patho respi- 1 tranx
TRANSCRIPT
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Respiratory function:
Ventilation- entry of air
Perfusion- blood in capillaries
Respiratory gas exchange
Anatomy:The lungs is divided intosegments or lobules or lobes, the right
lung is divided into 3 lobes while the left
lung is divided into 2 lobes
Anteriorly: mostly upper lobe
Posteriorly: mostly lower lobes; upper
parts of the lower lobe are quite thin and
are located laterally.
Trachea- contains C-shaped cartilage
rings but as you go down distally these
rings will be replaced by cartilage plates
and will eventually disappear as you go
more distally along the airway.
Acinus- main respiratory unit; where gas
exchange occurs
- Starts with the respiratory
bronchiole alveolar duct
alveolar sacs
- Before the respiratory bronchiole
we have the terminal bronchiole
- Group of 3 acini = lobule
- As you go down distally smooth
muscles also disappears.
Cross-section of the acinus
Pores of Kohn- holes in between
alveolar spaces that facilitate
Subject: PhathologyTopic: DISEASES OF THERESPIRATORY TRACT- 1Lecturer: Dra. Dela FuenteDate of Lecture: October 2011
Transcriptionist: The SoloistPages: 14
SY
2011-2
012
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movement of air from one alveolar sac
to another and not only air but also
exudates in cases of infections which
promotes spread of infection from one
alveolar space to another.
On a closer view: alveolar structure
that is lined by pneumocytes and also
characterized by the presence of
macrophages.
Alveolar capillaries- are closely
apposed to the alveolar epithelium
that they share a common basement
membrane which helps in the efficient
diffusion of gases between the
capillaries and the alveolar spaces.
Lining: Ciliated Pseudostratified
columnar epithelium with goblet cells.
The cilia are responsible for themucociliary movement. As you go
down the ciliated epithelium is
replaced by the mucus-secreting
epithelium.
In between the epithelium and the
cartilage, we have the bronchial
glands or mucus glands and we also
have smooth muscles.
In some disease states, these glands
undergo hyperplasia and hypertrophy
inc. mucus secretion (seen in
chronic bronchitis)
Smooth muscles can also undergo
hypertrophy which is seen in Bronchial
asthma
Above: here the walls become thinner
(to facilitate easier diffusion of gases)
as you go down. Terminal
bronchioleresp. bronchiole
alveolar duct alveolar sac
In some disease states the thin wall of
the alveoli may become thickened and
this would lead to inefficient diffusion
of gases.
Familiarize yourself with this
diagram for it will be the basis of
lung pathologies
Alveolar space- lined by 2 types of
pneumocytes (alveolar epithelium).
Types 1 and 2.
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Though type 1 comprises 90% of the
lining epithelium Type 2 is more
plentiful than type 1.Type 1
pneumocytes are membranous,
flattened/plate-like. Type 2 are round
in shape
Type II cells are important for at least
two reasons: (1) They are the sourceofpulmonary surfactant, contained
in osmiophilic lamellar bodies seen
with electron microscopy, and (2) they
are the main cell type involved in
the repair of alveolar epithelium
after destruction of type I cells. But
the problem with this is that type 2
cells are not membranous, they are
thick. Such that their proliferation
impairs gas exchange.
The surfactant reduces the surface
tension throughout the lungs,
contributing to its compliance which in
turn prevents it from collapsing.
Within the alveolar space are the
alveolar macrophages which are the
last line of defense in the pulmonary
defense mechanism. These cells are
phagocytic and are capable ofsecreting mediators which can cause
changes in the alveolar epithelium.
Interstitium- In between alveolar
spaces which is composed of
interstitial cells. When the lungs is
injured, these cells proliferate and
causes the interstitium to become
fibrotic.
Pulmonary capillaries are alsolocated in the interstitium through w/c
blood will pass. Shares a common
basement membrane with the alveolar
space.
Factors involved in the maintenance
of adequate respiration:
1. Adequate air intake
2. Rapid diffusion along alveolar ducts
and thru alveolar walls (approx 10
ms)
3. Adequate blood flow or perfusion-
pulmonary capillaries
Inadequate air supply to the alveoli
(hypoventilation)
1. CNS lesions affecting respiratory
ctrs
2. Paralysis of muscles of respiration
(diaphragm and intercostals)
3. Injuries/deformities of thoracic
skeleton
4. Pleural effusion or pneumothorax
5. Bronchial obstruction (tumor,
foreign body, mucus, narrowing of
walls due to bronchoconstriction,
fibrosis)- can be intraluminal or
extraluminal (tumors)
Impaired diffusion of gas
1. Reduction in total alveolar surface
area
No of alveoli- 700 million
Surface area- 1 tennis court or
70 sq. meters
2. Increase in distance over which
diffusion takes place
Alveolar diameter- approx. 20
micrometer
Increasing the diameter will
slow down gas diffusion/ gas
exchange
3. Increase in thickness of alveolar
capillary membrane- fibrosis
Altered pulmonary perfusion- enough
ventilation but not enough blood
perfusion
1. Occlusion of large vessels by
multiple emboli
Usual source of emboli: deep
leg veins
2. Slowing of pulmonary circulation
3. Reduction in pulmonary capillary
bed (in diffuse lung
disease)
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4. Pulmonary vascular spasm due to
hypoxia
In systemic circulation when you
have hypoxia, blood vessels will
tend dilate to compensate but in
the lungs hypoxia induces
vasoconstriction in order to shunt
the blood in well ventilated areas.
Ventilation-Perfusion Mismatch
Dead air space areas of the
lung that are ventilated but not
perfused (not enough blood
flow)
Shunt areas of the lungs that
are perfused but not ventilated
Pulmonary Defense Mechanisms
Nasal clearance (>10 m) LARGER
particles
Tracheobronchial clearance (2-10
m) coughed-out by mucociliary
apparatus
Alveolar macrophages (
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Pulmonary Sequestration
- non-functioning lung tissue
- separate from normal
bronchopulmonary tree
- separate blood supply
- 2 types: Extralobar and
intralobar
Extralobar outside the visceral
pleura
- outside normal lung pleura
- venous drainage via systemic
veins (75%)
- more often associated with other
anomalies
- with separate blood supply
Intralobar within the visceral pleura
- within visceral pleura
- surrounded by normal lung
- venous drainage via pulmonary
veins (95%)
- not often associated with other
congenital anomalies
- may be an acquired post-
inflammatory process
Clinical significance of congenital
cysts:
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Compression or displacement of
significant lung volume
Development of infection
Progressive cystic dilatation
Rupture
ATELECTASIS- collapsed of lung
parenchyma- becomes liver-like
-refers either to incomplete expansion
of the lungs (neonatal atelectasis) or
to the collapse of previously inflated
lung, producing areas of relatively
airless pulmonary parenchyma.
Acquired atelectasis, encountered
principally in adults, may be divided
into resorption (or obstruction),compression, and contraction
atelectasis
Obstructive- Resorption
atelectasis is the consequence of
complete obstruction of an airway,
which in time leads to resorption of
the oxygen trapped in the
dependent alveoli, without
impairment of blood flow through
the affected alveolar walls. Sincelung volume is diminished, the
mediastinum shifts towardthe
atelectatic lung. Resorption
atelectasis is caused principally by
excessive secretions (e.g.,
mucous plugs) or exudates within
smaller bronchi and is therefore
most often found in bronchial
asthma, chronic bronchitis,
bronchiectasis, andpostoperative states and with
aspiration of foreign bodies.
NOTE: Although bronchial
neoplasms can cause atelectasis,
in most instances they cause
subtotal obstruction and produce
localized emphysema.
Compressive- results whenever
the pleural cavity is partially orcompletely filled by fluid exudate,
tumor, blood, or air (the last-
mentioned constituting
pneumothorax) or, with tension
pneumothorax, when air pressure
impinges on and threatens the
function of the lung and
mediastinum, especially the major
vessels. Compression atelectasis is
most commonly encountered in
patients with cardiac failure who
develop pleural fluid and in
patients with neoplastic
effusions within the pleural
cavities. Similarly, abnormal
elevation of the diaphragm, such
as that which follows peritonitis or
subdiaphragmatic abscesses or
occurs in seriously ill postoperative
patients, induces basal atelectasis.
With compressive atelectasis,
the mediastinum shifts away
from the affected lung
Contraction- fibrotic changes
(localized or generalized) in the
lung and pelura which prevents fullexpansion
NOTE: Significant atelectasis reduces
oxygenation and predisposes to
infection. Because the collapsed lung
parenchyma can be re-expanded,
atelectasis is a reversible disorder
(except that caused by
contraction).
Morphology:
Collapsed lung parenchyma
Red-blue, rubbery, subcrepitant
( no air inside)
Slit-like alveoli (instead of wideopen)
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Right lung: Atelectatic Left: Normal
>>The arrow to the left points the non-
atelectatic alveoli while the one on the
lower right points the atelectatic alveoli
(slit-like alveoli)
*Closer view of the slit like
alveoli*alveolar membrane are close to
each other
Obstructive Atelectasis- towards
atelectatic side
Compressive Atelectasis- mediastinal
stucture are pushed toward the non-
atelectatic lung
Case: stab wound on the right side of the
chest will result to compressive
atelectasis due to hemothorax andpneumothorax pushing mediastinal
structure towards the non atelectatic
lung.
PULMONARY EDEMA
Outward forces: Vascular hydrostaticpressure & tissue oncotic pressure (at a
lesser degree) - causing edema
Inward forces: Intravascular oncotic
pressure and Tissue hydrostatic pressure
Albumin- plasma proteins (responsible
for plasma oncotic pressure)
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Pulmonary Edema: Mechanisms
1. Hemodynamic disturbance
a. Increased venous & capillary
pressure (hydrostatic pressure)- seen in
left-sided heart failure, mitral valve
stenosis, volume overload and pulmonary
vein obstruction
b. Decreased oncotic pressure-
hypoalbuminemia- liver failure,
malnutrition, nephrotic syndrome-
albumin is excreted in the urine; seen
also in protein-losing enteropathy
c. Lymphatic obstruction
2. Microvascular injury
- increased capillary permeability(Bacterial, viral, mycoplasma and
ricketssial) The last 3 causes damage to
the pulmonary capillaries
Causes: Lifted from Robbins
Infections: pneumonia, septicemia
Inhaled gases: oxygen, smoke
Liquid aspiration: gastric contents, near-drowning
Drugs and chemicals: chemotherapeutic agents
(bleomycin), other medications (amphotericin B),
heroin, kerosene, paraquat
Shock, trauma
Radiation
Transfusion related
3. Undetermined origin
a. High altitude- w/o
acclimatization, oxygen in air is less and
causes hypoxia vasoconstriction which
then causes hypertension (inc. pulmonary
and endothelial damage. Occur at 8000
ft. High but may occur at 400o ft in
susceptible individuals
Dexamethasone- facilitates resorption
of edema fluid
b. Neurogenic (CNS trauma)
seen in subarachnoid hemorrhage
which increases intracranial pressure.
>>Edema fluid (pink amorphous) w/in the
alveoli
The most common hemodynamic
mechanism of pulmonary edema is that
attributable to increased hydrostatic
pressure, as occurs in left-sidedcongestive heart failure. Whatever the
clinical setting, pulmonary congestion and
edema are characterized by heavy, wet
lungs. Fluid accumulates initially in the
basal regions of the lower lobes because
hydrostatic pressure is greater in these
sites (dependent edema). Histologically,
the alveolar capillaries areengorged,
and an intra-alveolar granular pink
precipitate is seen. Alveolar
microhemorrhages and hemosiderin-
laden macrophages ("heart failure"
cells) may be present. In long-standing
cases of pulmonary congestion, such as
those seen in mitral stenosis,
hemosiderin-laden macrophages are
abundant, and fibrosis and thickening of
the alveolar walls cause the soggy lungs
to become firm and brown (brown
induration). These changes not only
impair normal respiratory function, butalso predispose to infection.
The second mechanism leading to
pulmonary edema is injury to the
capillaries of the alveolar septa. Here
the pulmonary capillary hydrostatic
pressure is usually not elevated, and
hemodynamic factors play a secondary
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role. The edema results from primary
injury to the vascular endothelium or
damage to alveolar epithelial cells (with
secondary microvascular injury). This
results in leakage of fluids and proteins
first into the interstitial space and, in
more severe cases, into the alveoli. When
the edema remains localized, as it does in
most forms of pneumonia, it is
overshadowed by the manifestations of
infection. When diffuse, however, alveolar
edema is an important contributor to a
serious and often fatal condition, acute
respiratory distress syndrome.
ACUTE LUNG INJURY:
Abrupt onset of significant
hypoxemia & diffuse pulmonary
infiltrates in the absence of cardiac
failure (Non-cardiogenic pulmonary
edema)
Acute Interstitial Pneumonia
idiopathic origin; widespread
ALI/ARDS
Acute Respiratory Distress
Syndrome
-Rapid onset of severe life-threatening respiratory insufficiency,
tachycardia, cyanosis and severe
arteriolar hypoxemia that is refractory
to oxygen therapy
A.K.A. Shock lung, Traumatic wet lung
Acute alveolar injury and Diffuse alveolar
injury
-Diffuse alveolar capillary &
epithelial damage
-Severe respiratory insufficiency
-Profound hypoxemia
-Refractory to oxygen therapy
-Decreased lung compliance
-Bilateral pulmonary infiltrates
NOTE: More than 50% of cases areassociated with:
o sepsis
o diffuse pulmonary infections-
viral, mycoplasma and
pneumocystis pneumonia,
military TB
o gastric aspiration
o mechanical trauma (head
injury)
CAUSES:
Direct LungInjury
Indirect LungInjury
pneumonia sepsisaspiration severe trauma
inhalation injury acute pancreatitisnear drowning cardiopulmonary
bypasspulmonarycontusion
massive transfusion
fat embolism drug overdose
ARDS pathogenesis: main player:
cytokines
increased synthesis ofIL-8; release of
similar compounds endothelial
activation; pulmonary microvascular
sequestration & activation of neutrophils
(IL-1 & TNF) activated neutrophils
release mediators that damage the
alveolar epithelium & promote more
inflammation
IL-8 potent neutrophil chemotactic
agent/activating agent
NOTE: Normally neutrophils can be found
in the lungs but in ARDS there is an
increase in number of activated
neutrophils which promoted endothelial
damage.
Endothelial/epithelial injury
o increased vascular permeability
o leakage of protein-rich fluid into
the interstitium
o exudation of fluid into alveolar
spaces
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o deposition of plasma proteins,
fibrin & cell debris in the injured
alveolar walls
o hyaline membrane
ARDS PATHOGENESIS:
Diffuse damage to alveolarcapillary walls leakage of
protein-rich fluid into the
interstitium
End result: INTERSTITIAL &
ALVEOLAR EDEMA
Damage to pneumocytes type I
exudation of fluid into alveolar
space
deposition of plasma proteins,
fibrin & epithelial debris on alveolar walls
HYALINE MEMBRANE
Disruption of surfactant airspace collapse
Ventilation perfusion
mismatch
Stiffening of the lungs with
decreased compliance (due to
fibroblast proliferation)
ARDS: Main events & outcome:
Morphology:
1. Acute stage (1st wk after
pulmonary injury)
- heavy, red & boggy lungs
- hyaline membrane
2. Resolution
- organization of fibrin exudatefibrosis
>>Above: ARDS Interstitial edema
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Above:Thickened alveolar walls due to
inflammation and edema
>> Take note the presence ofhyaline
membrane on the alveolar walls (Pink
amorphous material lining the walls) with
a lot of inflammatory infiltrates in the
intersitium.
Diseases of Vascular Origin
Pulmonary Embolism &
Infarction
Pulmonary Hypertension
Diffuse Pulmonary Hemorrhage
Syndromes
PULMONARY EMBOLISM:
Risk Factors
1. Prolonged immobilization- hip
fracture
2. Hypercoagulable states- either
primary(e.g., factor V Leiden,
prothrombin 20210 A,
hyperhomocysteinemia, and
antiphospholipid syndrome) or
secondary(e.g., obesity, recent
surgery, cancer, oral contraceptive
use, pregnancy)
3. Indwelling central venous lines-
right atrial thrombus
4. Underlying disorders- cardiac
disease or cancer
NOTE:The pathophysiologic response
and clinical significance of pulmonary
embolism depend on the extent to which
the pulmonary artery blood flow is
obstructed, the size of the occluded
vessel(s), the number of emboli, theoverall status of the cardiovascular
system, and the release of vasoactive
factors such as thromboxane A2 from
platelets that accumulate at the site of
thrombus.
Emboli result in two main
pathophysiologic consequences:
respiratory compromise owing to the
nonperfused, although ventilated,
segment and hemodynamic
compromise owing to increased
resistance to pulmonary blood flow
engendered by the embolic obstruction.
The latter leads to pulmonary
hypertension and can cause acute right-
sided heart failure.
MORPHOLOGY:
Large emboli may impact in the main
pulmonary artery or its major branches or
lodge at the bifurcation as a saddle
embolus. Sudden death often ensues,
owing largely to the blockage of blood
flow through the lungs. Death may also
be caused by acute failure of the right
side of the heart (acute cor pulmonale).
Smaller emboli can travel out into the
more peripheral vessels, where they may
cause infarction. In patients with
adequate cardiovascular function, thebronchial arterial supply can often sustain
the lung parenchyma despite obstruction
to the pulmonary arterial system. Under
these circumstances, hemorrhages may
occur, but there is no infarction of the
underlying lung parenchyma. Only about
10% of emboli actually cause infarction.
Although the underlying pulmonary
architecture may be obscured by the
suffusion of blood, hemorrhages aredistinguished by the preservation of the
pulmonary alveolar architecture; in such
cases, resorption of the blood permits
reconstitution of the preexisting
architecture.
Saddle Embolus
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Above: a big emboli in the pulmonary
artery (can be unilateral or bilateral)-
lethal; immediate death
Small emboli- lodge in smaller
branches and patients may survive.
Patients may either have infarction or
no infarction because the lungs has adual blood supply (Pulmonary artery
and Bronchial artery- arises from the
aorta). Usually, however, in individuals
with a normal cardiovascular system
small emboli induce only transient chest
pain and cough or possibly pulmonary
hemorrhages without infarction. Only in
the predisposed, in whom the bronchial
circulation itself is inadequate, do small
emboli cause small infarcts
In cases of small emboli in the branches
of pulmonary artery, the branches from
the bronchial artery can still supply this
area. These emboli can cause a transient
occlusion but reperfusion can cause
hemorrhage. In cases of the elderly and
patients with atherosclerosis (aorta), the
blood supply coming from the bronchial
artery may not be sufficient to re-supply
the areas that are affected and you mayhave an infarction.
Pulmonary infarct is hemorrhagic
because it has dual blood supply and it
has a very loose parenchyma and not
compact. Appears as a raised, red-blue
area in the early stages. Often, the
apposed pleural surface is covered by a
fibrinous exudate. The red cells begin to
lyse within 48 hours, and the infarct
becomes paler and eventually red-brownas hemosiderin is produced. With the
passage of time, fibrous replacement
begins at the margins as a gray-white
peripheral zone and eventually converts
the infarct into a contracted scar.
Histologically, the diagnostic feature of
acute pulmonary infarction is the
ischemic necrosis of the lung substance
within the area of hemorrhage, affecting
the alveolar walls, bronchioles, and
vessels. If the infarct is caused by an
infected embolus, it is modified by a more
intense neutrophilic exudation and more
intense inflammatory reaction. Such
lesions are referred to as septic
infarcts, and some convert to abscesses.
ABOVE: SEVERE PULMONARYHEMORRHAGE
ABOVE: EMBOLI IN PULMONARY ARTERY
Clinical features depend on:
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1. Extent of blood flow
obstruction
Saddle embolus= DEATH
2. Size of occluded vessel
3. Number & size of emboli
4. Cardiovascular status ofpatient
5. Vasoactive factors released
by platelets
MOST
COMMON
SOURCES OF
LUNG
EMBOLI
(deep leg
veins)
LEAST
COMMON
SOURCES OF
LUNG EMBOLI
External iliac
v.
Right side of
heart
Femoral v. Gonadal v.
(ovarian &
testicular)
Deep femoral
v.
Uterine v.
Popliteal v. Pelvic venous
plexus
Post. Tibial v. Lateral
circumflex
Femoral v.
Soleal plexus Great
saphenous v.
Small
saphenous v.
Physiologic Effects
Respiratory compromise
Affected area is ventilated
but not perfused
Hemodynamic compromise
Multiple emboli--- d
resistance to pulmonary
blood flow
pulmonary HPN
Consequences
1. Resolution
2. Pulmonary HPN
3. Development of second emboli
4. Death
PULMONARY HYPERTENSION
Ppa = QR + Pla
Ppa = pulmonary arterial pressure
Increased is seen in Pulmonary
congestion
Q = pulmonary blood flow
R = pulmonary vascular resistance
Pla = left atrial pressure
INCREASE:
Flow: in L R shunts (ASD &VSD)due to increased pressure in the left side
of the heart
Resistance: vasoconstrictioncapillary
destruction (seen in extensive
lung disease)
postcapillary
Left atrial pressure: mitral stenosis
LV
failure
CLASSIFICATION (WHO Venice 2003
Revised Classification System)
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WHO Group I - Pulmonary arterial
hypertension (PAH)
Idiopathic (IPAH)
Familial (FPAH)
Asso.(APAH): collagen vascular disease
congenital shunts between thesystemic & pulmonary
circulation, portal hypertension,
HIV infection, drugs,
toxins, or other diseases or
disorders
1. Associated with venous or
capillary disease
WHO Group II - Pulmonaryhypertension associated with left
heart disease
Atrial or ventricular disease
Valvular disease (e.g. mitral
stenosis)
WHO Group III - Pulmonary
hypertension asso. with lung
diseases and/or hypoxemia
COPD, (ILD)
Sleep-disordered breathing,
alveolar hypoventilation
Chronic exposure to high
altitude
Developmental lung
abnormalities
WHO Group IV - Pulmonary
hypertension due to chronic
thrombotic and/or embolic
disease
Pulmonary embolism in the
proximal or distal pulmonary
arteries
Embolization of other
matter, such as tumor cellsor parasites
WHO Group V - Miscellaneous
Pulmonary HPN: Mechanisms
BMPR2 (bone morphogenetic
protein receptor type 2)
Endothelial dysfunction
Organization & incorporation of
small emboli
Neurohormonal vascular reactivity
- chronic vasoconstriction
Ingestion of substances which mayinjure the endothelium
Pulmonary HPN: Morphology
Recanalized or organized thrombus
Medial hypertrophy
Intimal & adventitial fibrosis
Reduplication of elastic
membranes
Plexogenic pulmonary arteriopathy
Small arteries and arterioles are
usually affected
Pulmonary HPN: Grades
Grade I: medial hypertrophy
Grade II: + intimal proliferation
Grade III: intimal fibrosis; +/- occlusive
Grade IV: plexiform lesions
Grade V: rupture of pulmonary arteries
Grade VI: fibrinoid necrosis
HISTO: PULMONARY HPN
http://en.wikipedia.org/wiki/Collagen_vascular_diseasehttp://en.wikipedia.org/wiki/Portal_hypertensionhttp://en.wikipedia.org/wiki/HIVhttp://en.wikipedia.org/wiki/Mitral_stenosishttp://en.wikipedia.org/wiki/Mitral_stenosishttp://en.wikipedia.org/wiki/Sleep-disordered_breathinghttp://en.wikipedia.org/wiki/Pulmonary_embolismhttp://en.wikipedia.org/wiki/Tumorhttp://en.wikipedia.org/wiki/Parasitehttp://en.wikipedia.org/wiki/Collagen_vascular_diseasehttp://en.wikipedia.org/wiki/Portal_hypertensionhttp://en.wikipedia.org/wiki/HIVhttp://en.wikipedia.org/wiki/Mitral_stenosishttp://en.wikipedia.org/wiki/Mitral_stenosishttp://en.wikipedia.org/wiki/Mitral_stenosishttp://en.wikipedia.org/wiki/Sleep-disordered_breathinghttp://en.wikipedia.org/wiki/Pulmonary_embolismhttp://en.wikipedia.org/wiki/Tumorhttp://en.wikipedia.org/wiki/Parasite -
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ABOVE: Medial hypertrophy
ABOVE: Plexogenic Pulmonary
Arteriopathy
So called because a tuft of capillary
formations is present, producing a
network, or web, that spans the lumens of
dilated thin-walled, small, arteries
__________END OF
TRANSCRIPTION__________
Batch 2014,
Kindly read your books for a more
detailed discussion of each of the topics.
Ive already added some information from
Robbins.
Hopefully you guys will enjoy studying
respiratory module as much as I did.
Hi nga pala sa mga Groupmates ko sa
anatomy lab, Tel, max, al, karla and Iami.
Miss ko na mga gaguhan sessions ntn lalo
na mga green jokes n Iami!
Pizza party daw ulit tau sabi ni Iami sya
sagot sa lahat ng gastos..di ba iami??