Pathology of lung Flashcards
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
pneumonia influenza
lung endemaotus, weight is decreased
-may be hemorrgic and inhomogenous apperance
interstitium
-change in pneumo, maciro, fluid exsudate
increase pneumo 2
infectiosu interstial pneumonia
cmv pneumonia
rsv pneumo
pneumocystis pneumonia
one of most complicaiotn of pneumonia
lung fibrosos
alveolar fibrosis
-superficial alveolar exsuadative process->exsuadative fibrin
- pseudoalveoli
-anlergemnt of thickness of alveolar capp membran->diffusing problema–>
-hypoxia and vaaoconstriction–>PULMO HYPERTENSION
-
typical comlication of lung fibrosis
secodnary pneumopathic lung parenchyme infleucning right heart function–>chronic pulmonary hear(cor pulmonale)
interstital fibrossi
-within interalveolar walls
-sueprfical alveoalr fibrosis
idiopathic interstitial oneumoan ex
hamman rich syndrome:
liebow and carrington
hamman rich syndorme
rapid and progressive developming lung fibrosis
-honeycomb
-parenchyme firbotized, dialed air psaces w mucin w chnaged consistenyc
IS NOT CHRONIC ABSTRCUTION PULMO DISEASE
Diffuse parenchymal lung disease (DPLD)
idiopathic
-infective and post ifnective, inhaled substances:pneumoconioses and extrisinc allergic elveolitis, non inhaled,
chronic brochitis deinfintion and epidemiology
persistent productive cough with expectortion
-thre monts for 2-3 years
epidemiologt
-middle aged men
-development of COPD or cor pulmonale
-emphysema
etiology of chornic brocnitig
-oevr secretion of mucos
-smoking
- impary ciliary movemnt
2.inhibit funciton of alveolar macrophages - leads to hypertrophy and hyperplasia of mucus secreting galnds
- sti vagus and causes bronchoconstriciton
- atmopshric poluciton
6-occupation - infeciton
morpholgt and symtons if chronic broncitits
morpholgy
-brocnhial wall thickened
-hyepremic
-edematus
symtpoms
-perisitent cough
-recurrent resp inf
-dyspnoe
-blue blaters: cyanosis and edema
-RHF-cor pulonale
-enlarged heart w promiennt vv
reid index
ratio of thickness of submucosal mucus secreting gland and thickness bt epi and cartilaeg
basiclaly:Mucosal glands and bronchial wall
bronchiolotis
-infla affecting small airway
-older
chronic restictive pulmo disease
-reduced expansion of lung parenchyma w decreased totoal lung capacity
general symotoms: dyspnea, non prod coughm cyaosis, pulmo hypertension, cor pulmonae chromnio
tyøes pf chronci restrictive pulmo disaes
- restrciton due to chest wall disorder, pleura or neuromusclualr apparatus
-no primarly lung disease
- kuphoscoliosis, poliomyelitis, obesity, pleural disease - restriction due to interstitial and infiltrative disease
- ILD-interstitial lung ideaae
Sacoidosis
-noncaetoing epitheloid cell granulomas+ no necrosis
-later-hyalonized fibrous tissue
gian cells:a steroid bodies+schaumanns bodies
-LN and lungs
COPD
chrinic, aprtia or complete obst.
CHRONIC BRONCHITIS
EMPHYSEMA
BRONCHIAL ASTHMA
BRONCHIECTASIS
bronchiectasos
what and where
-abnoormal and irreversible dialtion of bronchi and brochioles(GREATER THAN 2MM)
-cant clear out mucus–>bacteria
- persiient cough +expectorian of foul smelling,purulent sputum
emphysema
what and etiopathogenesis
-abnormal permamntnet enlargmedn of airpsaces distal to terminal broncioles+destruction of their wallWITHOUT fibroris
-ACINUS part
etio:
- elastin syn and degradation
-cigarette smoking or herediatry a1-antitrypsin
TERMINAL BRONCIOLES-ACINUS PART
^DEGRADATION OF ELASTIN (SMAOKIN)–>CENTRILOBULAR EMPHYSEMA
A1-ANTITRYPSIN DEFICIENCY->PARAACINAR /PARALOBULAR EPHYSEMA
symtoms of emphysema
- dyspnoe
- distress
- barrel shaped
- cough appaer late after dyspnoe
- pink puffers
6.weight loss - RHF and HYPERCAPENIC RESP FAILURE
- small heart with hyperinflated lings
lung atelactasi
incomplete expansion/collapse of air filled alveoli
etiology
1.compressive
-from iytside
-lower lobessss
-samller so lesser pressure needed
- obstructive or absorptive
- contraction
-localized fibrosis
pulmonary edema
acc of transudate in alveolar spaces
Increased permeability of alveolar-capilary membrane
* Increase hydrostatic pressure
* Decreased oncotic pressure
* Blockage of lymphatic drainage
most common cause of sec pulmoanry edema
True: in left HF→venous congestion →congestion in capillariesfluid moves into the interstitium of the lungs
cause of primary pulmonary edema
ulmonary hypertension:* primary/idiopathic and secondary (more common)
Primary pulmonary edema is caused directly by damage to the lung tissue or pulmonary capillaries, like in acute respiratory distress syndrome (ARDS).
Secondary pulmonary edema results from other conditions that indirectly cause fluid accumulation in the lungs, most commonly left-sided heart failure (cardiogenic pulmonary edema).
pulmonary thormoembolsim
-most ftala
-veins in leg or varicose veins
consequence
- suden death: massice pulmo embolsim, MI-dyspnoe and shock
-acute cor pulmonale: enlarg and failure of RV
-Pulmo infarction
-pulmo hemorrahe
-resolutuiom
-Åulmo hypertension, chornic cor pulmonale, arterioscelosis
People with successive pulmonary embolism run the risk of developing
Pulmonary hypertension occurs when there are multiple (Successive) small thromboemboli undergoing organisation rather than resolution
pulmoanry hypertension
systolic BP in pulmo arterial circualiton above 30mmhg
divided into primiary/idiopathic and secondary
idopathic/primary pulmo hypertension:
cause
-young fenales or children
causes
-neurohumoral vasocontricotr mechnism->CHRONI VASCOCONSTRICITON
-collagen disease
-familial
secondayr pulmo hypertnsion
-over 50
etiopa
- passive pulmonary hypertension: mitral stenosis, chornic LV failure
-Hyperkinetic/reactive : patent ductus arteriosus, atrial or ventricualr septal defect
-vasoocclusic
- Diffuse, pneumoniaFalse: Diffuse pneumonias are evenly divided between noninfectious (cryptogenic organizing pneumonia) and infectious (CMV, respiratory viruses, Pneumocystis pneumonia [PCP]). - UpToDate
- Generally speaking, fibrotization of the alveolar spaces, lead to pulmonary hypertension, in this case it would be considered a secondary “Pneumopathic” hypertension - UpToDate and Compendium
- Alveolitis and Hamman richFalse: Hamman-Rich disease ← Cryptogenic fibrotizing alveolitis.
- Diffuse bilateral fibrosis of lungs with multiple small cysts giving a honeycomb appearance, the pleura is thickened and adhesive in places with intervening nodularity.
- Generally speaking, fibrotization of the alveolar spaces, lead to pulmonary hypertension, in this case it would be considered a secondary “Pneumopathic” hypertension - UpToDate and Compendium
didduse alveolar hemorrhage ynsdorme
-Triad:a nemia, hemoptysis, diffuse pulmo infiltartes
ANTIBODY AGAIN COLLAGEN IV-BASEMEMNT MEMRBANE OF GLOMERULI AND ALVELOLI(LGGGGGGGGG
being tumors of tree
-pri
-sec
systemic
Primary
-being:bronchus or in alveolar pulm. parenchyma
-Maligannt: central/hillar part of bronchu +lungs
-
secondary
- MTS from other
systemic:
bronchogenic
hilus=centraø part of lung
pulmary parenchyme
distal parts moslty
cmmon tumor of lungs
Carcinoma
rare
neuroepi/neurendocrine origin carcinoid (NEN)
epithelial(papilloma adn adenoma
mesenchymal-CHONDORMA
-HAMAROMA
-lymphoid tumor=BALT
bening epi tumors
papillom and adneoma
most cmmon being mesenchymal tumor of tree
chondroma
most common benign tumor of lung
hamartorma1
catgroeis of cqarcinoma
1.epidermoid(SCC
2.adenocarcinoma
3.large +small cell
NSCLC
SCC, adeno + large cell
SCLC
Small cell ca
NEN/NET
carcinoid +atypical carcinoid
hilar/bronchogenid
small cell + SCC
PERIPHERY
ANDEONM + LARGE CELL
Bronchogeniq SCC
Grade 1: keratinized
G 2: non keratinized
keratin perals
form basal cells
smoking
causes large lesion of tumor mass in lung
adenocaricnoma
-from pneumo 2
-genetical alteration of EGFR
- precurso: pre or non invasive lesions, minmallt inavse adenocarcinoma
True: Adenocarcinomas are the most common type of lung cancer, accounting for approximately 40% of cases
True: EGFR (More common) and ALK are the most common markers shown in adenocarcinomas of the lungs.
n fact, adenocarcinoma is the most common type of lung cancer in never-smokers, accounting for approximately 50-70% of cases, while in smokers, it is still the most common type but to a lesser degree
hardly detactable bc located in periphery
Inasive adenocacinoma grades
1: lepidiv and papillary
2: acinary +micropapillary
3. solid, mucin
small cell lung ca
smokin
oat tumor
Is associated with ectopic hormone production
Tumor mass in central lung and mediastinum
Undifferentiated neuroendocrine
they are assocaited with a very poor prognosis.
small blue cell
True: SCLC is usually located centrally in the major airways, frequently also involving the mediastinal lymph nodes, but it may occur peripherally in the lungs in about 5% of cases. Metastatic spread, most frequently to the liver, bone, brain, ipsilateral and contralateral lung, and adrenal glands, is commonly present at the time of presentation. Malignant pleural and pericardial effusions are also common
large cell ca
-variable postion: peripherla or central part
-smoking
-uncommni
Large cell neuroendocrine carcinoma represents a high-grade malignant tumor
neuroendocrine neiplasia
low grade: carcinoid, atypicla carcinoid of lungs
high gradE: neuroendocine carcinoma->Small cell CA->Small cell NeCa+large cell NeCa
grading of neurendocrine neoplasms
accoridng to mitoctyc act index, prolif KI-67 indec and necrosis
-g1: carcinoid
g2 atypical carcinoid
-g3: NE carcinoma
Grading: gastroenteropancreatic NENs \ lung NEN
-G1: NET, G1/carcinoid
-G2: NET, G2/atypical
-G3: NE ca, small or large cell
protein positivit of genes
- EGFR, ALK, ROS 1
2.PD/PD-L1 - chemo
mesothelioma
mesothelial cells
-lung surface
-very bad
