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Pulmonary Pathology I, BACTERIAL PNEUMONIA-ID CAUSATIVE AGENT-P. carinii in AIDS Bronchopneumo-patchy consolidation-lobular -usually extension of bronchiolitis -infancy and old age-lower resistance -often terminates long course of other dz Lobar pneumo-acute, but infrequent now b/c ABX -more extensive exudation->spreads through pores of Kohn -if extending to surface->pleuritis->can resolve or form ADHESIONS* PATHOGENESIS-w/ impaired defenses or lower immunity NL defenses: Nasal, tracheobronchial, alv clearance Interference: loss of cough reflex, injured mucociliary app(hot gas, cig), interference w/ alv macs (EtOH, tob smoke, anoxia, O2 intox), pulm congestion/edema, accumulated secretions (CF, obstruction) Most common cause of death in influenza pts Hematogenous spread from OR to lungs COMPLICATIONS 1. Tissue destruction/necrosis->abscess (esp w/ type 3 pneumococci, K. pneumo) 2. Spread to pleural cavity->intrapleural fibrosuppurative 'EMPYEMA' 3. Organization of exudate->solid tissue 4. Bacteremic dissemination CLINICAL-MALAISE, FEVER, SPUTUM COUGH -Rub, pleuritic pain with pleuritis TX-ABX->few S/Sx after 48-74 hrs -Identify org % hospitalizable pneumo is fatal-due to complication Infections -mostly viral TUBERCULOSIS -new emergence w/ AIDS, resistance Primary Pulm TB -initial focus-Ghon complex subpleural lesion near fissure + enlarged caseous LNs draining into focus -most pts (-)Sx->fibrosis, calcification -OR progressive spread w/ cavitation, TB pneumonia, miliary TB Secondary (Reactivation) Pulm TB-often from subclinical primary -bacilli move up to apices (based on O2 tension) -reactivation in 5-10% pts->more dmg than primary MORPH-in apex of both lungs, less often in hilus -often regional nodes w/ sim activity -hope caseation of primary is away from bronchus ->fibrous encapsulation->scar->adhesions -coalescent granulomas-epithelioid cells w/ fibs, lymphos -necrosis in centers of tubercles ->coalescence->sccar (in favorable case) -can't find bacilli in late fibrous phase Tx complicated by advanced dz, resistance, or: AIDS, DM, reactive amyloidosis, BACTERIAL PNEUMONIA-ID CAUSATIVE AGENT-P. carinii in AIDS Bronchopneumo-patchy consolidation-lobular -usually extension of bronchiolitis -infancy and old age-lower resistance -often terminates long course of other dz Lobar pneumo-acute, but infrequent now b/c ABX -more extensive exudation->spreads through pores of Kohn -if extending to surface->pleuritis->can resolve or form ADHESIONS* PATHOGENESIS-w/ impaired defenses or lower immunity NL defenses: Nasal, tracheobronchial, alv clearance Interference: loss of cough reflex, injured mucociliary app(hot gas, cig), interference w/ alv macs (EtOH, tob smoke, anoxia, O2 intox), pulm congestion/edema, accumulated secretions (CF, obstruction) Most common cause of death in influenza pts Hematogenous spread from OR to lungs COMPLICATIONS 1. Tissue destruction/necrosis->abscess (esp w/ type 3 pneumococci, K. pneumo) 2. Spread to pleural cavity->intrapleural fibrosuppurative 'EMPYEMA' 3. Organization of exudate->solid tissue 4. Bacteremic dissemination CLINICAL-MALAISE, FEVER, SPUTUM COUGH -Rub, pleuritic pain with pleuritis TX-ABX->few S/Sx after 48-74 hrs -Identify org % hospitalizable pneumo is fatal-due to complication Types Lobar Pneumonia 95% Pneumococci (protected by mucoid capsule) types 1,2,3,7 - type 3 esp virulent K. pneumo, Staph, Strep, H.influenzae Pseudomonas, Proteus (due to ABX resistance) MORPHOLOGY - 4 stages 1. Congestion-engorged vessels, intra-alv fluid, few PMNs -lots of bac - HEAVY, BOGGY, RED 2. Red hepatization-RBCs, PMNs, fibrin into alv spaces -RED, FIRM, AIRLESS 3. Gray Hepatization-disintegrated RBCs, fibrin stays 4. Resolution-digestion of all the funk, resorbed/coughed up, Lung Pathology Pleura NONINFLAM EFFUSIONS Hydrothorax-clear/straw colored fluid -often results from edema dzs (transudates) -CARDIAC FAILURE, renal failure, liver cirrhosis, Meig syndrome (rt side) -->compression/atalectasis on lung parts Hemothorax-almost always fatal-smooth clots -complication of rupture Ao aneur, trauma -makes adhesions if slow enough Chylothorax-milky, lymphatic fluid w/ fats -more often just on left side -via thoracic duct trauma/obstruction -via malig conditions in thorax, Lung Pathology Vascular Origin ADULT RESP DISTRESS SYNDROME-classic restrictive dz =shock lung, diff. alv. dmg, wet lungs, etc. -caused by diffuse alv capillary dmg -rapid onset of severe resp insuff, cyanosis, arterial hypoxemia refractory to O2 Tx can ->multisystem organ failure Most pts have severe pulm edema (noncardiogenic) ->diffuse alv infiltration on CXR ->hyaline membranes on histo (like in newborn) Causes, usually a combo of (usually eap endoth injury): -Direct lung injury: diffuse pulm infx, O2 toxicity, toxins, irritants, asp of gastric contents -Systemic: septic shock, trauma shock, hemorr panc'titis, burns, abd surgery comps, narcotics/drugs, hypersens, hemodialysis, cardiac surgery w/ bypass pumps MORPHOLOGY Acute edematous stage:heavy, firm, red, baggy lungs -congestions, hyaline membranes (remnants of dead ccells) -type II epith cells proliferate to restore alv, but can't -->organization of fibrin exudate->fibrosis->septa thicken -fatal cases often w/ bronchopneumonia PATHOGENESIS-end results of many alv injuries -endotoxin (for instance) ->more WBCs->toxic to endoth ->injured cap walls->inc. perm->fluid, fibrin exudates -doesn't resolve (resolves w/ cardiogenic infiltrates) Final Common Pathway: diffuse dmg to alv cap walls CLINICAL-usually already in hosp for other condition -then dyspnea, tachypnea, initial CXR NL ->cyanosis, hypoxemia, resp failure, CXR infiltrates -resp acidosis, unresponsive to O2 Tx Lung: focally stiff, dec. func vol, collapsed alvs, some tissue still NL -continued perfusion though, so V/Q mismatch -help by inhaling NO (vasodilator-> dec. PVR THERAPY-frequently fatal - even O2 Tx can be toxic -some recover and resorb fluid 150000 cases/yr, 60% fatal, Lung Pathology Infections -mostly viral LUNG ABSCESS-necrosis in lung -from oropharynx surgery, sinobronchial infx, dental sepsis, bronchiectasis Common orgs: aerobe/anaerobic Strep, S. aureus, gram(-)s -often mixed -60%-dental anaerobes-Bacteroides, Fusobac, Peptococcus Pathogenesis: 1. Asp of infective material**-alcoholism, coma, anesthesia, sinusitis, gingivodental sepsis, cough suppression 2. Antecedent primary bac infx-esp S. aureus, K.pneumo, type 3 pneumococcus; fungi, bronchiectasis-IMMUNOSUPPRESSED 3. Septic embolism-including from rt heart valves (IVDA) 4. Neoplasia-2ndary infx in obstructed segment 5. Misc-direct trauma, infx spread from close organ, hematog seeding OR Primary Cryptogenic Lung Abscesses-no known cause MORPHOLOGY-suppurative destruction of parenchyma w/in central area -if communication w/ air passage->drainage->air cavity -saprophytic infx flourish in abscess debris -continued infx->gangrene of lung -chronic->fibrous wall -asp more common on right and single -pneumo or BE->multiple, basal, scattered -septic, pyemic->anywhere, multiple CLINICAL-like BE-cough, fever, lots of smelly purulent/bloody sputum -fever, chest pain, wt loss -clubbing of fingers, toes w/in weeks -Dx from bronchscopy, X-ray - rule out CA Tx-most resolve w/ proper Tx Complications-extension into pleura, hemorrhgage, brain abscesses, mening (septic emboli), 2ndary AA amyloidosis, Lung Pathology Complications of Tx DRUG-INDUCED LUNG DZ Drugs->bronchospasm, pulm edema, chronic pneumonitis w/ fibrosis, hypersens pneumonitis Amiodarone concentrates in lung -control arrhythmias-->pneumonitis Bleomycin, other CTX->pneumonitis, fibrosis, Lung Pathology Complications of Tx RADIATION-INDUCED LUNG DZ Radiation Pneumonitis in XRT -Acute 1-6 mos after Tx ->fever, dyspnea, infiltrates at site -atypical hyperplastic type II cells -STEROID TX WORKS WELL -Chronic-interstitial fibrosis at site -Atypical epith cells, foam cells in vessel walls -results from direct toxicity on endoth, epith, Lung Pathology Atelectasis Incomplete expansion or Collapse of prev-inflated lung ->reduces O2-->PRONE TO INFX -reversible except for contraction Obstruction/Resorption ->from obstruction of airway ->resorption of O2 trapped in alv-unimpaired blood -lung vol dec, so mediastinum shifts TOWARDS -usually from excess secretions in airway -eg bronchial asthma, chronic bron, bronchiectasis, aspiration, post-op states Compression-pleural cavity filled w/ fluid, tumor, air, tension pneumothorax -most common in cardiac failure w/ effusions, CA pts -also from elevated diaphragm -mediastinum shifts AWAY from affected lung Patchy-loss of pulm surfactant-NEONATAL and ARDS Contraction -fibrotic changes inhibit full expansion, BACTERIAL PNEUMONIA-ID CAUSATIVE AGENT-P. carinii in AIDS Bronchopneumo-patchy consolidation-lobular -usually extension of bronchiolitis -infancy and old age-lower resistance -often terminates long course of other dz Lobar pneumo-acute, but infrequent now b/c ABX -more extensive exudation->spreads through pores of Kohn -if extending to surface->pleuritis->can resolve or form ADHESIONS* PATHOGENESIS-w/ impaired defenses or lower immunity NL defenses: Nasal, tracheobronchial, alv clearance Interference: loss of cough reflex, injured mucociliary app(hot gas, cig), interference w/ alv macs (EtOH, tob smoke, anoxia, O2 intox), pulm congestion/edema, accumulated secretions (CF, obstruction) Most common cause of death in influenza pts Hematogenous spread from OR to lungs COMPLICATIONS 1. Tissue destruction/necrosis->abscess (esp w/ type 3 pneumococci, K. pneumo) 2. Spread to pleural cavity->intrapleural fibrosuppurative 'EMPYEMA' 3. Organization of exudate->solid tissue 4. Bacteremic dissemination CLINICAL-MALAISE, FEVER, SPUTUM COUGH -Rub, pleuritic pain with pleuritis TX-ABX->few S/Sx after 48-74 hrs -Identify org % hospitalizable pneumo is fatal-due to complication Infections -mostly viral LUNG ABSCESS-necrosis in lung -from oropharynx surgery, sinobronchial infx, dental sepsis, bronchiectasis Common orgs: aerobe/anaerobic Strep, S. aureus, gram(-)s -often mixed -60%-dental anaerobes-Bacteroides, Fusobac, Peptococcus Pathogenesis: 1. Asp of infective material**-alcoholism, coma, anesthesia, sinusitis, gingivodental sepsis, cough suppression 2. Antecedent primary bac infx-esp S. aureus, K.pneumo, type 3 pneumococcus; fungi, bronchiectasis-IMMUNOSUPPRESSED 3. Septic embolism-including from rt heart valves (IVDA) 4. Neoplasia-2ndary infx in obstructed segment 5. Misc-direct trauma, infx spread from close organ, hematog seeding OR Primary Cryptogenic Lung Abscesses-no known cause MORPHOLOGY-suppurative destruction of parenchyma w/in central area -if communication w/ air passage->drainage->air cavity -saprophytic infx flourish in abscess debris -continued infx->gangrene of lung -chronic->fibrous wall -asp more common on right and single -pneumo or BE->multiple, basal, scattered -septic, pyemic->anywhere, multiple CLINICAL-like BE-cough, fever, lots of smelly purulent/bloody sputum -fever, chest pain, wt loss -clubbing of fingers, toes w/in weeks -Dx from bronchscopy, X-ray - rule out CA Tx-most resolve w/ proper Tx Complications-extension into pleura, hemorrhgage, brain abscesses, mening (septic emboli), 2ndary AA amyloidosis, Lung Pathology Infections -mostly viral VIRAL, MYCOPLASMAL PNEUMONIA -(primary atypical pneumonia)-acute, febrile dz -patchy inflam in lungs, in alv septa, pulm interstitium -"atypical" b/c no alv exudate -AKA-interstitial pneumonitis Mycoplasma pneumoniae-Most common cause Influenza A & B, RSV, adenovirus, rhinovirus, rubeola, VZV Chlamydia psittaca, Coxiella burnetta (Q fever) -most agents often cause URI or LRI w/ other circumstances MORPHOLOGY - patchy or lobar, bi- or unilaterally -smooth pleura, infrequent pleuritis/effusions -localized to alv walls - interstitium - hyaline membranes -walls widened, edematous, mononuc inflam (PMNs if acute) ->alveolocapillary block ->restored architecture upon relief Superimposed bac infx->ulcerative bronchitis, bronchiolitis ->can look like regular bac pneumo HSV, VZV, adenovirus->necrosis of bronch, alv epith; inflam Cytomegalic inclusion Dz - epith giant cells w/ inclusions CLINICAL-varied-severe URI or chest colds -few localizing Sx, cough can be absent -can have fever, HA, myalgia, leg pains -usually mild-1% mort-can be epidemic w/ viral epidemics (flu) -ELEVATED COLD AGGLUTININS-differentiate -in half of Mycoplasma, 20% adenovirus, not in other viral