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50 Cards in this Set

  • Front
  • Back
protective mechanisms of URT
- nasal hair
- cilia of trach/bronch mucosa
- lymphoid tissue of oro/nasopharynx
- **alveolar macrophages
sinus mucosa cover
- secreted by goblet cells in sinus epithelium, consisting of 2 layers
2 layers of sinus mucosa cover
superficial - traps inhaled particles, covers cilia
deep - lubricates cilia
ciliary movement
- moves superficial layer with entrapped debris
- keep sinus epi free of pathogens
mucous contains 2 types of defenses that aid in protecting sinuses from pathogens
specific and non-specific

-> maintain healthy lung sterility despite direct contact w/ ext air***
URTIs common:
adults
children
adults: 2-3 viral URTIs/yr
children: 3-8 viral URTIs/yr
common cold
- mild, self limiting infection
- caused by many groups of viruses (adeno-,rhino-,flu-,parainflu-)
common cold:
mechanism
- inflammation of nasal mucous memb w/ excessive production of mucous AND loss of superficial ciliated cells
rhino-sinusitis
- group of disorders characterized by inflamm of:
- nasal mucosa
- paranasal sinuses (frontal, maxillary, sphenoid, ethmoid)
rhino-sinusitis:
1. MC
2. acute
3. chronic
1. one of MC type of URTI (1 bill cases viral/bacT sinusitis/yr US)
2. inflamm predom caused by **viral or bacT microorganisms
3. inflamm d/t a **number of other causes
rhino-sinusitis:
pathogenesis
viral URTI -> dysfnxn of epi cells -> disturbance of sinus hometostasis -> accum and stag of secretions and bacT in sinuses -> bacT superinfxn -> **acute bacT rhinosinusitis (ABRS)
ABRS:
inc risk
- immunosuppressed (cortisone & AIDS pts)
- presence of asthma, allergy, CF
- 2*/environmental smoke exposure or snort coke
--> last 2 both damage nasal mucosa -> pt prone to infxn
ABRS:
etiology
s. pneumonia, h. flu (m. catarrhais, s. pyogenes, s. auereus, anaerobes)
the same bugs (streps, h-flu, m-cat, anaerobes) are also a/w:
- community acquired PNA (CAP)
- acute exacerb of chronic bronch
- acute otitis media
ABRS:
micro
- acutely inflamed mucosa shows congestion, edema and hyperactive mucosal glands
why is it imp to use right abx therapy w/ tx of ABRS?
- resistance (esp S. pna, H. flu)
acute laryngo-tracheitis
- URTI including phonation, mainly children
- bugs: strep, H-flu, paraflu, RSV
-clinical: hoarse, high pitch cough and stridor
-MC complication: trach obstruction
- loss cilated epi inflamm mucosa
acute bronchitis
- inflamm of large bronchi
- bugs: flu, bacT, cold, chemicals
- micro: vasc congestion & infiltration of mononuc (virus), PMNs (bacT), fibrin & occasionally ulceration of bronchial mucosa
why is acute bronchitis a problem esp w/ babies?
- abundant mucus secretion can block bronchioles (can't open if infected)
PNA
- inflamm of lung parenchyma, characterized by presence of inflamm exudate w/in alveoli and or/interstitium

- cause infectious or non-infectious
PNA:
classifications
anatomical: distribution of lesions (lobar, broncho, interstitial)
etiological: bacT, viral, mycoplasma PNA
clinical setting: where infxn occurs --> PNA syndromes
PNA syndromes
1. CAP
--> acute PNA
--> atypical PNA
2. nosocomial PNA
3. aspiration PNA
4. chronic PNA (granulomatous)
5. necrotizing PNA & lung abscess
6. PNA in immunocomp host
CAP:
1. cause
2. mechanism
1. bacT (may follow URT infxn) or atypical (viral or mycoplasma)
2. bacT invades lung parenchyma & causes alveoli to be filled w/ inflamm exudates -> causes consolidation of pulm tissue
CAP:
predisposing condidtions
1. age
2. chronic ds (COPD,CHF,DM)
3. congen or acquired immune deficiencies
4. dec or absent splenic fnxn causes inc risk of encapsulated bacT (ie pneumococcus)
bacT PNA:
1. cause
2. who
1. G+/-
2. age group 10-40
bacT PNA:
highest risk group
1. immunosupp/AIDS/elderly
2. asplenic pts
3. SCA pts
4. mult myeloma
5. cirrhosis/ alcoholics
6. renal failure
7. influenza
8. COPD
9. diabetics
bacT PNA:
high risk group should...
get vaccinated, highly recommended***
classifications of bacT PNA
1. bronchoPNA: inflamm involves bronchi and corresponding lobule
2. lobar PNA: involve alveoli of entire love w/o involvement of bronchi
bronchoPNA
1. definition
2. histo
1. patchy consolid. centered around inflamed bronchi, usually multifocal and bilat
2. suppurative bronchitis and bronchiolitis w/ acute inflamm exudates containg polymorphs, fibrin and organisms
bronchoPNA
1. bugs
2. high risk pts
1. staph, strep, pneumo, H-flu, coriform bacT
2.
- very young/old
-pre-existing trachea-bronchitis
- cardio/renal failure
- ca or stroke pt
bronchoPNA:
1. mechanism
2. where
1. bilat involv of several lobular bronchi and their corresponding lobules w/ multiple firm areas of consolid. around bronchi --> filled w/ mucopurulent material
bronchoPNA
1. complications
2. s/sx
1. prog of ds may cause confluence of consolidated areas
2.
- fever
- cough w/ expectoration of purulent sputum
- hx of being bedridden
- underlying serious condtn
- URT infxn
broncho PNA
outcome and complications
1. resolution
2. oganization of suppurative exudates
3. lung abscess
4. empyema, pericarditis
5. distant effects of bacTemia
6. death -*very common terminal manifestation for many pts (due to mult organ failure)
describe resolution in bronchoPNA
only occurs if tx is started early before structural damage was done
describe organization in bronchoPNA
- organization of suppurative exudates leads to fibrous scarring which can lead to fibrosis
lobar PNA
acute bacT infxn w/ large areas of consolidation in one or more lobes
lobar PNA:
1. etiology
2. sites
1. 90-95% caused by pneumococci which is esp dangerous infxn in children
- types 1,2,3,7 w/ 3 most virulent
- occasionally caused by klebsiella p, stap, strep and h-flu
2. sharply confined to a love, rarely more than one lobe affected
lobar PNA:
4 stages
1. congestion
2. red hepatization
3. gray hepatization
4. resolution
congestion
boggy, engorged, congestive alveolar vessels
--deep red firm lobe
red hepatization
- lobe filled w/ intra-alveolar PMNs and RBCs; resembles liver tissue
- red and firm, makes it airless and sink in water
- alveoli fills w/ inflamm exudates, fibrin, PMNs, bacT, etc
gray hepatization
- looks pale as PMNs destroy and inject RBCs and debris
- lobe appears gray and dry w/ no more congestion and lung is preserved
resolution
- return to nL or near-nL state
- exudate is digested & absorbed by macrophages
- lung fibroblasts help return alveoli to nL
lobar PNA:
1. s/sx
2. outcomes
1. typical infxous symp: fev/chills/malaise
- others: inspiratory chest pain & blood-stained sputum
- sudden improvement of symps during resolution stage
2. typically completely resolved in most tx'd cases
lobar PNA:
complications
- most likely in cases by Klebsiella or S. aureus
1. hemorrhagic pleuritis, esp in rickettsias or typhus
2. lung abscesses
3. suppurateive pleuritis leads to empyema
4. pulm fibrosis
5. poss bacTemia leading to meningitis or endocarditis
lobar PNA:
CXR
homogenous opacification w/ vol of lobe unchanged, not reduced like atelectasis
aspiration PNA
- aspiration of gastric content while unconscious
- high risk: ppl who fall asleep while eating or vom in sleep
--debiliated pt
--alcoholics
--impaired esophageal fnxn (scleroderma, diverticula, achalasia)
- impaired cough/gag reflex
aspiration PNA
bugs
anaerobic oral flora mixed w/ aerobic common pathogens (H-flu, strep, staph, etc)
lung abscess
localized destruction (liquificative necrosis) of lung parenchyma containing pus-surrounded by fibrous tissue
lung abscess:
1. bug
2. patho
1. staph, strep, G- bacT and anaerobes
2. aspiration of infx'd material (fb like teeth)
--following pulm infxn
--a/w ds from other site - may cause sepsis in steroid abuser or IV drug use
lung abscess:
complications
1. communication w/ bronchus and expectoration of copious sputum
2. comm w/ pleural cavity leadint to empyema or fistulas
3. metastatic abscess, particularly brain - sym inc erratic behavior & h/a