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51 Cards in this Set

  • Front
  • Back
How are the bronchi unlike the bronchioles?
They have cartilage and submucosal glands
What are the components of the acinus?
respiratory bronchiole, alveolar duct/sac
What are the structures included in the upper respiratory tract?
nose, pharynx, larynx
Nasal polyps

What do they consist of?
Benign outgrowth of nasal mucosa following recurrent rhinitis
Nasal polyps

Risk factors? (5)
Recurrent rhinitis, asthma, allergies, CF, aspirin
Nasal polyps

Microscopic appearance?
Hyperplastic mucosa overlying edematous and inflamed stroma
What is a sinonasal papilloma?
Benign neoplasm arising in the squamous or columnar epithelium of the sinonasal tract
What is the most important type of sinonasal papilloma? What does it do?

What viruses is it associated with?
Inverted

Grows backwards into the mucosa, can be locally aggressive and recur

HPV 6 and 11
Nasopharyngeal angiofibroma

what is it? How does it present?
Benign vascular tumor IN BOYS

Presents as epistaxis, can be locally aggressive
What would you expect to find on a sluture with allergic fungal sinusitis?
High mucin --> amorphous, pink

High eosinophils
Nasopharyngeal carcinoma
a. what is it?
b. populations?
c. viral association?
a. malignant tumor of nasopharynx
b. adult, male, chinese, pediatric african
c. EBV
What are 3 histological types of Nasopharyngeal angiofibroma

How do you treat
1. keratinizing squamous cell carcinoma
2. non-keratinizing
3. Undifferentiated (lots of lymphocytes, syncytium of epithelial cells)

Radiosensitive
What are vocal polyps?

How gets it mostly
Reactive nodules on true vocal cord due to irritation

smokers and singers
What do vocal polyps look like histologically?
Squamous epithelium overlying fibrous tissue
Laryngeal/squamous papilloma

a. where is it?
b. what does it look like?
c. Viral association?
a. benign, on true vocal cords
b. raspberry like mass, fibrovascular core
c. HPV 6 and 11
Juvenile laryngeal papillomatosis

viral association?

transmission?
characteristics?
HPV 6 and 11

vertical transmission of HPV in delivery

Multiple nodules, recurs
Carcinoma of the larynx
a. whom does it affect most
b. predominant type
c. predominant area
d. Field effect?
a. men>40, smokers, drinkers, asbestos-exposed, radiation-exposed
b. squamous cell
c. glottic area (vocal cords) --> hoarse
d. cigarettes expose multiple areas --> can get multiple sq. cell carcinomas
Conditions associated with HPV?
HPV -
sinonasal papillomas
laryngeal papilloma
squamous carcinomas and precursor lesions
Conditions associated with EBV?
Nasopharyngeal carcinoma
Hairy leukoplakia - white tongue in HIV
What happens in neonatal atelectasis?

Acquired atelectasis?

What does this result in?
Neonatal - inadequate expansion of the lungs

Acquired - collapse of lung

Results in collapse of alveoli, hypoxia, superimposed infections
Acquired atelectasis

3 methods of acquiring?
1. Resorption/obstruction
2. Compression
3. Contraction
Acquired atelectasis

What happens in reabsorption/obstruction?

What can cause this?
Obstruction in distal airway, air resorbed distally, mediastinum pulled in, alveolar collapse

mucous, asthma, COPD, bronchiectasis, foreign body
Acquired atelectasis

How do you acquire from compression?

What causes it?
accumulated fluid or air in pleural cavity causes collapsed lung, mediastinal shift away

pleural effusion, pneumothorax, hemothorax
Acquired atelectasis

What happens in contraction?

What causes this?
Irreversible fibrosis prevents expansion, mediastinum shifts towards

pulmonary fibrosis
What is the definition of bronchial asthma?
recurrent episodic, reversible bronchoconstriction of hyperreactive airways in response to various stimuli
What is the difference between atopic and non-atopic asthma?
Atopic: Type I hypersenstivity to environmental antigens, IgE, family hx positive, childhood

Non-atopic: Non-IgE mediated rxn to viral/cold/stress/etc., family hx neg, adults
What are the two phases that account for the pathogenesis of atopic asthma?
1. Sensitization
allergen --> TH2 resonse --> IgE (IL4) binds to mast cells, eosinophils recruited (IL5), and mucus produced (IL13)

2. Re-exposure --> antigen cross links IgE --> mast cells release mediators --> bronchoconstriction, mucus production, vascular congestion, edema
What are the mast cell mediators that lead to atopic asthma?
Histamine
Heparin
Leukotrienes
Proteases

Bronchconstrict, mucus production, vascular congestion, edema
What happens in the late phase of an atopic asthmatic response?
Recruitment of leukocytes --> more mediators released --> epithelial damage and bronchoconstriction

Leads to airway remodling
What is the pathogenesis of non-atopic asthma?
Virus-induced inflammation of respiratory mucosa lowers the threshold of subepithelial vagal receptors to irritants
Asthma

gross appearance?
over inflation of lungs, areas of atelectasis, mucus plugs
Asthma

histology?
mucus lugs contain curschmann's spirals (whorls of shed epithelium), entrapped eosinophils, and Charcot-leyden crystals

Airway remodling
What are the 4 processes that occur in airway remodling?
1. hypertrophy/hyperplasia of bronchiolar wall
2. overgrowth of submucosal glands
3. basement membrane thickening
4. increased vascularity
What is a typical presentation of acute asthma?

What is status asmaticus?
Severe dyspnea, wheezing, non-productive nighttime cough, difficulty in expiration

Severe asthma that persists for days, does not respond to meds
What is emphysema?
Permanent enlargement of airspaces of the acinus accompanies with destruction of walls (no fibrosis)
What are 3 types of emhysema?
1. centriacinar - respiratory bronchioles, upper lobes, smoking-related

2. panacinar - all of acini, lower lobe, a1 antitrypsin deficiency

3. distal - distal acini, subpleural upper lung near fibrosis or atelectasis, forms bullae
How does smoking lead to emphysema?
Nicotine activates macrophages --> mediators --> neutrophils --> secretes proteases (elastase), also inactivates a1-antitrypsin (antiprotease)

also create free oxygen radicals, deplete antioxidants
What is the gross appearnace of emphysema?
hyperinflated lungs
What is the microscopic appearance of emphysema?
enlarged alveoli with free-floating septa, thin walled, no fibrosis
What is the clinical presentation of emphysema?
"Pink puffers"

progressive dyspnea, shallow breathing, breath through pursed lips, barrel chest, weight loss

No cough
What are 3 complications of emphysema?
1. Pulm Ht, cor pulomonale
2. respiratory failure
3. tension pneumo
What is chronic bronchitis?
persistnet productive cough for 3 months for at least 2 years in a row
What are the 3 types of chronic bronchitis?
Simple chronic - productive cough, no obstruction

chronic asthmatic - hyper-responsive airways with bronchospasm and wheezing

chronic obstructive - chronic obstruction (coexists w/emphysmea)
What is the pathogeneis of chronic bronchitis?
smoking/pollution --> inflammation of the bronchioles, hypersecretion of mucus --> obstruction
What characterizes the morpholgy of chronic bronchitis?
Hyperplasia/hypertrophy of submucosal mucus glands

Reid index >0.4 (thickness of mucous gland/thickness of bronchial wall)
What is the clinical presentation of chronic bronchitis?
Blue bloater

history of cough and sputum with frequent exacerbations

chronic hypoxemia
pulm HT, cor pulmonale
What is bronchiectasis?
Permanent dilation of bronchi and bronchioles caused by destruction of smooth muscle and supporting elastic tissue associated with chronic necrotizing infections
What are some pathogens that can cause bronchiectasis?
s. aureaus, klebsiela, aspergillus, mycobact. TB
What are 3 congenital causes of bronchiectasis?
CF, immunodeficiencies, kartagener syndrome
How does bronchiectasis look
a. grossly
b. histologically
a. lower lobes, abnormal dilation of airways can be followed to pleural surface

b. enlarged airway, giant cells with necrotizing inflammation
What is the clinical course of bronchiectasis?

Complications (4)
Foul-smelling sputum
Hemoptysis

1. Lung abscess --> embolize
2. pulm HT
3. metastatic brain abscess
4. reactive amyloidosis