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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??