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Y2 - Path - Exam 4 > 8: Pulm 1 > Flashcards

8: Pulm 1 Flashcards

1
Q

Normal Lung anatomy:

conducting zone versus respiratory zone?

A

CONDUCTIVE

  • Trachea
  • Main stem bronchi
  • Bronchi
  • Bronchioles
  • Terminal Bronchioles

RESPIRATORY - these 3 layers form pulmonary acinus; structure is simpler for gas exchange

  • Respiratory Bronchioles
  • Alveolar ducts
  • Alveoli
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2
Q

Histology of LARGE AIRWAYS (trachea/bronchi)

A
  • pseudostratified, tall columnar, ciliated epithelium - cilia to move things out
  • goblet cells - to make mucus to capture pathogens
  • basal cells
  • neuroendocrine cells - receive neuronal input –> put hormones into blood
  • submucosal mucous glands
  • **cartilage - key feature of conductive zone
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3
Q

histology of SMALL AIRWAYS (bronchioles)

A
  • lack of cartilage
  • lack of submucosal glands
  • gradually thinner epithelium
  • gradually less mucous cells
  • non ciliated columnar clara cells (terminal bronchioles)
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4
Q

Type I versus Type II pneumocytes?

A
  • Type I pneumocyte: forms part of the barrier across which gas exchange occurs
  • Type II pneumocyte secretes surfactant;/ acts to repair larger, cuboidal cells and occur more diffusely
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5
Q

Alveoli:

composition of alveolar SURFACE,

composition of alveolar LINING

A
  • Alveolar SURFACE:
    • 95% type I pneumocytes; 5% type II pneumocytes
  • Alveolar LINING:
    • 40% type I pneumocytes, *60% type II pneumocytes
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6
Q

Alveoli:

structure

A
  • capillary network
  • fusion of BM and endothelium and epithelium (gas-exchange areas)
  • pores of Kohn (b/w alveoli)
  • macrophages
  • surfactant layer
  • interstitium
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7
Q

define: atelectasis

A

Incomplete expansion of the lung, or collapse of previously inflated lung leading to loss of lung volume

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8
Q

effect of Atelectasis on function?

A
  • Reduces oxygenation (ventilation-perfusion imbalance)
  • Predisposes to infection
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9
Q

Types of Atelectasis?

A
  • Resorption (obstruction) - most common are mucus plugs
    • airways are obstructed there is no further ventilation to the lungs and beyond
    • early stages, BFcontinues and gradually the oxygen and nitrogen get absorbed
  • Compression (relaxation)
    • The loss of negative pressure in pleura permits the lung to relax, due to elastic recoil.
  • Contraction atelectasis
    • compression of parts of the lung by fibrotic changes in the pleura
  • Patchy (micro-atelectasis)
    • occurs in the absence of surfactant, such as can occur in newborns
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10
Q

Hemodynamic Pumonary Edema is the accumulation of fluid in the lungs caused by the disruption of Starling’s forces;

What are the causes?

A
  • Increase hydrostatic pressure (left-sided HF, volume overload, PV obstruction, etc.)
  • Decrease oncotic pressure (hypoalbuminemia)
  • Lymphatic obstruction
  • Accumulation of fluid in dependent basal regions of lower lobes
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11
Q

What are the causes of Edema due to microvascular injury?

A
  • capillary hydrostatic pressure not elevated
  • primary injury to vascular endothelium and/or alveolar epithelium
  • leakage of fluids into interstitial space and then alveolar space
  • Non cardiogenic pulmonary edema
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12
Q

causes of microvascular injury?

A
  • infections (viruses, mycoplasma, etc.)
  • inhaled gases (oxygen, cyanides, smoke, etc)
  • liquid aspiration (gastric acid and contents)
  • drugs and chemicals
  • shock, trauma, sepsis, radiation
  • pancreatitis, uremia, TTP, DIC, etc.
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13
Q

Histologic findings of Pulmonary Congestion and Edema?

A
  • engorged capillaries
  • granular pink precipitate in alveolar spaces
  • microhemorrhages
  • hemosiderin-laden macrophages and fibrin
  • fibroblastic plugs (repair) and interstitial fibrosis (chronic)
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14
Q

acute phase versus subacute phase

histo findings of pulmonary congestion and edema

A
  • ACUTE:
    • congestion of capillaries
    • edema fluid (granular precipitate) in alveolar spaces
  • SUBACUTE
    • hemosiderin laden macrophages – stains golden brown in lung
    • fibrin in alveolar spaces
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15
Q

histo features of ORGANIZATION/REPAIR phase in pulmonary congestion/edema?

A
  • immature fibrous tissue (plugs) in alveolar spaces
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16
Q

Adult Respiratory Distress Syndrome (ARDS):

causes

A
  • Acute respiratory failure/ acute lung injury - MOST COMMON CAUSE OF ARDS
    • *Specifically in pt w/ SEPTIC SHOCK
  • Decreased lung compliance
  • Hypoxemia refractory to oxygen therapy
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17
Q

Adult Respiratory Distress Syndrome (ARDS):

diagnosis, course, mortality

A
  • Dx: Bilateral radiologic opacities
    • Frequent superimposed infections
  • Course: Progression to multi-organ failure
  • Mortality over 50% (v high mortality)
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18
Q

what is this histologic pattern and what pulmonary disease does it correlate with?

A

DIFFUSE ALVEOLAR DAMAGE (DAD): assoc w/ ARDS (adult resp distress syndrome)

  • EARLY (injury phase) of DAD
    • edema, +/- hemorrhage
    • fibrinous exudate
    • hyaline membranes (fibrin-rich layer with necrotic cells)
    • mild interstitial inflammation
    • fibrin microthrombi
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19
Q

which phase of diffuse alveolar damage is pictured below?

A

TYPE II PNEUMOCYTE HYPERPLASIA;

part of the repair (organizing) phase

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20
Q

which phase of diffuse alveolar damage is pictured below?

A

INTERSTITIAL/ AIRSPACE fibroblastic proliferation (fibrous plugs);

with marked thickening of alvolar septae

(part of Repair (organizing) phase)

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21
Q

presenting clinical symptoms of PULMONARY EMBOLISM?

A
  • Chest pain
  • Dyspnea (difficult or labored breathing)
  • Tachypnea (abnormally rapid breathing)
  • Hemoptysis (coughing of blood or blood-stained mucus)
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22
Q

sources of pulmonary embolism?

what is MOST COMMON source?

A
  • MOST COMMON SOURCE OF PE: DEEP VENOUS THROMBOSIS (DVT)
  • Other sources
    • pelvic vein thrombi
    • foreign body emboli
    • bone marrow emboli
    • amniotic fluid emboli
    • air emboli
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23
Q

pulmonary embolism:

PREDISPOSING FACTORS

A

venous stasis

hypercoagulable state

endothelial injury

24
Q

pulmonary embolism:

RISK FACTORS

A
  • immobilization
  • obesity
  • pregnancy
  • estrogenic oral contraceptives
  • hereditary clotting disorders
25
Q

how does pulmonary embolism compromise respiration and hemodynamics?

A
  • Respiration
    • Clot in lungs –> ventilated segment is NOT perfused –> compromised resp
  • Hemodynamics
    • Clot –> increased resistance to pulmonary blood flow (vasoconstriction) –> hemodynamic compromise
26
Q

Consequences of PE depends on size of embolus and adequacy of bronchial circulation;

Compare Large and Small emboli consequences

A
  • LARGE emboli (5%)
    • saddle embolus - sitting at bifurcation of pulmonary trunk
    • –> sudden death OR CV collapse
  • SMALL emboli (60-80%)
    • asymptomatic, OR
    • transient chest pain, hemoptysis
    • repeated small emboli –> may have same effect as large emboli
27
Q

Consequences of PE depends on size of embolus and adequacy of bronchial circulation;

Consequences of MIDDLE-SIZED EMBOLI

A

Middle sized emboli (20-35%) – PULMONARY INFARCTION

  • Hemorrhagic
  • pleural-based
  • wedged-shaped
  • fibrinous exudate on pleural surface
  • form contracted scar w/ resolution
  • predominantly lower lobes
28
Q

Chronic Obstructive Pulmonary Disease (COPD):

hallmark sign, and pathogenesis

A
  • Hallmark of COPD: decreased expiratory flow rate (hard to get air out of lungs)
    • (Total lung capacity is normal or increased)
  • Path: Chronic/recurrent airflow obstruction
    • narrowed/small airways
    • loss of elastic recoil
29
Q

what is most common trigger for COPD and Emphysema?

A

Chronic injury such as **CIGARETTE SMOKING

30
Q

define: emphysema

A
  • abnormal permanent enlargement of airspaces distal to terminal bronchioles
  • w/ destruction of alveolar walls

(no structure left to lung bc structure is destroyed –> filled w/ spaces of air)

31
Q

emphysema:

gross and histo morphology

A
  • gross: voluminous lung, as if inflated balloon
  • histo:
    • enlarged airspaces
    • thin alveolar walls
    • compressed septal capillaries
    • rupture of walls
32
Q

compare the types of emphysema:

centriacinar (centrilobular) and panacinar (panlobular)

A
  • Centriacinar (centrilobular)
    • Central/proximal acinus (Distal alveoli spared )
    • Apical segments/upper lobes
    • Smokers
  • Panacinar (panlobular)
    • All portions of acinus
    • Lower basal zones
    • Alpha-1-antitrypsin deficiency
    • Worse in smokers
  • Paraseptal (distal acinar)
  • Irregular
33
Q

which type of emphysema is caused by Alpha-1-antitrypsin deficiency ?

A

panacinar (panlobular) emphysema

34
Q

there are 2 theories of pathogenesis of emphysema:

descirbe the protease-antiprotease hypothesis

A
  1. Irritation (smoke particles)
  2. Activation of macrophages
  3. Recruitment of neutrophils
  4. Release/enhancement of neutrophilic elastase
  5. Inactivation of a1-AT
  6. Destruction of alveolar wall
35
Q

there are 2 theories of pathogenesis of emphysema:

descirbe the oxidant-antioxidant imbalance hypothesis

A
  • Lung has a substantial amount of antioxidants (glutathione, superoxide dismutase)
  • Agents that contain abundant oxidants can deplete these stores
  • Net effect is oxidative damage to antiproteases, giving a functional deficiency
36
Q

how does emphysema affect lung function?

A
  • decreased gas-exchange area
    • reduction of diffusion capacity
  • small airway collapse (loss of support structures) –>
    • airflow obstruction
  • clinically apparent after reduction of 25% of lung volume
37
Q

clinical presentation of pure emphysema:

A
  • exertional dyspnea –> (walking capacity decreases –> requires oxygen)
  • minimal cough or sputum
  • use accessory muscles –> barrel chest (huge, expanded lungs)
  • hyperresonance (occurs in the chest as a result of overinflation of the lung)
  • depressed diaphragm
38
Q

chronic bronchitis is defined by duration and trigger factor:

what are these definitions?

A
  • Persistent cough w/ sputum for 3 months in at least 2 consecutive years
  • Trigger: Chronic irritation (tobacco smoke)
39
Q

effects of chronic bronchitis on mucus glands and bronchi/bronchioles

A
  • Mucous glands hypertrophy/ hypersecretion
  • Bronchitis and bronchiolitis (inflammation of the bronchi and bronchioles)
  • Secondary infections
40
Q

histopathology of CHRONIC BRONCHITIS

A
  • Hyperemia and edema of mucous membranes
  • Mucinous secretions/casts filling airways
  • Mucous glands hyperplasia in trachea and bronchi
  • Bronchial/bronchiolar mucous plugging
  • Bronchial and bronchiolar epithelium with squamous and goblet-cell metaplasia
  • Inflammation
  • Fibrosis
41
Q

Chronic bronchitis:

clinical presentation

A
  • Copious mucoid sputum
  • Hypercapnia (elevated CO2)
  • Hypoxemia (low O2)
  • Cyanosis (bluish color to skin)
42
Q

Associated conditions of CHRONIC BRONCHITIS

A
  • Cor pulmonale (RHF)
  • **Secondary bacterial infections - predisposed to secondary bacterial infections
  • Pulmonary hypertension
43
Q

define: asthma

A
  • Chronic OBSTRUCTIVE, reversible inflammatory disorder of airways
  • causes recurrent episodes of wheezing, breathlessness, cough
44
Q

mechisms of Asthma, and types

A
  • Paroxysmal contraction of bronchial smooth muscle in response to various stimuli
    (hyperresponsiveness)
    • Increased mucous secretion
    • Reversible airway narrowing
  • Types of Asthma
    • ATOPIC
    • NON-ATOPIC
45
Q

ATOPIC asthma = allergen-triggered asthma;

what are key cells found in this type of asthma?

A

MAST CELLS and eosinophils; usually in response to allergen

immediate phase (minutes), and late phase (hours)

46
Q

ATOPIC ASTHMA:

cause, epidemiology

A
  • IgE mediated hypersensitivity reaction <– triggered by environmental pathogens
  • Epi: most common type of asthma
    • begins in childhood
    • often w/ family hx

Recall: other atopic diseases incl

47
Q

ATOPIC ASTHMA:

pathogenesis

A
  • T-helper 2 lymphocytes play a critical role in initial sensitization
    • Excessive reaction against environmental antigens
    • Cytokines produced by T Helper-2 cells account for most of the asthma features
  • Subsequent IgE-mediated reaction to inhaled allergens elicits an immediate response and a late-phase reaction
48
Q

which cytokines are produced by T helper 2 cells in atopic asthma; and what are their functions?

A
  • IL-4 stimulates IgE production which binds mast cells in the mucosal surface
  • IL-5 activates eosinophils
  • IL-13 stimulates mucous production
49
Q

NON-ATOPIC ASTHMA:

triggers, etiology

A
  • Triggers: respiratory tract infections, chemicals, and drugs
  • Etiology: NO FHx
    • unknown primary etiology
    • theory is virus-induced inflammation –> hypersensitive airways
50
Q

ASTHMA:

gross and micro morphology

A
  • GROSS: overinflated lungs, patchy atelectasis; airways w/ mucous plugs
  • Micro: AIRWAY REMODELING
    • Edema
    • Sub-basement membrane thickening
    • Inflammation with eosinophils (bronchitis-olitis)
    • Hypertrophy of smooth muscle and mucous glands
    • Curschmann’s spirals (whorled mucous plugs mixed with epithelial shed)
    • Charcot-Leyden crystals (debris of eosin. Membranes)
51
Q

ASTHMA:

clinical presentation

A
  • Acute dyspnea
  • Wheezing
  • Reversible (spontaneous or with therapy)
  • Status asthmaticus - emergency
    • hypoxia
    • hypercapnia
    • acidosis
    • fatal
52
Q

define: BRONCHIECTASIS

A

Chronic necrotizing obstructive lung infection –> affecting bronchi and bronchioles

53
Q

effect of Bronchiectasis on lungs?

A
  • Leads to abnormal dilatation of airways with destruction of the muscle and elastic supporting tissue
  • Basal segments (worse drainage)
54
Q

what are the conditions associated w/ bronchiectasis?

(anything that affects function of cilia)

A
  • Congenital or hereditary conditions including cystic fibrosis, intralobar sequestration, immunodefeciency states and primary ciliary dyskinesia.
  • Postinfectious conditions including necrotizing pneumonia (mycobacterium and staphylococcus aureus), viruses (adenovirus and infleunza), and fungi (aspergillus).
  • Bronchial obstruction (tumor, foreign body and mucous impaction)
  • Others, such as collagen vascular disease, inflammatory bowel disease, chronic lung rejection post-transplantation and GVHD
55
Q

BRONCHIECTASIS:

histopathology

A
  • Dilatation of airways
  • Severe necrotizing acute and chronic inflammation (bronchitis/bronchiolitis)
  • Squamous metaplasia
  • Fibrosis
  • Abscesses
56
Q

BRONCHIECTASIS:

clinical presentation

A
  • cough
  • fever
  • abdundant purulent sputum
  • obstructive respiratory insufficiency (dyspnea/cyanosis)
  • cor-pulmonale (Right heart failure)
  • Metastatic brain abscesses
  • Amyloidosis
57
Q

BRONCHIECTASIS:

complications

A
  • Cor pulmonale (right heart failure)
  • Brain abcscesses
  • Amyloidosis

Y2 - Path - Exam 4 (13 decks)

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