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
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
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)
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
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
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
7
Q
define: atelectasis
A
Incomplete expansion of the lung, or collapse of previously inflated lung leading to loss of lung volume
8
Q
effect of Atelectasis on function?
A
- Reduces oxygenation (ventilation-perfusion imbalance)
- Predisposes to infection
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
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
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
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.
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)
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
15
Q
histo features of ORGANIZATION/REPAIR phase in pulmonary congestion/edema?
A
- immature fibrous tissue (plugs) in alveolar spaces
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
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)
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
19
Q
which phase of diffuse alveolar damage is pictured below?
A
TYPE II PNEUMOCYTE HYPERPLASIA;
part of the repair (organizing) phase
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)
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)
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
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
how does pulmonary embolism compromise **respiration** and **hemodynamics**?
* Respiration
* Clot in lungs --\> ventilated segment is NOT perfused --\> compromised resp
* Hemodynamics
* Clot --\> increased resistance to pulmonary blood flow (vasoconstriction) --\> hemodynamic compromise
26
Consequences of PE depends on **size** of embolus and **adequacy of bronchial circulation**;
Compare Large and Small emboli consequences
* 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
Consequences of PE depends on size of embolus and adequacy of bronchial circulation;
Consequences of MIDDLE-SIZED EMBOLI
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
**Chronic Obstructive Pulmonary Disease (COPD):**
hallmark sign, and pathogenesis
* 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
what is most common trigger for COPD and Emphysema?
Chronic injury such as **\*\*CIGARETTE SMOKING**
30
define: **emphysema**
* 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
**emphysema**:
gross and histo morphology
* gross: voluminous lung, as if inflated balloon
* histo:
* enlarged airspaces
* thin alveolar walls
* compressed septal capillaries
* rupture of walls
32
compare the types of emphysema:
**centriacinar (centrilobular)** and **panacinar (panlobular)**
* **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
which type of emphysema is caused by **Alpha-1-antitrypsin deficiency ?**
**panacinar (panlobular)** emphysema
34
there are 2 theories of pathogenesis of emphysema:
descirbe the **protease-antiprotease hypothesis**
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
there are 2 theories of pathogenesis of emphysema:
descirbe the **oxidant-antioxidant imbalance** hypothesis
* 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
how does **emphysema** affect lung function?
* 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
clinical presentation of **pure emphysema:**
* **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
**chronic bronchitis** is defined by duration and trigger factor:
what are these definitions?
* Persistent **cough w/ sputum for 3 months** in at least 2 consecutive years
* Trigger: Chronic irritation **(tobacco smoke)**
39
effects of **_chronic bronchitis_** on **mucus glands** and **bronchi/bronchioles**
* Mucous glands **hypertrophy/ hypersecretion**
* Bronchitis and bronchiolitis (**inflammation** of the bronchi and bronchioles)
* Secondary **infections**
40
histopathology of CHRONIC BRONCHITIS
* **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
Chronic bronchitis:
clinical presentation
* Copious **mucoid sputum**
* **Hypercapnia** *(elevated CO2)*
* **Hypoxemia** (*low O2)*
* **Cyanosis** *(bluish color to skin)*
42
Associated conditions of CHRONIC BRONCHITIS
* **Cor pulmonale (RHF)**
* **\*\*Secondary bacterial infections** *- predisposed to secondary bacterial infections*
* Pulmonary hypertension
43
define: **asthma**
* Chronic **OBSTRUCTIVE**, **reversible** inflammatory disorder of airways
* causes recurrent episodes of wheezing, breathlessness, cough
44
mechisms of **Asthma**, and types
* 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
**ATOPIC asthma = allergen-triggered asthma;**
what are key cells found in this type of asthma?
MAST CELLS and eosinophils; usually in response to allergen
immediate phase (minutes), and late phase (hours)
46
**ATOPIC ASTHMA:**
cause, epidemiology
* **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
ATOPIC ASTHMA:
pathogenesis
* **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
which cytokines are produced by T helper 2 cells in atopic asthma; and what are their functions?
* **IL-4** stimulates IgE production which binds mast cells in the mucosal surface
* **IL-5** activates eosinophils
* **IL-13** stimulates mucous production
49
**NON-ATOPIC ASTHMA:**
triggers, etiology
* Triggers: respiratory tract infections, chemicals, and drugs
* Etiology: NO FHx
* unknown primary etiology
* theory is virus-induced inflammation --\> hypersensitive airways
50
ASTHMA:
gross and micro morphology
* 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
ASTHMA:
clinical presentation
* Acute dyspnea
* Wheezing
* **Reversible** (spontaneous or with therapy)
* ***Status asthmaticus - emergency***
* hypoxia
* hypercapnia
* acidosis
* fatal
52
define: **BRONCHIECTASIS**
Chronic necrotizing **obstructive** lung infection --\> affecting bronchi and bronchioles
53
effect of Bronchiectasis on lungs?
* Leads to **abnormal dilatation of airways** with destruction of the muscle and elastic supporting tissue
* Basal segments **(worse drainage)**
54
what are the conditions associated w/ **bronchiectasis**?
(anything that affects function of cilia)
* **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
BRONCHIECTASIS:
histopathology
* Dilatation of airways
* Severe necrotizing acute and chronic inflammation (bronchitis/bronchiolitis)
* Squamous metaplasia
* Fibrosis
* Abscesses
56
**BRONCHIECTASIS**:
clinical presentation
* cough
* fever
* abdundant **purulent sputum**
* **obstructive respiratory insufficiency** (dyspnea/cyanosis)
* **cor-pulmonale** (Right heart failure)
* Metastatic brain abscesses
* Amyloidosis
57
**BRONCHIECTASIS**:
complications
* Cor pulmonale (right heart failure)
* Brain abcscesses
* Amyloidosis
