Gomez - Intro to Resp Path/Rad Flashcards

1
Q

What other name is nasal mucosa called by?

A

Schneiderian mucosa

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2
Q

What does nasal histology look like?

A

Pseudostratified ciliated columnar epithelium with submucosal glands

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3
Q

What are the nasal vestibules lined by?

A

Nonkeratinized squamous epithelium

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4
Q

What causes acute infectious rhinitis?

A

Rhinoviruses are most common

many others can also cause it

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5
Q

Describe the disease process of acute rhinitis

A

Run nose (rhinorrhea)

Transmission by contact

Can cause other conditions like pharyngitis, sinusitis, tonsillitis, otitis media

Self-limiting

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6
Q

Describe allergic rhinitis

A

Type I hypersensitivity (IgE mediated)

Pt presents with runny nose and congestion

Associated with seasonal allergies

Tx: antihistamine

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7
Q

Describe the pathway of Type I hypersensitivity rxns

A

Allergen stims TH2 response and IgE production

IgE binds to Fc receptors on mast cells

Subsequent exposures to same allergen activate mast cells to degranulate, releasing histamine and other inflammatory mediators

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8
Q

What is chronic rhinitis?

A

Caused by many different factors

Defined as persistence of cardinal sx for >1month

Sx: sneezing, rhinorrhea, congestion, postnasal drip

Appears to follow acute rhinitis

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9
Q

Describe nasal polyps

A

Inflammatory polyp

often results from recurrent attacks of rhinitis

suggestive of allergies but most pts are not atopic

May cause obstruction

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10
Q

What is the important anatomical relationship of all sinuses?

A

All communicate in some way with nasal cavity

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11
Q

What are the three types of sinusitis?

A

Acute (w/ empyema)

Subacute

Chronic

Only differentiating factor is time

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12
Q

What is a mucocele of the sinus?

A

Mucus accumulation that obstructs sinus

No bacterial involvement

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13
Q

What are some serious complications of sinusitis?

A

Orbital cellulitis

Osteomyelitis

Cranial vault extension

Septic thrombophlebitis of dural venous sinus

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14
Q

Describe acute (infectious) sinusitis

A

Can be viral or bacterial in nature

Anything that causes common cold or ear infections can cause this

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15
Q

What is the ASA triad?

A

Chronic rhinosinustis

Nasal polyps

Severe bronchial asthma

Induced by taking aspirin

Can lead to chronic sinusitis

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16
Q

What is immotile cilia syndrome?

A

During development, if cilia aren’t motile, can result in defective migration of cells to wrong side of body and may cause situs inversus in 50% with this abnormality

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17
Q

What is Kartagener syndrome?

A

Defective ciliary action and situs inversus

18
Q

What is the most common bacterial cause of sinusitis?

A

Staph aureus

19
Q

What is a mycetoma?

A

Ball of fungus resulting in fungal sinusitis

Destructive lesion

20
Q

What is a complication of invasive fungal sinusitis?

A

Major destruction of surrounding tissues

21
Q

Discuss cocaine’s effect on upper airways

A

Cocaine is a potent vasoconstrictor, and can cause tissue destruction from ischemia

22
Q

What are two significant causes of infectious necrotizing lesions of upper airways?

A

Rhinocerebral mucormycosis

Hansen disease/lepromatous leprosy

23
Q

What is a major malignancy causing necrotizing lesions of the upper airway?

A

Extranodal NK/T cell lymphoma

Often localize to the midline

can be quite lethal

24
Q

Discuss rhinocerebral mucormycosis

A

Caused by sarophytic mold fungi

More prevalent in diabetics or immunocompromised individuals

Produce irregular-shaped hyphae w/ few to no septa

Very aggressive

25
Where do a lot of lung cancers occur? What sequelae are important to recognize because of this?
Around the hilum Important because these cancers can invade esophagus, trachea, and aorta
26
What structures are present in the trachea/bronchus?
Ciliated epithelium Goblet cells Seromucus glands Cartilage Histologically, differentiate trachea and bronchus based on size
27
What structures are present in the bronchiolus?
Smooth muscle cells Clara cells Capillaries Basal membrane Surfactant No cartilage
28
What structures are present in the alveoli?
Type I pneumocyte Type II pneumocyte Alveolar septum
29
What is a major difference between Type I and Type II pneumocytes?
Type I are terminally differentiated Type II will regenerate if there is alveolar injury
30
What are pores of Kohn?
Gaps in between alveoli Serve to equalize pressure between adjacent alveoli
31
What is atelectasis?
Collapse of alveoli
32
What is resorption of lung tissue?
Obstruction of an area leads to no air getting in, but air is diffusing into tissues, leading to collapse of that area Mediastinum will shift towards side of resorption Other lung will have compensatory hyperinflation
33
What is compression of lung tissue?
External pressure on lung (incl. elevation of diaphragm) Mediastinal shifting away from affected lung
34
What is contraction of lung tissue?
Secondary to fibrosis of lung or pleura Does not allow lung to expand properly Irreversible
35
All atelectasis increases the risk for what?
Infection
36
What are the two main types of pulmonary edema?
Hemodynamic Microvascular
37
Describe hemodynamic pulmonary edema
Most common form Increased hydrostatic pressure from L heart failure Presence of "heart failure" cells If chronic, can lead to alveolar fibrosis (appearance of brown induration of lung)
38
Describe microvascular injury resulting in pulmonary edema
Caused by increased permeability resulting from infection, toxic injury, etc. If diffuse, can lead to ARDS
39
What are the criteria for acute lung injury?
Acute onset of dyspnea Hypoxemia Bilateral infiltrates Absence of primary L-sided heart failure
40
Describe ARDS (aka diffuse alveolar damage)
Occurs in pts w/ severe disease Diffuse damage to alveolar capillary walls, leading to neutrophil migration Vascular injury and secondary loss of surfactant
41
What are the main causes of ARDS?
Diffuse pulmonary infection (PNA, viral, etc) Gastric aspiration Mechanical trauma, incl. head inj.
42
Describe Acute Interstitial Pneumonia
aka Hamman-Rich Syndrome Sx similar to ARDS No real causative disorder Acute respiratory failure following illness Pts get progressively worse High mortality rate