Flashcards in P- URT and Obstructive Lung Disease Deck (62):
Which lung is aspirated material and foreign bodies more likely to enter?
Right, because it is more vertically oriented
What structures compose the acini?
1. respiratory bronchioles
2. alveolar ducts
3. alveolar sacs
What structures make up the upper respiratory tracts?
What are nasal polyps?
What patients do they typically arise in? (4)
They are benign nasal mucosa outgrowths that arise in patients with inflammatory or infectious sinonasal maladies like:
1. chronic rhinosinusitis
4. cystic fibrosis
What is the microscopic appearance of a nasal polyp?
-respiratory mucosa with overlying edematous and inflamed stroma
-Lots of eosinophils.
What is Samter's triad?
2. nasal polyps
3. aspirin sensitivity
These all occur because the person produces extra LTs.
What is a Schneiderian papilloma? What cells do the neoplasms arise from?
What are the 3 types?
It is a papillary neoplasm arising from columnar or squamous epithelial cells of the sinonasal tract.
1. exophytic/septal (most common)
2. inverted ( lateral nasal wall)- grows inward
What infections are associated with Schneiderian papillomas?
HPV 6 and 11
What is the treatment for Schneiderian papillomas?
What are the clinical features of nasopharyngeal angiofibroma? Who usually presents with it?
It is a benign vascular tumor seen in adolescent boys due to excess testosterone.
It presents with:
epistaxis and nasal airway obstruction
It can invade bone due to locally aggressive nature
What is the morphology of nasopharyngeal angiofibroma?
What is the treatment?
There are numerous thin-walled blood vessels embedded in cellular fibrous stroma.
Treatment is surgical excision. Usually embolized prior to excision as they bleed out profusely intraoperatively.
What are the salient epidemiological features of nasopharyngeal carcinoma?
Who does it affect? What infectious agent is it associated with?
What are the 3 histological patterns?
It affects adult Chinese and pediatric Africans and is associated with EBV.
2. Non-keratinizing differentiated
3. non-keratinizing undifferentiated
What histological pattern is the most common nasopharyngeal carcinoma?
What are the morphological features?
1. large neoplastic epithelial cells in syncytium-like pattern
2. heavy non-neoplastic lymphocytic infiltrate
What is the treatment for nasopharyngeal carcinoma?
Radiation +/- chemo
What are the 4 etiologies associated with necrotizing lesions in the upper respiratory tract?
1. Acute infections esp. in DM, TB, immunocompromised
2. Drug use- cocaine
3. Wegener's granulomatosis
4. carcinoma, NK/T cell lymphoma
What is the clinical presentation of someone with Vocal cord nodules and polyps?
What is the morphology?
What is treatment?
It is common in smokers or people who abuse their voice (singer's nodule) with a small protrusion on their true vocal cords (bilateral usually)
It is a non-neoplastic reaction to inflammation/trauma and is associated with:
1. benign squamous epithelium
2. edematous myxoid stroma
1. spontaneous regression
2. surgical excision
What is the clinical presentation of laryngeal squamous papilloma?
What is the morphological presentation?
Adults- single lesion
Raspberry-like excrescenses on true vocal cords.
Squamous epithelium lined finger-like projections with central fibrovascular cores.
Caused by HPV 6 and 11
What lesions of the nose, pharynx and larynx are associated with HPV?
Laryngeal papilloma - 6 and 11
sinonasal (Schneiderian) papilloma - 6 and 11
What is the most common manifestation associated with laryngeal carcinoma?
What are the etiological factors that contribute to it?
Hoarseness in men >40
(this is a good first sign, because they come into the hospital earlier)
3. poor nutrition
What is "field effect"?
Smoking exposes multiple areas to carcinogens so people can develop multiple head and neck cancers
What is the morphology and treatment of laryngeal carcinoma?
Morphology: squamous cell carcinoma with keratin pearls and intercellular bridges
Treatment : surgery, radiation or combo
What are the 5 major predisposing factors to laryngeal squamous cell carcinoma?
5. poor nutrition
What is atelectasis?
What are the 3 common types?
Which are reversible?
"incomplete expansion"- it is the collapse of a previously inflated lung that can result in hypoxia
1. Obstructive/resorptive - reversible
2. compressive- reversible
3. Contraction - reversible
What is the main cause of neonatal atelectasis?
Not enough surfactant production
Describe resorptive/obstructive atelectasis.
What are common causes?
Does the mediastinum shift toward or away from the affected hemithorax?
It is when the alveoli collapse due to resorption of air distal to a completely obstructed airway.
1. foreign body
2. mucus plug
The mediastinum shifts toward the problem.
Removal of the cause will fix the problem (reversible)
Describe compressive atelectasis.
What are the most common causes?
Does the mediastinum shift toward or away from the affected hemithorax?
Is it reversible or irreversible?
It is when the lung is compressed by an external force.
2. pleural effusion
Mediastinum shifts away from the problem
It is reversible.
What is a contraction atelectasis?
What is the main cause?
Does the mediastinum shift toward or away from the problem?
Is it reversible?
It is when the airway collapses due to pulmonary fibrosis.
Mediastinum shifts toward the problem and it is irreversible.
What is an obstructive lung disease?
What are the PFTs?
What are the 4 major types? Are they acute/reversible or chronic/irreversible?
It is increased resistance to airflow during respiration caused by obstruction. (trouble getting air out)
FEV/FVC is <80% TLC is increased.
1. Asthma- acute/reversible
2. Chronic bronchitis - chronic/irreversible
3. emphysema- chronic/irreversible
4. bronchiectasis- chronic/irreversible
What are the clinical presentation features of asthma?
1. hyperreactivity to various stimuli
2. episodic/reversible bronchospasm
3. expiratory wheezing, dyspnea, cough especially at night
4. prolonged expiration
What are the 3 major types of asthma?
What are the main triggers for each?
1. atopic/extrinsic- allergic stimuli resulting in type I hypersensitivity (IgE-mediated) - pollen, dust
2. non-atopic/intrinsic- triggered by non-immune stimuli like respiratory tract infections, exercise, cold weather, occupational agents
3. drug-induced asthma- aspirin sensitive asthma in patients with nasal polyps and allergic rhinitis (inhibition of cyclooxygenase makes extra LTs)
Describe what happens in initial sensitization of a patient with atopic/extrinsic asthma.
The geneticall predisposed person encounter an allergen which elicits a Type II CD4 TH2 cell response
IL4- IgE production
IL5 - mast cell/ eosinophil recruitment
IL13- mucus production
What happens during reexposure to an antigen in a person with atopic asthma?
(early and late responses, what mediators are involved, what is the time frame?)
The antigens bind and cross-link IgE that are bound to mast cells.
Mast cells degranulate and release histamine, heparin, LTs and protease that open epithelial tight junctions. More antigens enter, more mast cells release mediators, etc, etc
In addition, subepithelial vagal receptors cause bronchoconstriction, vascular congestion, and edema
Late Response (4-8 hours)
Chemokines from mast cells and epithelial cells recruit leukocytes from the blood causing a fresh round of mediator release
What is airway remodelling?
What are the 4 major morphological changes noted?
Repeated immune reactions cause:
1. hypertrophy and hyperplasia of bronchial smooth muscle (bronchial wall thickening)
2. Overgrowth of submucousal glands and mucous metaplasia of epithelium
3. deposition of subepithelial collagen (BM thickening)
4. increased vascularity
What is the gross appearance of the lungs with asthma?
2. areas of atelectasis
3. mucus plugs and vascular congestion in the bronchi and bronchioles
What are the histological findings in someone with asthma?
1. Curschmann's spirals- mucus plugs with whorls of epithelium
2. entrapped eosinophils
3. Charcot-Leyden crystals
4. goblet cell metaplasia
What histological findings are made on autopsy for someone who died of status asthmaticus?
extensive desquamation of the cilia and epithelium (impeding removal of mucus)
What are the 2 major complications of asthma?
1. respiratory failure
What are the 3 common symptoms associated with all COPD?
1. dyspnea on exertion
2. chronic cough
3. chronic irreversible obstruction of the airways
What is emphysema and what are the 4 major types?
It is permanent enlargement of the air space distal to terminal bronchioles due to destruction of the septal wall WITHOUT fibrosis.
3. Distal Acinar (paraseptal)
Describe centriacinar/centrilobar emphysema. What part of the acini is affected?
Which lobe is more commonly affected?
Who get this type?
How does it look grossly?
Enlargement of air space in the proximal acini (respiratory bronchioles)
Cigarette smokers (smoke rises)
It looks like normal preserved acini mixed with septal loss
Describe panacinar emphysema.
What part of the acini is affected?
What lobe is affected?
Who gets this type?
What does it look like grossly?
It affects the whole acinus.
People with a-1 antitrypsin deficiency
Grossly, all alveoli have septal loss and the lesions are a lot larger than the centriacinar.
Describe distal acinar emphysema.
What lobe is affected?
Who gets this type?
It affects the distal part of the acini next to the pleura.
It is more severe in upper lobes
It occurs around areas of scarring and atelectasia and predisposes to pneumothorax by forming cyst called bullae
What is irregular emphysema?
Who is likely to get it?
It is isolated airway distension associated with scarring from TB.
How does emphysema cause an obstructive lung disorder?
Airways usually remain patent during expiration despite increased pressure becasue of structural integrity and elastic recoil.
It emphysema, this is lost so the bronchioles collapse on expiration.
This causes more work to "blow them back up" during inspiration, so the bronchiole walls will thicken due to smooth muscle hypertrophy and fibrosis.
What are the two critical imbalances that cause emphysema?
1. Protease-Antiprotease Imbalance (too much elastase, not enough a1-antitrypsin)
2. Oxidant-Antioxidant imbalance
How does smoking cause a protease-antiprotease imbalance in the lungs?
How does it cause an oxidant-antioxidant imbalance?
1. Nicotine attracts neutrophils which release proteases and inactivates antiproteases.
2. Nicotine produces abundant ROS and depletes antioxidants causing tissue damage
The normal a1 antitrypsin gene is _________. Individuals with _______ have severely reduced a1 trypsin activity and individuals with ______ and _______ have significantly reduced a1 antitrypsin activity.
Normal - PiMM
Markedly reduced- PiZZ
Significantly reduced - PiZS and PiSS
What do emphysema lungs look like grossly?
What do they look like microscopically in early stages and late stages?
Grossly- inflated and voluninous
Microscopically early- alveolar wall destruction with enlarged alveoli and free floating septa
Microscopically late- larger spaces with subpleural blebs
What is the clinical presentation of someone with emphysema?
1. pink puffer- overventilation with increased RR but shallow breaths to get oxygen. pursed lips
2. progressive dyspnea
3. barrel chest
4. weight loss
In addition to emphysema, what other malady is commonly associated with a1 antitrysin deficiency?
What are the three most severe complications of emphysema?
1. respiratory failure
2. tension pneumonthorax (ruptured bullae in paraseptal/distal acinar)
3. pulmonary hypertension (cor pulmonale)
What presentation must a patient have for them to be classified as having chronic bronchitis?
Productive cough with mucoid or mucopurulent sputum lasting:
-3 months of the year
- 2 consecutive years
What is the pathogenesis of chronic bronchitis?
What are the 2 major risk factors?
Chronic smoking and air pollution lead to significant inflammation of the bronchioles.
Inflammatory cells like neutrophils and mononuclear cells (CD8+ T lymphocytes) cause:
Hypertrophy of submucousal mucus glands and hypersecretion of mucus into the small airways leading to:
airway obstruction with reduced air flow
What is the Reid index?
Thickness of mucus glands/ thickness of lamina propria.
This ratio goes up markedly in chronic bronchitis
What is the clinical presentation of chronic bronchitis?
1. Blue bloater- significant hypoxia and hypercapnia
2. chronic productive cough
3. decreased RR
4. deep laborious breathing
What are the 5 most serious complications of chronic bronchitis?
1. pulmonary hypertension/cor pulmonale due to reduced numbers of alveolar capillaries
2. Respiratory acidosis
3. pulmonary failure
4. cellular atypia/dysplasia--> carcinoma
What is bronchiectasis?
What are the 3 main conditions that predispose to bronchiectasis?
permanent abnormal dilation of the bronchioles and bronchi (larger airways) caused by destruction of supporting tissue as a result of chronic necrotizing infections.
1. bronchial obstruction by foreign body or tumor, bronchitis, asthma
2. CF, immunodeficiency, Kartagener's
3. Necrotizing pneumonia- MTb, S. aureus, Klebsiella
What are the two processes crucial for the formation of bronchiectasis?
Which must come first?
It doesnt matter which happens first but there must be:
2. Chronic persistent necrotizing infection
Describe the gross morphology associated with bronchiectasis. Which lobes are more affected?
It can involve the whole lung or just a lobe.
Dilated bronchi may reach almost to the subpleural space.
Lower lobes are generally more affected.
What is the histological appearance of bronchiectasis?
necrotizing inflammation of bronchi and bronchiole walls.
Peribronchiolar fibrosis in chronic stages.
What is the clinical presentation of bronchiectasis?
1. clubbing of fingers
2. purulent foul smelling sputum with/without hemoptysis