Intro to Resp (Gomez) Flashcards
Upper Airway Structures
Basic Structures Sinonasal Tract Nasal Cavity Rhinosinuses Pharynx (“Throat”) Nasopharynx Oropharynx Hypopharynx Larynx
Major function of upper airway structures
Conduit air to and from lungs Heat/Humidify inspired air to 98°/98% Particle removal from inspired air Immune surveillance of pathogens Smell Speech
Sinonasal Respiratory Mucosa
Nasal (Schneiderian) mucosa
lines nasal cavity & rhinonasal sinuses
Three types of epithelial cells
Ciliated pseudostratified columnar cells
Mucin-containing goblet cells
Basal (reserve) cells
Two characteristics of lamina propria
Prominent vascularity
Subepithelial seromucous glands
Acute (infectious) Rhinitis
Symptoms: Runny and blocked nose Sneezing Sore throat and cough Sinus and ear pain Headache Fever Anorexia Malaise and lethargy
Common cold = coryza
rhinorrhea = runny nose
transmitted by contact
Can progress –> pharyngitis, tonsillitis, sinusitis, otitis media
Self-limited
Up to 50% of all adult “colds” due to rhinoviruses, (enterovirus)
Allergic Rhinitis - “Hay Fever”
Onset: children/young adults & again 30-40s
Classifications:
seasonal
perennial
episodic
Immediate (Type I) hypersensitivity reaction
Immediat rxn (mast cells, edema) late-phase rxn (late-phase rxn)
Chronic Rhinitis
over 1 month of cardinal symptoms (sneezing, rhinorrhea, nasal congestion, postnasal drainage)
most have onset after age 20
Nasal Polyps
Recurrent attacks of rhinitis
most patients are not atopic
Usually multiple
May cause obstruction
Sinusitis/Rhinosinusitis
Inflammation of sinuses usually associated with inflammation of nasal mucosa
Acute rhinosinusitis- less than 4 days
- Empyema of sinus
Subacute rhinosinusitis 4-12 days
Chronic rhinosinusitis more than 12 weeks
Mucocele of sinus - mucus accumulation from obstruction; no bacterial involvement
Acute (Infectious) Sinusitis (ARS)
** Purulent rhinorrhea, nasal congestion and/or facial pain
can be viral (usually clears in 7 days) or bacterial
Moraxella catarrhalis (mainly children)
suggested by
Presence of symptoms for seven or more days
Symptoms initially improve and then worsen
Sinusitis associated with dental disease
Predisposing genetic/ medical Factors for Development Chronic Sinusitis
ASA triad; aspirin induced chronic rhinosinusitis, nasal polyps, and severe bronchial asthma
immotile cilia syndrome– Kartagener (defective ciliary action and situs inversus)
cystic fibrosis
chronic sinusitis- most is obstructive
ostiomeatal complex (OMC) -
channel that links thefrontal, anterior and middle ethmoid, and the maxillary sinuses to the middle meatus
OMC patency is critical for normal sinus ventilation and drainage
- Frontal sinus–>infundibulum of middle meatus
- Anterior ethmoid sinus–>middle meatus
- Middle ethmoid sinus–>ethmoid bulla of middle meatus
- Maxillary sinus–>middle meatus
chronic obstructive sinusitis symptoms and obstructions
major etiology
Common Symptoms Facial pain, pressure, fullness Nasal obstruction/congestion Nasal drainage/postnasal drip Decreased sense of smell
Obstruction may be
non-infected (“mucocele”)
suppurative (“empyema”)
Mostly staph aureus
Fungal Sinusitis types
Allergic Fungal
Sinusitis– will see lots of fungus
Fungus ball (Mycetoma)
Invasive Fungal Sinusitis
Allergic vs Allergic Fungal Sinusitis
fungal will have hyphae
allergic will have mucus (no fungi)- Charcot Leyen Crystals
allergic fungal will have both
Causes of nectrotizing lesions of upper airways
Vascular
Granulomatosis with polyangiitis/Wegener
Infectious
Rhinocerebral mucormycosis/Rhinocerebral zygomycosis
Hansen disease/lepromatous leprosy
Malignancies: extranodal NK/T cell lymphoma
miscellaneous (sarcoidosis, etc.)
Mucormycosis
Caused by saprophytic mold fungi (Mucoromycotina)
In infected tissues produce irregular shaped hyphae that have few or no septa
Usually uncontrolled diabetes where ketoacidosis is present
Lung intimate neighbors
aorta and esophagus, vena cava, heart
Conducting Vs. Respiratory
Conducting:
- Trachea2. Carina & stem bronchi3. Interpulmonary bronchi4. Segmental bronchus5. Bronchiole
5a. Terminal bronchiole (2 mm)
Respiratory:
5b. Respiratory bronchiole6. Alveolar duct7. Alveolus (7 mm)
Inhaled Particle Issues
0.5-5 micron most dangerous
> 5 µ cleared by mucociliary action
3-5 µ reach bronchioles
less than 2 µ reach the alveoli
Lancet (needle) shaped objects can go further than ovoid objects of same maximum size
Microscopic Anatomy
Trachea & bronchi
- Ciliated & goblet cells
- Mucus
- Smooth muscle
- Seromucous glands
- Cartilage
Bronchioles
- Ciliated & Clara cell
- Surfactant
- Smooth muscle
Alveoli
Type I pneumocyte
Type II pneumocyte
Lamellar bodies
Alveolar septa
difference between type II and type I pneumocytes
type 1 cannot replicate; type 2 have to do that
Alveoli
Air sac (small pockets) invaginations (200 um) O2 & CO2 exchange (blood-air barrier) Cellular Components Surface alveolar lining cells 95% Type I (non-div.) 5% Type II (div.) Capillary endothelial cells Fused basal laminae of alveolar and endothelial cells Occasional Interstitial cells Alveolar macrophages Pores of Kohn (inter-alveoli openings) Anastomosing pulmonary capillaries
Atelectasis
Incomplete expansion (Neonatal)
Acquired collapse (Adult):
Resorption (obstruction)
- Airway obstruction; mucus, foreign body, tumor
- **Mediastinal shift toward involved lung
Compression
- External pressure including elevated diaphragm
- Mediastinal shift away from involved lung
Contraction
- Secondary to fibrosis of lung or pleura
Irreversible
All atelectasis at risk for infection
linear (plate-like) atelectasis
esp. seen after surgery due to pt not breathing as deep… leads to collapsed peripheral lung areas (absorption atelectasis)
Two Main Types of Pulmonary edema
Hemodynamic
Most Common
“heart failure” cells
chronic –> alveolar fibrosis: brown induration of lung
Microvascular (alveolar) injury (infection, toxins, etc., can –> Acute Respiratory Distress Syndrome
Non-cardiogenic Pulmonary Edema criteria
1-Acute onset of dyspnea
2-Hypoxemia
3-Bilateral infiltrates
4- Absence of Primary left-sided heart failure
Can –> ARDS/ DAD (diffuse alveolar damage)
AIP (acute interstitial pneumonia)
Adult Acute Respiratory Distress Syndrome
(Diffuse Alveolar Damage)
Occurs in patients with severe disease
Diffuse damage to alveolar capillary walls –> neutrophilic migration
Have secondary loss of surfactant
Conditions Associated with Development of Acute Respiratory Distress Syndrome
Sepsis, diffuse pulmonary infection, gastric aspiration
mechanical trauma, including head injures
near drowning
fractures with fat embolism
burns, ionizing radiation
smoke, gases, chemicals
Paraquat - inhaled
drug overdoses
Reperfusion injury after lung transplant
ARDS (Diffuse Alveolar Damage) Clinical
Patients are already ill when ARDS is superimposed
Diffuse bilateral infiltrates on xray
High mortality
Acute Interstitial Pneumonia
(AIP, Hamman-Rich Syndrome)
Symptoms similar to ARDS But, no associated causative disorder Ave. age – 59 years, M=F Acute respiratory failure following illness
