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respiratory medicine midterm > The Lung part 7 > Flashcards

The Lung part 7 Flashcards

1
Q

Diffuse pulmonary hemorrhage syndromes

A
  • complication of interstitial lung disorders; include:
  • Goodpasture’s syndrome
  • Idioathic pulmonary hemosiderosis
  • vasculitis associated hemorrhage found in conditions like hypersensitivity angiitis, Wegner’s granulomatosis, and SLE
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2
Q

Goodpasture’s syndrome

A
  • uncommon autoimmune dz
  • kidney and lung injury caused by circulating autoAb against non-collagenous domain of a3 chain of collagen IV
  • if only kidney involved, called glomerular BM dz
  • Abs initiate inflammatory destruction of BM in renal glomeruli and pulmonary alveoli leading to RPGN and a necrotizing hemorrhagic interstitial pneumonitis
  • teens or 20s (but any age can be affected), males
  • majority of patients are smokers!
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3
Q

Pathogenesis of Goodpasture’s syndrome

A
  • trigger for anti-BM Abs unknown
  • env insult like viral infxn, exposure to hydrocarbon solvents (drycleaning), or smoking thought to be required to unmask cryptic epitopes
  • genetic predisposition–associated with HLA-DRB1*1501 and *1502
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4
Q

Goodpasture’s syndrome morphology

A
  • heavy lungs w/areas of red-brown consolidation
  • Histo: focal necrosis of alveolar walls associated with intra-alveolar hemorrhages
  • alveoli contain hemosiderin-laden macrophages
  • later stages: fibrous thickening of septae, hypertrophy of type II pneumocytes, organization of blood in alveolar spaces
  • IF: LINEAR deposits of Ig along BM of septal walls
  • kidneys=focal prolif GN in early cases or crescentic GN in pts with RPGN
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5
Q

Diagnostic morphology for Goodpastures

A

-Linear deposits of Igs and complement by IF along glomerular BM even in the patients w/o renal disease

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6
Q

Clinical features of Goodpastures

A
  • begin w/resp symptoms–hemoptysis
  • radiography: focal pulmonary consolidations
  • Soon see GN–> to rapidly progressive renal failure
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7
Q

Most common cause of death in Goodpasture’s syndrome

A

-UREMIA!

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8
Q

Prognosis and treatment for Goodpasture’s

A
  • before prognosis was dismal but now much better due to PLASMAPHERESIS–removes circulating anti-BM Abs and chemical mediators of immunologic injury
  • simultaneous immunosuppressive tx inhibits further Ab production, relieving both lung hemorrhage and GN
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9
Q

Idiopathic pulmonary hemosiderosis

A
  • rare
  • intermittent, diffuse alveolar hemorrhage
  • mostly young children! but can see in adults
  • gradual onset of productive cough, hemoptysis, anemia associated with diffuse pulmonary infiltrations similar to Goodpasture’s
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10
Q

Cause and pathogenesis of idiopathic pulmonary hemosiderosis

A
  • unknown!
  • No anti-BM Abs detectable
  • favorable response to long term immunosuppression w/prednisone/ azathioprine indicates immunologic mechanism involved in pulm capillary damage/bleeding
  • some pts develop other immune disorders
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11
Q

Polyangiitis with granulomatosis

A
  • Wegner’s granulomatosis
  • involves upper respiratory tract and/or lungs
  • hemoptysis is common presenting symptom
  • transbronchial biopsy=only tissue available for Dx; since amt of tissue is small, necrosis and granulomatous vasculitis may not be present
  • Diagnostically important are capillaritis and scattered, poorly formed granulomas (unlike those of sarcoidosis which are rounded and well-defined!)
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12
Q

Majority of resp tract infections are

A
  • Upper respiratory tract infections (cold, pharyngitis)

- Bacterial, viral, mycoplasmal and fungal infections of lung (pneumonia) still pretty common

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13
Q

Pneumonia results whenever

A
  • local degense mechanisms are impaired or systemic resitance of host is lowered by things like:
  • chronic disease, immunologic deficiency, treatment with immunosuppressive agents, leukopenia
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14
Q

Examples of how local defense mechanisms of the lung are compromised (5)

A
  • Loss or suppression of cough reflex
  • Injury to mucociliary apparatus
  • Accumulation of secretions
  • Interference with the phagocytic or bactericidal action of alveolar macrophages
  • Pulmonary congestion and edema
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15
Q

Loss or suppression of cough reflex caused by

A

-from coma, anesthesia, neuromuscular disorders, drugs, or chest pain (may lead to aspiration of gastric contents)

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16
Q

Injury to mucociliary apparatus by

A

-by either impairment of ciliary function or destruction of ciliated epithelium due to cigarette smoke, inhalation of hot or corrosive gases, viral diseases, or genetic defects of ciliary function (immotile cilia syndrome)

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17
Q

Accumulation of secretions–seen in conditions like

A

cystic fibrosis and bronchial obstruction

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18
Q

Interference with the phagocytic or bactericidal action of alveolar macrophages by what substances?

A

-alcohol, tobacco smoke, anoxia or oxygen intoxication

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19
Q

Defects in innate immunity (neutrophil and complement) and humoral immunodeficiency typically leads to increased incidence of infections with

A

-pyogenic bacteria

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20
Q

Germline mutations in ___is associated with dustructive bacterial (pneumococcal) pneumonias

A

-MYD88–adaptor for many TLRs that is important for activation of transcription factor NFkb

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21
Q

Cell-mediated immune defects (congenital and acquired) lead to

A

-increased infections with intracellular microbes like mycobacteria and herpesviruses as well as with microorganisms of very low virulence like Pneumocystis jiroveci

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22
Q

Most common cause of death in viral influenza epidemics is

A

-superimposed bacterial pneumonia

23
Q

portal of entry for most bacterial pneumonia is the

A
  • respiratory tract
  • BUT hemategenous seeding of lungs from another organ may occur making it difficult to distinguish it from primary pneumonia
24
Q

Many patients with chronic diseases acquire terminal pneumonia while

A
  • hospitalized (nosocomial infection)
  • Bacteria common to hospital environment may have acquired resistance to antibiotics; opportunities for spread are increased
  • invasive procedures like intubations and injections common and bacteria may contaminate equipment used in resp care units
25
Q

Community acquired acute pneumonia

A
  • lung infection acquired from env in otherwise healthy (in contrast to hospital acquired)
  • may be viral or bacterial–hard to differentiate
26
Q

CRP in viral vs. bacterial pneumonia

A
  • produced in liver

- significantly elevated in bacterial more than viral

27
Q

Bacterial infection usually follows

A
  • an upper respiratory viral infection
  • Bacterial invasion of lungs causes alveoli to be filled with inflammatory exudate, causing consolidation (solidification) of pulmonary tissue
28
Q

Predisposing conditions associated with community acquired pneumonia

A
  • extremes of ages
  • chronic diseases (COPD, CHF, diabetes)
  • congenital or acquired immune deficiencies
  • decreased splenic function (sickle cell disease, post-splenectomy)
29
Q

Most common cause of community acquired acute pneumonia

A

-Streptococcus pneumoniae

30
Q

Streptococcus pneumoniae

A
  • Dx w/gram stained sputum
  • see many neutrophils with typical gram-pos, lancet shaped diplococci
  • is part of endogenous flora in 20% of adults so results may be false positive!
  • Isolation from blood cultues is more specific but less sensitive
  • Pneumococcal vaccines w/capsular polysaccharides from common srotypes used in ppl w/high risk pneumococcal sepsis
31
Q

Haemophilus influenzae

A
  • pleomorphic, gram negative; occurs in encapsulated and non-encapsulated form
  • six serotypes of encapsulated (a to f); b is most virulent
  • Abs against capsule protects from H. influenzae–this is why capsular polysaccharide b is incorporated in widely used vaccine against H. influenzae=declined incidence
32
Q

Haemophilus influenzae–non encapsulated forms

A
  • incidence of non encapsulated forms (nontypeable forms) increasing; less virulent, spread along surface of upper respiratory tract
  • produce otitis media, sinusitis, bronchopneumonia
  • Neonates and children with comorbidities like prematurity, malignancy, immunodeficiency at high risk for development of invasive infection
33
Q

H. influenzae pneumonia

A
  • follows viral respiratory infection
  • pediatric emergency; high mortality rate
  • Descending laryngotracheobronchitis results in airway obstruction as smaller bronchi are plugged by dense, fibrin rich exudates containing neutrophils (similar to pneumococcal pneumonia)
  • Pulmonary consolidation is lobular and patchy but may be confluent and involve entire lung lobe
34
Q

Before the vaccine, H. influenzae was a common cause of

A
  • suppurative meningitis in children up to 5 yrs of age
  • H. influenzae also causes acute, purulent conjunctivitis (pink eye) in children
  • in predisposed older pts, may cause septicemia, endocarditis, pyelonephritis, cholecystitis, suppurative arthritis
35
Q

H. influenzae is the most common bacterial cause of

A

-acute exacerbation of COPD

36
Q

Morexella cararrhalis

A
  • bacterial pneumonia in elderly
  • second most common bacterial cause of acute exacerbation of COPD
  • Along with S. pneumoniae and H. influenzae, M. catarrhalis is one of the 3 most common causes of otits media in children
37
Q

Staphylococcus aureus

A
  • important cause of secondary bacterial pneumonia in children and healthy adults following viral resp illnesses (measles in children, influenza in children and adults)
  • lots of complications–lung access and empyema
  • IV drug users at high risk for staph pneumonia
  • also important cause of hospital-acquired pneumonia
38
Q

Klebsiella pneumonia

A
  • most frequent cause of gram-negative bacterial pneumonia
  • affects debilitated and malnourished people, esp CHRONIC ALCOHOLICS
  • thick mucoid sputum is characteristic bc the organism produces abundant viscid capsular polysaccharide, which patient may have difficulty expectorating
39
Q

Pseudomonas aeruginosa

A
  • most commonly causes hospital-acquired infections
  • occurrence in cystic fibrosis and immunocompromised patients
  • common in patients who are neutropenic and has propensity to invade blood vessels with consequent extra pulmonary spread
  • Pseudomonas septicemia=fulminant disease
40
Q

Legionella pneumophila

A
  • agent of Legionnaire’s disease–epidemic and sporadic forms of pneumonia
  • causes Pontiac fever–self limited URI
  • flourishes in artificial aquatic environments like water-cooling towers and tubing systems of domestic (potable) water supplies
  • mode of transmission=either inhalation of aerosolized organisms or aspiration of contaminated drinking water
41
Q

Legionella pneumonia is common in individuals with

A
  • predisposing conditions like cardiac, renal, immunologic or hematologic disease
  • Organ transplant recipients particularly susceptible
  • can be severe requiring hospitalization and immunosuppressed patients have fatality rates up to50%
  • Rapid diagnosis by seeing Legionella Ags in urine or by positive fluorescent Ab test on sputum samples
  • culture is diagnostic gold standard
42
Q

Mycoplasma pneumoniae

A
  • common in children and young adults

- occur sporadically as local epidemics in closed communities (schools, military camps, and prisons)

43
Q

Two patterns of anatomic distribution in bacterial pneumonia

A
  • Lobular bronchopneumonia

- Lobar pneumonia

44
Q

Lobar pneumonia vs bronchopneumonia dominant characteristics

A
  • Bronchopneumonia=patchy consolidation of lung
  • Lobar pneumonia=consolidation of large portion of a lobe or of entire lobe
  • patterns overlap
45
Q

Most important in determining bronchopneumonia vs. lobar pneumonia clinically

A

-IDENTIFICATION OF CAUSATIVE ORGANISM AND DETERMINATION OF EXTENT OF DISEASE

46
Q

Four stages of inflammatory response in LOBAR pneumonia

A

1) congestion
2) Red hepatization
3) gray hepatization
4) resolution

47
Q

Congestion stage (1) of lobar pneumonia

A
  • lung is heavy, boggy, and red

- vascular engorgement, intra-alveolar fluid w/few neutrophils; presence of numerous bacteria

48
Q

Red hepatization (2) stage of lobar pneumonia

A
  • massive confluent exudation as neutrophils, red cells, and fibrin fill alveolar spaces
  • Grossly, lobe is red, firm and airless with a liver like consistency–hence the term hepatization
49
Q

Stage of gray hepatization (3) in lobar pneumonia

A

progressive disintegration of red cells and persistence of fibrinosuppurative exudate resulting in a color change to grayish brown

50
Q

Stage of resolution (4) in Lobar pneumonia

A
  • exudate within alveolar spaces is broken down by enzymatic digestion to produce granular, semifluid debris that is resorbed, ingested by macrophages, expectorated or organized by fibroblasts
  • Pleural fibrosis reaction to underlying inflammation often present in early stages if consolidation extends to surface (pleuritis) may similarly resolve
  • more often undergoes organization leaving fibrous thickening or permanent adhesions
51
Q

Bronchopneumonia morphology

A
  • consolidated areas of acute suppurative inflammation
  • consolidation may be confined to one lobe but more often multi lobar and frequently bilateral and basal bc of tendency of secretions to gravitate to lower lobes
  • Well developed lesions are slightly elevated, dry, granular, gray-red to yellow and poorly delimited at their margins
  • Histologically, rxn elicits neutrophil rich exudate that fills bronchi, bronchioles, adjacent alveolar spaces
52
Q

Complications of pneumonia

A

1) tissue destruction and necrosis causing ABSCESS (esp with type 3 pneumococci or Klebsiella infxns)
2) spread of infection to pleural cavity causing intra-pleural fibrinosuppurative reaction called empyema
3) bacteremic dissemination to heart valves, pericardium, brain, kidneys, spleen or joints, causing metastatic abscesses, endocarditis, meningitis or suppurative arthritis

53
Q

Clinical course of community acquired pneumonia

A
  • abrupt onset of high fever, shaking chills and cough producing mucopurulent sputum; some patients have hemoptysis
  • When pleuritis is present, it is accompanied by pleuritic pain and pleural friction rub
  • whole lobe is radiopaque in lobar pneumonia whereas there are focal opacities in bronchopneumonia
54
Q

Community acquired pneumonia treatment

A
  • antibiotics
  • treated patients afebrile with few clinical signs 48-72 hours after initiating antibiotics
  • need to identify organism and determine its antibiotic sensitivity
  • Much fewer hospitalizations and death results from complication like empyema, meningitis, endocarditis, pericarditis or chronic alcoholism

respiratory medicine midterm (17 decks)

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