemoptysis,
and fever
to a more rapidly spreading acute condition, usually seen in immunocompromised
patients, with cavitation, spread to other organ systems, and frequently
a fatal outcome)
(pulmonary cryptococcosis
: most cases are asymptomatic or characterized by cough, dull chest pain,
and low grade fever,
although a few cases are fulminant in the lungs (peribronchitis
or diffuse pneumonia)
limited to one only lobe => fever,
hypophonesis, small
bronchi coarse crackles,
productive
cough
,
nephropathies,
systemic
arterial hypertension,
neurological
disorders,
immune
deficiencies.
Mortality : 1%.
(3÷14%, expecially in alcoholists, diabetics and individuals affected
by COPD. Raspberry gel-like sputum)(4%)
(fever,
rales, and infiltration of a middle or lower lobe; the recovery period
is usually prolonged)
(a mild type of bacterial pneumonia, usually seen in infants whose mothers
are infected; eosinophilia)
(Louisiana pneumonia : a form of pneumonia seen in Louisiana)
(Q fever pneumonia : it is usually benign and self-limited, with
granulomatous infiltrates and linear atelectasis visible radiographically:
3%)
(typhoid pneumonia : children may
develop bronchopneumonia
and adults may develop lobar pneumonia,
with suppuration and pleural empyema)
(tuberculous pneumonia : part
of the earliest reaction to infection
(Eaton agent pneumonia / mycoplasmal pneumonia : 10%, expecially
in youngs with age 5-19)
(influenzal or influenza virus pneumonia : some cases are mild,
but it can develop into a fulminant condition characterized by massive
pulmonary
hemorrhagic edema with consolidation. It may be accompanied by a superinfection
with bacterial pneumonia; 8%)
(measles virus pneumonia : it ranges from a mild type occurring
during a bout of measles to severe, even fatal, giant
cell pneumonia)
(seen in infants and young children and occasionally in immunocompromised
or otherwise debilitated adults; also wheezing, and crackles due to bronchiolitis)
(it is usually mild, but in neonates and the immunocompromised it can be
fatal. Characteristics range from interstitial inflammation without necrosis
to a necrotizing bronchitis and bronchiolitis
with desquamation that may occlude the lumen, and areas of hemorrhagic
consolidation alternating with areas of atelectasis)
(varicella pneumonia : developing as a complication 2 to 6 days
after the appearance of varicella (chickenpox), seen in adults more often
than children. Symptoms may be severe, with violent cough, hemoptysis,
and severe chest pains. Radiologically, there are numerous nodular densities,
which may coalesce, at the base of each lung, and often hilar lymphadenitis;
small nodular calcifications may persist),
immunodeficiency,
antibiotic-resistance, consciousness impairment, tachypnea
(> 25 / min), hemodynamic instability, septic shock, multilobar involvement,
massive pleural effusion, cavitation, leukopenia
(< 4,000 / mL) or leukocytosis (> 20,000
/ mL), anemia, socioeconomical difficulties.
,
endotracheal
intubation
for > 3 days (preventable by oropharynx disinfection; nasogastric
tube
decreases pneumonia risk but increases sinusitis risk !), thoracic surgery
lasting > 4 hrs, hypoalbuminemia),
(Friedländer's bacillus pneumonia : usually lobar in type and
often limited to the right upper lobe; characteristics include large amounts
of inflammatory, sometimes bloody, mucoid exudates in the lung; 9.1%)
(early)
(herpes simplex virus pneumonia : in conjunction with other manifestations
of the herpesvirus infection)
(cytomegalovirus pneumonia) => ARDS
: giant
cell pneumonia / Hecht's pneumonia : multinucleate giant cell inclusion
bodies
(sometimes progresses to life-threatening conditions such as meningitis,
pericarditis, endocarditis, and epiglottitis that can cause obstruction
of the airway; 8%)(interstitial
plasma cell pneumonia / pneumocystosis / pneumocystiasis is characterized
by cellular detritus containing plasma cells appearing in the lungs; if
untreated it leads to pulmonary consolidation, hypoxemia, and death),
normophonesis, no coarse crackles, dry
cough
antibacterials;
Weill's
sign : absence of expansion in the subclavicular region of the affected
side in infantile pneumonia.
: densities for up to 18 weeks
for a pathogenic microorganism]
or urinoculturepositive
per Streptococcus pneumoniae,
...)
of the lung
DNA sequences, as well as an overexpression of human IL-6 and human cyclin
D1 in myofibroblastic cells; the spectrum of expressed viral genes is not
the same as can be observed in Kaposi's
sarcoma
or multicentric
Castleman's disease,
suggesting that HHV-8 plays a different role in the pathogenesis of its
associated diseases. Lung IPT secondary to buttressing material may follow
lung
volume reduction surgery (LVRS)ref.
The underlying cause and pathogenesis remain uncertain and may be an unregulated
reparative response of injured tissue. A history of lower respiratory tract
infection is present in 18 to 30% of casesref1,
ref2.
ref.
It is speculated if solitary BOOP
may evolve into inflammatory pseudotumor of the lungref.
Although variable success in the treatment of these lesions with corticosteroids,
radiation, and antibiotics has been reported, surgery remains the preferred
treatment modalityref1,
ref2,
ref3.
Early and complete surgical resection of the IPT provides cure and prevents
local recurrenceref.
However, complete resection is usually extremely difficult. Persistence
of the mass and symptoms may necessitate further operations, as in our
patient.
from the lungs:
a benign tumor, usually a circumscribed nodule or coin lesion located in
peripheral lung parenchyma or in a bronchus; tissue types and degree of
calcification vary
: p53-, pRb+,
pituitary
adenomas
and duodenal carcinoid (Zollinger-Ellison
syndrome),
bronchial
carcinoid)
: lung cancer mortality rates in Xuan Wei are among the highest in China
in both nonsmoking women (which in this region traditionally start the
fires and cook, spending more time inside homes that lack ventilation and
exposing to indoor emissions from the burning of smoky coal : 16.3% have
mutations in KRAS
and TP53).
The strongest family link was found in the relatives of patients who developed
the disease at age 60 or younger. In Iceland the parents of patients who
developed the disease before age 60 had nearly a 3.5 times higher risk
of also developing the disease compared to the general population. For
brothers and sisters in such cases the risk was > 3 times higher and for
children slightly less than that. Aunts and uncles, cousins, nieces and
nephews of lung cancer victims of any age also run a higher risk, though
at lower levels than the immediate familyref.,
including chromated
copper arsenate (CCA),
more prominent among cigarette smokersref.
such as broccoli and cabbage (World Cancer Research Fund. Food, nutrition
and the prevention of cancer: a global perspective. Washington: American
Institute for Cancer Research, 1997). Such vegetables are rich in isothiocyanates,
which have been shown in animals to have strong chemopreventative properties
against lung cancerref.
In a review of studies of the effect of cruciferous vegetables, a definite
protective effect against any type of cancer could not be identified, in
view of the small size of studies and potential for confounding from other
dietary sources (IARC Handbook of cancer prevention. Cruciferous vegetables,
isothiocyanates and indoles. Lyon, France: IARC Press, 2004). Confounding
could, however, be addressed by adoption of a mendelian randomisation approachref.
Isothiocyanates are thought to be eliminated by glutathione-S-transferase
enzymes, most notably GSTM1
and GSTT1ref1,
ref2.
Both GSTM1 and GSTT1 genes have null alleles with homozygous null genotypes,
resulting in no enzyme being produced. Individuals who are homozygous for
the inactive form of either or both genes probably have higher isothiocyanate
concentrations because of their reduced elimination capacity. Furthermore,
and implicit in the mendelian randomisation approach, the roles of GSTM1
and GSTT1 genes are likely to be independent of other dietary and lifestyle
factors, reducing the possibility of confounding from these sources. These
results provide strong evidence for our a-priori hypothesis that the protective
effect of cruciferous vegetables is most apparent in those who have low
values of circulating GST enzymes, because they have null alleles for GSTM1
and GSTT1 genes. The results also accord with those of several smaller
studies of lung cancer, breast cancer, and colorectal adenomas, which showed
a protective effect in GSTM1 and GSTT1 null carriersref.
However, we cannot draw definitive conclusions from these individual studies
because of their small sample size (the 3 previous studies of lung cancer,
based in Shanghai, Singapore, and Texas, consisted of a total of 968 cases
and 1362 controls)ref1,
ref2,
ref3.
Taking into consideration the size of the protective effects that have
been reported in this and other studies, which are likely to have been
substantially diluted by measurement error, these findings raise the prospect
of an important chemopreventive effect against lung cancer for cruciferous
vegetables in general, and isothiocyanates in particularref
arises from stem cells
infection in Asian patients
of the lung
of the lung : c-kit+ (55%), (4q-, 5q-, 10q-, 13q-, 15q-),
flattened 3D clusters with peripheral palisading, moderate to large single
cells with scant (alcohol-fixed) or moderate (air-dried) cytoplasm; and
large, oval, or polygonal nuclei with irregular contours, thickened nuclear
membranes, and finely or coarsely granular chromatin, showing some molding
and crush artifact. Nucleoli are generally present, and occasionally prominent.
Mitosis and necrosis are apparent. Neuroendocrine stains are applied to
all specimens, with at least one marker, commonly synaptophysin, positive
in 90% of specimens
of the lung / small cell lung cancer (SCLC) / microcytoma (18.2-25%
of all lung cancers; nonsurgical lesion, dense nuclei, sparse cytoplasm)
: p53+, pRb-, c-kit+ (46%); PCNA+
> 70%;
it has small oval undifferentiated cells that are intensely hematoxyphilic.
,
adrenal
gland metastases,
renal
metastases,
pancreas,
bowels,
bone
metastases,
and rarely cutaneous
metastasesref)
are common at diagnosis.
,
paraneoplastic symmetric polyarthritis
> TK
or TPA
on lungs (ipsilateral hemithorax, mediastinic and supraclavear lymph nodes,
and contralateral hilar lymph nodes => 1 only radiotherapeutic irradiation
field) + radioprophylaxis on encephalon at the end of the lung treatment.
Clinical presentation can mimic that of (tracheo)bronchial
asthma
of the lung (ACL) / non-smoker's carcinoma / scar carcinoma or cancer
(25-30.7%) : a type of bronchogenic carcinoma associated with scarring
(the scar may either precede the carcinoma or be a fibrotic response to
it) and made up of cuboidal or columnar cells in a discrete mass, usually
at the periphery of the lungs. Most such tumors derive from and form
bronchial mucus glandular structures containing mucin, although a minority
are solid and without mucin. Growth is slow, but there may be early invasion
of blood and lymph vessels, giving rise to metastases while the primary
lesion is still asymptomatic (40%, peripheral nodules, possibly
hilar masses, more common women; aggressive distant metastases, vacuolization,
mucus synthesis, glandular differentiation)
ref
;
in some cases inclusion of a tumor in this category rather than in one
of the more specific categories of bronchogenic carcinoma has been questioned.
due to ectopic PTH incretion),
SCC,
and CEA
> TK
or TPA
and/or the cardiovascular operative risks are too high. Stage IIIA requires
both neoadjuvant and adjuvant chemotherapy:
,
erlotinib
(survival improved by 40% (6.7 months compared to 4.7 months for those
on standard therapy))
and erlotinib
gave response rate of about 20%, while median survival was 12.5 months
: the treatment resulted in only mild side effects, including rash and
diarrhea
(55-60 Gy with conventional fractionation or hypofractionation)
2 weeks later (up to 50 Gy)
only
>
bone metastases
> brain metastases,
adrenal
gland metastases,
or contralateral lung)
or CT
(for all patients)
(for all symptomatic patients)
(for NSCLC patients with stage > II) => X-rays if hypercaptating
areas are detected
(for patients with pleural effusion)
(for patients with N2-N3 at chest CT)
(for patients with T3-T4 or M1 brain)
(expensive; for patients with N2/3M1)
in (superior) pulmonary sulcus
tumor (one at the apex of the lung along the superior pulmonary sulcus,
extending outward to destroy the ribs and vertebrae and invading the brachial
plexus).
Tumor involving the upper part of the lung, with invasion of the surrounding
structures as the plexus brachialis, ribs and extending in the nods, possibly
causing a Claude-Bernard
Horner syndrome.
It may cause hypotrophy of the innervated hand. After a first decription
in 1924 (Pancoast HK. Importance of a careful roentgen-ray investigation
of the apical regions. JAMA 83:1407 (1924)), it was better described in
1932 (Superior pulmonary sulcus tumors characterized by pain, Horner's
syndrome, destruction of bone and atrophy of hand muscles. JAMA 99:1391
(1932)). Actually already in 1838 Hare wrote one of the first published
descriptions of superior pulmonary sulcus tumor (Hare ES. Tumor involving
certain nerves. London Medical Gazette. 23:16 (1838))
(1-4%)
(5-10%)
:
: increased density only if neoangiogenesis occurrede (cysts and fibrotic
tissue appears normodense). If borders are irregular, a biopsy is required.-assisted
(if neoplasm is in medioparenchymal location)-assisted
(if neoplasm is near chest wall)
(probe enters via jugular incision and explores spaces around bronchi to
make biopsies of paratracheal and hilar lymph nodes : N2)
: examination of pleural cavity when cytology is negative but pleural effusion
has been detected
detects high levels of alkanes and benzene derivatives
can detect stage I (curable) lung cancer in persons at riskref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7
(Henschke CI, Yankelevitz DF, Smith JP, Miettinen OS. The use of spiral
CT in lung cancer screening. In: DeVita VT, Hellman S, Rosenberg SA, eds.
Progress in oncology 2002. Sudbury, MA: Jones and Barlett, 2002) as per
the International Early Lung Cancer Action
Program (IELCAP) protocol. a positive result on the initial low-dose
CT scan was defined as the identification of at least one solid or partly
solid noncalcified pulmonary nodule 5 mm or more in diameter, at least
one nonsolid noncalcified pulmonary nodule 8 mm or more in diameter, or
a solid endobronchial noduleref.
If none of the noncalcified nodules identified met the study criteria for
a positive result or if the test was negative, CT was repeated 12 months
later. The diameter of the nodule was defined as the average of the length
and width of the cross-sectional area of the largest nodule in the CT images.
The consistency of the nodule was defined as solid if the nodule obscured
the entire lung parenchyma, partly solid if it obscured part of the lung
parenchyma, and nonsolid if it obscured none of the parenchymaref.
If the result was positive, the type of workup depended on the diameter
of the largest nodule. For nodules 5 to 14 mm in diameter, the preferred
option was to perform another CT at 3 months; if the images showed growth
of the noduleref,
then biopsy, ideally by fine-needle aspiration, was to be performed, whereas
if there was no growth, the workup was stopped. The other option was to
perform PET immediately, and if the results were positive, biopsy was to
be performed; otherwise, CT was to be performed at 3 months. For nodules
15 mm in diameter or larger (whether solid, partly solid, or nonsolid),
immediate biopsy was an option in addition to the options already specified
for smaller nodules. When infection was suspected, a 2-week course of antibiotics
followed 1 month later by CT was an alternative to all the options mentionedref,
and if no resolution or growth was observed, biopsy was to be performed;
otherwise, the workup was stopped. For all participants for whom the workup
was stopped or for whom the biopsy did not lead to a diagnosis of lung
cancer, CT was to be repeated 12 months after the baseline CT. For annual
screenings, a positive result was considered to be any newly identified
noncalcified nodule, regardless of size. If no new nodule was identified,
CT was to be repeated 12 months later. If one or more new nodules were
identified, the workup depended on the diameter of the largest nodule.
If all nodules were < 3.0 mm in diameter, or if the largest nodule was
> 3.0 mm but < 5.0 mm in diameter, CT 6 or 3 months later, respectively,
was to be performed. If no growth was seen in any of the nodules, the workup
was stopped. If at least one of the noncalcified nodules was > 5.0 mm in
diameter, then an immediate 2-week course of a broad-spectrum antibiotic
was prescribed, followed 1 month later by CT. If the nodules showed no
resolution or growth, biopsy was to be performed; otherwise, the workup
was stopped. PET was an alternative to immediate biopsy; if the result
was positive, biopsy was to follow. If the result was indeterminate or
negative, CT was to be performed 3 months later, and if the scans showed
growth, biopsy was to follow. Otherwise, the workup was stopped. For all
patients for whom the workup was stopped or when biopsy did not result
in a diagnosis of lung cancer, CT was to be repeated 12 months after the
previous annual CT
)
due to septic
embolism,
septic
arthritis,
brain
abscess,
meningitis,
secondary amyloidosis)
,
chest pain, postural cough, vomiting,
digital hippocratism
(round and opaque ==vomiting=>
hydroaereal level and transparent)
and is underestimated by the initial chest x-ray. Respiratory failure in
these patients may not be immediate, and frequent reevaluation is warranted.
(MPM),
which also allows the intracavitary evaluation of the extension of the
disease
(pleuritis / pleurisy) : inflammation of
the pleura, with exudation into its cavity and upon its surface. The inflamed
surfaces of the pleura may become permanently united by adhesions
in patients with systemic
lupus erythematosus..
Accompanied by a lymphocyte-rich exudate.,
often accompanying uremic
pericarditis;
there are often painful friction rubs and hemothorax.
not uncommonly passes through the diaphragm to present as a right pleural
transudateref
in pleuritis with effusion varies in pitch during inspiration and expiration,
being raised on inspiration.
in pleuritis with effusion varies in pitch with the opening and closing
of the patient's mouth
(hydrothorax),
fever,
pneumonia, and hydrothorax occurring after a
puncture wound of the chest.
through a diaphragmatic hiatusref
drained into pleura through lymph vessels along DP
gradient,
...),
pain, sinusal
tachycardia,
dyspnea,
malaise,
thoracentesis,
culture
,
in
situ drainage, thoracoscopy,
pleural
decortication.
on the affected side, and pneumomediastinum.
=> systemic
arterial hypotension
and jugular venous distension (JVD) are enough for diagnosis
shows ...
).
or HRCT
)
until symptoms (straight trachea, normal jugular veins, normal breath sounds)
and CXR
(position of tube and lungs) reverse
by injecting irritating substances (Glc solution, talc) in pleural cavity
to induce a synechia
=> chronic
cor
pulmonale,
compensatory pulmonary emphysema in the unaffected lung.
intake
or even TIA.
.
Dopamine may activate oxytocin
production in the paraventricular nucleus of the hypothalamus. Oxytocin
may then activate cholinergic transmission in the hippocampus and, finally,
acetylcholine might induce yawning via the muscarinic receptors of the
effectors. This is an over-simplification; many other molecules can modulate
yawning, such as nitric oxide, glutamate, GABA, serotonin, ACTH, MSH, sexual
hormones and opium derivate peptides.
in the 1920s, with 'spasmodic yawning,' with epilepsy, not to speak of
hysteria.| virus | progression from upper respiratory infection to pneumonia | pulmonary copathogens | overall 30-day mortality with pneumonia |
| respiratory syncytial virus | 40% | 2.5-33% | 25-45% |
| parainfluenza | 18-44% | 53% | 35-37% |
| influenza A/B | 18% | 50% | 25-28% |
| virus |
|
|
|
|
|
|
| RSV | 1.0 (0.8–1.3) | 2.2 (1.5–3.2) |
| Parainfluenza | 1.3 (1.0–1.6) | 3.4 (2.4–4.7) |
| Influenza | 0.8 (0.4–1.4) | 2.6 (1.4–4.9) |
Acute chest pain :
Aetiology :
in angina pectoris; localized or irradiated to back, jaw, right body, epigastrium
or acute
myocardial infarction (AMI)
(mimicked with open hand over sternum, reversed location in situs viscerum
inversus)
dissection (enlargement at CXR,
far more common than echocardiography in emergency rooms)(pointed
pain; pericardial rubbing over 4th intercostal space while patients keeps
the breath; antalgic anteriorization displaces pericardial exudate forward
preventing rubbing and irritation of parietal pericardium; eventual disappearance
may mean worsening of inflammation; decreased amplitude on all EKG leads,
including Pardee's wave)
disorder, the physical symptoms being attributed to autonomic responses
to anxiety or to hyperventilation
(pain only at digital pressure over Valleix points (along parasternal,
mid-axillary, and paravertebral lines, where the intecostal nerves come
superficial, pain increases with inspiration
(Tietze's syndrome)
(diagnosis is difficult only at prodromal stages), ..)
(during flexion in obese patients) or hyatal
hernia
(sudden slimming))
or acute
myocardial infarction (AMI),
acute
pericarditis,
aortic
dissection,
pulmonary
embolism)
:
Copyright © 2001-2014 Daniele Focosi.
All rights reserved
| Terms of use | Legal
notices
|
|
|
|
|
