Respiratory Pathology

*NON-immune mediated asthma(Have normal serum igE)=INTRINSIC Asthma, which can also be caused by stuff like cigarette smoke,emotional extremes....Mechanism for Aspirin induced asthma is increased production of leukotrienes(By 5-lipooxygenase pathway) because arachidonic acid can't be metabolized to prostaglandins due to COX inhibition, so more of those metabolites are directed towards lipooxygenase pathway...They also really want you to know that Aspirin induced asthma is associated with NASAL POLYPS...

*Wheezing and Pulsus paradoxus along with Charcot-layden crystals on the image are Strongly suggestive of Asthma...*Charcot-layden crystals are result of Eosinophil breakdown in the sputum(note Double-pointed, eosinophilic crystal) don't confuse this with Curschmann spiral(Desquamated epithelium forming Mucus plugs in patients with asthma)...*Mass and Number of smooth muscle cells will be increased in the airways because SMC undergo HyperTROPHY and HyperPLASIA due to HYPERRESPONSIVENESS of Bronchi leading to episodes of REVERSIBLEBronchoconstriction(Needs SMC),Methacholine challenge is sensitive test used to rule OUT asthma and conceptually what we do there is we give DIRECT acting cholinomimetic to induce bronchoconstriction(Bronchoconstriction in asthmatic will be more significant than in normal patient)Just like with all other Obstructive diseases FEV1(How much air you blow out in 1st second) is decreased in asthmatics and FEV1 decreases MORE than FVC(Max air you can blow out after max inspiration),thus FEV1/FVC ratio goes DOWN....<SUPER HYjust remember Obstructive=dOwn.

*PULMONARY HYPERTENSION>Right sided heart failure is common in scleroderma and it is due to increased deposition of collagen in the lungs, FIRST vessels affected are small arterioeles and capillaries... Note that this Fibrosis more commonly just leads to RESTRICTIVE Lung disease and when the fibrosis is severe enough it can lead to pulmonary hypertension and RVHF.*Main players in this fibrosis are Fibroblasts induced by TGF-B which is secreted by Monoclonal T helper cells(CD4+)

*EXTRINSIC(Allergic)asthma-Most common one...

*Decreased apoptosis of endothelial cells and smooth muscle cells in arterioles seems to play a role in Primary pulmonary hypertension(usually presents in middle-aged females with shortness of breath/exercise intolerance)..While Lung transplant is definitive treatment vasodilators like Bosentan have proved to be useful.(Bosentan is COMPETITIVE ENDOTHELIN receptor antagonist)

*Because individuals with that stature(Thin,tall) have more NEGATIVE intrapleural pressure in apical lung....remember primary pneumothorax is usually due to rupture of APICAL SUBpleural BLEBS...Note that it usually manifests as Sudden onset Chest pain, HYPERresonanse and absent breath sounds.....

*Smoking>CENTRIacinar emphysema that predominantly involves UPPER lobes...vsAT1 deficiency>PANacinar emphysema usually involves LOWER lobes and anterior segments of the lung...just remember Centriacinar-Cmoking-UPper lobe relationship by CUP...

*Compensatory hyperinflation of lung parenchyma usually happens to "compensate" for Surgically removed/Collapsed lung segments/lobes...vs*Obstructive hyperinflation of segment happens in response to SUBTOTAL(Ball-Valve Obstruction) of the Bronchiole/Bronchus supplying that region, examples can include BRONCHOGENIC carcinoma/Mucus plug....Ball-valve obstruction basically means partial endobronchial obstruction which allows facile entry but not egress of air, resulting in a build-up of pressure in the terminal airways and potential rupture of alveoli,this type of obstruction can complicate with interstitial emphysema and even with TENSION Pneumothorax...

*Increase in Pulmonary capillary permeability is one of the mechanism by which ARDS causes EXUDATION of fluid into the alveoli...*PCWP however is usually NORMAL(abnormal PCWP should make you think of cardiogenic cause of pulmonary edema, because PCWP is reflects Pulmonary venous/LEFT ATRIAL pressure)...*Exudated fluid will also Increase V/Q mismatch,Work of breathing and will decrease the compliance...basically pathophysiology of ARDS is based on DIFFUSE ALVEOLAR damage

*Major Basic protein has been associated with bronchial damage in patients with Atopic (EXtrinsic Allergic)asthma...

*SRS-A=slow-reacting substance of anaphylaxis is basically mixture of Leukotrienes(LTD4,LTC4,LTE4) is contained within granules of Mast cells and Basophils..

*Occlusion of Pulmonary microvessels by FAT globules....He likely developed FAT emboli as fracture dislodged the fat globules from the marrow and allowed it to travel to the pulmonary vessels....
petechiae is likely due to thrombocytopenia because platelets bind to the coatings of those fat globules and thus less platelets are left in circulation...This patient could also develop ARDS because fatty acids released from fat globules could lead to toxic damage to endothelium in the lung>Potential for ARDS....Note that ARDS usually presents as acute onset RESTRICTIVE lung disease...

*Likely due to a lack of Vitamin A(Can happen in Cystic fibrosis due to fat/Fat soluble malabsorption due to atrophy of exocrine pancreas as a result of obstruction of the lumen and increased backflow pressure compromising the blood supply to that region)..Remember Vitamin A is needed to maintain specalized epithelia like Low columnar mucus secreting epithelia of CONJUCTIVA,urinary and RESPIRATORY tracts and note that this epithelium is also present in ducts of Exocrine pancreas and other Exocrine glands, so it makes sense that vitamin A deficiency(Like in patient with CF) could result in squamous metaplasia of specilized epithelium(in our case when Columnar epithelium is replaced by keratinizing squamous epithelia)...

*Walled of Foci usually in mid to lower lobes of the lung is known as Ghon Foci this combined with Adjacent lymph node involvement=Ghon complex and Ghon foci/Complex contian walled-off Dormant bacteria which can result in REACTIVATION of TB(usually reactivation involves APEX of the lung)vsRanke complex is when bacteria are completely cleared and scar is formed, this complex doesn't carry risk of reactivation(Histology would show Multinucleated giant cells/epitheloid cells around CENTRAL area of NECROSIS and CALCIFICATION)...

*Well maxillary sinus is most commonly affected because it is lowest of the sinuses and more importantly the draining site for it known as MIDDLE meatus is superior to it so it's harder to drain fluid out of this sinus and thus there is higher chance that it get stuck in the sinus eventually leading to inflammation and the pain over that area..They REALLY REALLY want you to know that maxillary sinuses drain into MIDDLE meatus...