Pathology of lung Flashcards
(78 cards)
Acute resp distress syndrome-ARDS/diffuse alveolar damage-DAD
what
caharacteristif
msot common cause
serious damage to lung parnechyam
Characteristics
-acute
-sever hypoxaemia
-bilat lung infiltartes
most common by shock
pathogenesis of ards/dad
1.exsudatove phase
-alevolar linging detaches and regressive/necrotic pneumocytes acc together with protien in alveoli
2- prolif phase
- interstitial fibrosis w carnificaiton
MORPHOLOGY OF ARDS/DAD
Interstitial oedema
2. Fibroblastic proliferation in the alveoli septum
3. Alveolar oedema
4. Alveolar fibrin and cell debris with the presence of hyaline membranes
5. Hyperplasia of type II pneumocytes
pneumonia
= inflammation of the lung parenchyma
o Inflammation of the respiratory bronchiole, alveolar structures and lung interstitium
o NOT pneumonitis!
bronchopeumipnia
= inflammation of small bronchi, bronchiole and surrounding lung parenchyma
o Inflammation of terminal bronchioles and related alveoli
pleuropneiomina
= pneumonia + pleuritis (inflammation of pleura)
interstitial pneumonia(pneummonitis)
= inflammation of lung interstitium
general about pneumonia
-lower airwsys
-3rd msot common cuase of eath
-streptocoocus pneomain
-children and adults over 50y
risk factor:
-chronic disades: hypettnesion, DM, renla, liver
-smoker
-aslchol and drugs
-elderly person
-young children
sign of lower airways infe
Cough
2. Dyspnoea
3. Tachypnoea
4. Pleural pain
5. Auscultation finding
+ systemic signs of infection: fever, leukocytosis (>10x109/L or >15% non-segmented leukocytes), shiver, chills, arthralgia,
fatigue, weakness)”
pneumonia acc to location
superficial/alveolar/lobar
-internal surface of alveol
-hele lower lung
-exsudate
interstitial:
-within lung intestitim
-act of alveolar macrophages, change inalveolar pneumo 2, small exsudate
extent of penumonia
1.localized(lobualr/folcal)
- bronchopneumoina
- can fuse–>lobar
-mer lower lungs
- diffuse(lobar)
- minst 1 lobe
-complete lung=alar
-lobar ppneumonia
epidemoological pneumoniaatypical bacteria
mycoplasma oneumonia
chlamidya pneumonia
legionella
hemophilus influenza
- CAP-community aquired–>bacterial and viral
-bacterial–>s.pneumonia(50%) and non s.pneumonnoa - HCAP–>HAP–>VAP
complication of pneumonia
Pleural effusion
* Fibrinous-purulent pleuritis
* Pyothorax – arises secondarily, from infected plural effusion
* Empyema
Bacteraemia
* Pulmonary fibrosis
* Pulmonary abscess
4th place of cause of deathin worl
COPD
-smoking. air plluy
pneumococcal pneumonia
most common community squired
not so high mortality now
vacinaiton is possibøe
Typicla pneumonia
-features on inflamatorry disease w fever, dypnoe, productive humogj couh
-cracklind-foca shadowing in lung
atypical pneumonai
-fulminant=severe and sudden
- in INTERSTITIUM
-atypical pahtogens, viruss or non infectio etiology
-^temp but not fever, dry irritative cogh, unsepcific/mininmal ascultaiton
-shadowing in lung
-NO alverolar effusuin
-
CAUSED BY MYCOPLASMA, CHLAMYDIA OR VIRUSES
EX:
Farmers lung: intesitnal oneumonai, type of hypersens pneumonitis
COVID 19:
PNeumocystis pneumonia:
bronchopneumonia/lobar oneumonia
what
way
etiology
mciro
-acyte localised superficial pneumonia
aka focal superficial
-terminal airwyas–>lung parenchyme
-secondary process
-bacteria: staphylo and strepto=pyogenic
mciro:
inhomogenous apperance
-small foci of inflaa–disperse->
-lung parenchyme is edeamtous
-weihgt is increased
-abscess->focal destruction - bc of puruelnt ocolliquaiton
lobar(croupons)pneumonia
-ALWAYS diffuse
-acute diffuse superfical /alveolar pneumonia
-streptococcus pneumonia
-all parts of infla in same stage
loabr pneumonia stages
1.inflammaotry edema-1 day
-alverolar edema w congestion of capp and vv
-^volune of fluid, but low infilatrate
2. red hepatization-2-3 day
-more neutro
3. grey hepatixaiton: 4-6 day(yellow hepatizaiton
-decreased neutro
-fibrin
-croupons
4. resolution 7day-3weeks
- macrophages–>eat
-Lymph vv –>coughing
-non speciifc grnaulaiton
-carnificaiton and superficial lung fibrosis
morphology of lobar pneumonia+ complicaiton
solidized klung tissue
lung tissue like liver
grey hepatization
complications
acute:
-pulmaonry hupestension–>pressure overload and RHF
-acute resp insfuficecny
-sepsis and shock
chronic:
-lung fibrosis
-pleuritis–>healing–>ahesions
intestitial pneumonia
-what
etiologt
within inetrstiitum-soft itusse within alveolar walls
etio
-infections: vial and atypical pathogens
-non inf:
Sars/corona
COVID-19 = term used for the viral infection caused by coronavirus SARS-CoV-2, that can progress to severe acute
respiratory syndrome (SARS) with pneumonia and acute respiratory distress syndrome (ARDS)
stages
1.acute/initial: plaque of unspecific changes=DAD
-pneumo 1 and 2 changes
-exsuadte–>alveoli
-low nr of cell elemnts
-acc of inflammaotry cells
- see protein in exsudate forming on alveoli surface=pseudomembrane
- HYALINE membrna eformaiton - prilif stagge
-âlveolar machropahes
-hyperplasia of pneumo 2
-firbotizaiton
complciaiton of covid 19
Pneumonia (75%)
o ARDS (15%)
o Acute liver injury (19%)
o Cardiac injury (7-17%)
o Coagulopathy/thromboembolic complications (10-25%)
o Acute renal injury (9%)
o Acute cerebrovascular disease (3%)
o Shock (6%)
+ organising oneumonia, PIMS-pediatris infla multiorgan syndorme