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Respiratory - Diseases (*Chronic Respiratory Diseases obstructive vs.…

- - - - P/C
        
        ARDS presents with bilateral pulmonary adema and hypoxemia
        
        usually is secondary to a traumatic event (RTA = road traffic accident) where there is pulmonary contusion or injury to the alveoli to start the inflammation process
      - Cardiogenic vs Non-cardiogenic ARDS
  - - - PE ABGs
        
        PE occludes blood flow to certain areas of the lungs
        
        V/Q mismatch and hypoxia
        
        central resp centre tries to compensate by hyperventilating to get more Oxygen
        
        this makes things worse, there is still V/Q mismatch so all the hyperventilating does in increase unloading of CO2
        --> hypocapnea
        
        respiratory alkylosis
        
        note that renal compensation with bicarb loss doesn't happen until 48 hours
        
        Clinical Cases
        
        Clinical Case
        
        Notes:
        
        note that
        
        Clinical Case
        
        PE = Pulmonary Embolism
        
        Clinical Case
        
        Notes:
        
        in PE there is primarily hypoxemia due to the V/Q (vent./flow) mismatch
        
        you then get dyspnea and SOB to try and increase the blood-arterial O2
        --> CO2 mostly travels (~70%) as HCO3- bicarbonate so in PE and hyperventilation it is cleared quicker at the alveoli
        --> hyperventilation causes hypocapnea
        
        hypocapnea means lower CO2 at the tissues --> pH rises
        
        note that in acute PE you see the opposite as chronic COPD
        
        acute PE has hypoxia, but secondary hyperventilation and hypocapnea
        
        chronic COPD has hypoxia, but is caused by emphysema and hypoventilation
        --> hypercapnea = respiratory acidosis with a lowered acidic pH
        --> since this is chronic you get renal compensation
        
        Saddle PE of the pulmonary Arteries
        
        cause of sudden death
        
        large thrmoboembolism lodges in the bifurcation of the pulmonary arteries
        
        Dual Blood supply to the Lungs - Protection in PE
        
        both pulmonary arteries and bronchialy arteries are dual blood supply tot he lungs
        
        infarction can be prevented by dual blood supply for procimal occlusion PEs
        
        more distal PEs can cause infarction and are not protected against
        
        Management of PE
        
        D-dimers first to rule it out = nonspecific
        --> D-dimers are breakdown product from fibrin clots
        
        CTPA = gold standard for Dx
        --> CTPA contraindicated for CKDs, radiolabel allergy
        --> can't hande the infusion of the contrast die
        
        CKD patients = V/Q scans
        --> V/Q mismatch Dx for PE
        --> other diseases can have defect in both alveoli V, which then casues lower flow = Q
        --> this gives a matched, but lower V/Q and is negative for PE
        
        *V/Q Sans
        
        CTPA contraindicated for CKDs, radiolabel allergy
        --> can't hande the infusion of the contrast die
        
        V/Q mismatch Dx for PE
        --> other diseases can have defect in both alveoli V, which then casues lower flow = Q
        --> this gives a matched, but lower V/Q and is negative for PE
        
        *FES = fat embolism Syndrome (PE from femur fracture)
        
        usually a RTA
        --> femur or pelvic fracture releases fat emboli into the circulation
        
        fat emboli of smaller sizes can get through the heart and into systemic circulation
        --> affect microvessels everywhere
        - FES triad:
        --> PE from larger fat emboli
        --> petechiae rash on skin (smallfat emboli in microvessels)
        --> confusion/TIA symptoms = smallfat emboli in microvessels of brain
  - - - Clinical Cases
        
        Clinical Case
        
        Notes:
        
        note that
        
        Clinical Case
  - - - Exudative pleural Effusion
        
        high protein/LDH in pleura
        
        from inflammation, vascular permeability allowing WBCs, etc. into the pleura
        --> exudate = EVIL
        
        pleural / serum protein ratio > 0.5
        
        pleural / serum LDH ratio > 0.6
        (LDH > 2/3 normal)
- - - - "PAH = poor PA system at the END of microphone, need a BOSE SENT IN"
        
        PAH / PA system = Pulmonary Arteries in PAH
        
        End of microphone = Endothelin receptors cause of PAH
        --> endothelin goes against NO cGMP and PGI2 prostacyclin cAMP
        
        BOSE SENT IN = Bosentan for PAH
        --> Bosentan = endothelin receptor antagonist
      - Pathophys of primary PAH
        
        endothelin receptors initiate growth of endothelium and vasoconstriction also
        --> main target therapy of bosentral
        
        note that endothelin goes against the actions of NO cGMP path and PGI2 = prostacyclin cAMP pathways that cause vasodilation
        
        BMPR gene mutation for PAH
  - - - TB = Tuberculosis case 1
        
        Notes:
        -
        
        Case example:
      - TB = Tuberculosis case 2
        
        shows how mycobacterium tuberculosis infect macrophages
        
        macrophages need to signal to cytotoxic CD8 cells by IL-12
        
        CD8 t cells then send them IFN - gamma in return for apoptosis
        
        Notes:
        -- recall the TH cells differentiate into either
        
        TH2 --> IL 4/5 for b cells and antibodies
        
        TH1 --> IL 12 and IFN - gamma killing macrophages and infected cells
        --> these TH cells (TH1) are themselves activated by infected macrophages
        
        Case example:
    - - SARCOIDOSIS
        
        S = Skin problems = erythemia nodosum
        --> rashes on front of lower legs
        
        A = ACE increase and African Americans
        --> from granulomas / macrophages in the liver
        --> Sarcoid is fairly rare diseaase overall, but 15 times more likely in African Americans
        
        R = respiratory granulomas + restrictive lung disease
        
        C = high CALCemia / high CD4+/CD8 ratio
        
        O = occular lesions
        
        I = Immune mediated type 4
        
        D = diabetes inspidus
        
        O = osteopathy
        
        S = Schaumann bodies (in the Langhans giant cells)
        --> Shawman Shuaman!!
        --> calcium and protein inclusions inside of Langhans giant cells as part of a granuloma
        
        I = interstital lung disease
        
        S = Seven nerve palsy = CN7 bells palsy
        --> (same as LYME disease FACE)
        
        Clinical Cases
        
        Clinical Case
        
        Notes:
        
        note that
        
        Clinical Case
        
        Sarcoidosis
        
        Notes:
        
        note that any presentation with dyspnea that has imaging showing pulmonary infiltrates and hilar adenopathy
        --> need to think of Sarcoidosis
        
        Case example:
        
        Sarcoidosis granuloma
        
        have Shaumann inclusions int he granulomas
        --> calcium deposits
        --> due to the hyperCALCEMIA seen in sarcoidosis
  - - - Clinical Case
      - Notes:
        
        note that
  - - - *Cystic Fibrosis
        
        Notes:
        
        note that in CF in both the lungs / GI and the sweat ducts it is the combination of CL- and Na+ collecting that the water follows them and creates the thick mucus in the GI/lungs or the high NaCL in the sweat
        
        Na+ always trying to get into the cell
        
        Cl- going out in the lungs and reabsorbed back in the sweat
        
        in the lungs the lack of salt in the mucus makes the water flow into the cells
        
        thick dry mucus in the lungs
        
        Cystic Fibrosis - Nasal Saline test
        
        nasal transepithelial potential difference test,
        
        recall that the CFTR normally inhibits the ENaC channel to stop Na coming into the cell
        
        in CF this inhibition is gone
        --> higher ENaC activity and increase Na absorption into the cell
        
        when saline put into the nasal mucosa
        --> Na gets absorbed, but the Cl- ions do not
        --> high voltage difference, cells more positive than the Cl- rich saline
        
        Clinical Cases
        
        Cystic Fibrosis example
        
        Notes:
        
        note that the CFTR works differently with the ENaC for Cl- depending on the tissue
        
        in the sweat glands both the CFTR and ENaC work together to try and reabsorb the salt from the sweat and back into the epithelial tissue
        --> reason why CFTR- people will have a positive sweat test = high NaCl in their sweat
        
        in the respiratory system the CFTR and ENaC work in opposite directions and the CFTR inhibits the ENaC
        --> Na+ is mainly what the water follows
        --> thus less electrolytes in the lung fluid
        --> thicker mucus
        
        Cystic Fibrosis example 2
        
        Notes:
        
        note that the CFTR mutation in cystic fibrosis causes the misfolding of this Cl- channel
        
        it is then brought within the cell to proteosomes to be degraded
        
        Clinical Case
        
        Clinical Case
        
        Notes:
        
        note that
      - *Karategner Syndrome
        --> imparied dynesin holding microtubules in cilia
        --> classic triad of : dextrocardia / situs inversus, recurrent RTIs/sinusitis, bronchiectasis
        
        Clinical Cases
        
        Clinical Case
        
        Notes:
        
        note that
        
        Clinical Case
  - - - Fine particle Clearance by Macrophages
        
        pneumoconiosis comes from inhalation of fine particles
        
        these get past the mucociliary escalaotr
        
        it is up to macrophages to clear fine particles and get rid of them
        --> macrophages getting activated by the fine particles is also what causes the activation of fibroblasts and interstitial lung disease that follows
      - Notes:
        
        Go to the CLUB at the terminal end of the night
        --> CLub cells in the terminal bronchioles
        --> terminal bronchioles is also start of the serous fluid and last ciliated columnar
      - *Silicosis Pneumoconiosis
        
        silicon ingested constantly by macrophages in the alveoli trying to clear out the toxin
        
        silicon builds up in macrophages and makes them useless
        
        more prone to infections like TB
        
        Silicosis = "SHELLicosis CALCIFICATION"
        
        silicosis "egg shell calcification" = calcficiation of the rim of the hilar lymph nodes
      - *Asbestosis Pneumoconiosis
        
        Asbestosis is Magnesium collections in the parenchyma and pleura
        
        ferruginous bodies collect and cause inflammation --> fibrosis
        --> think of asbestosis = magnesium (like Fe iron)
        --> Fe ferruginous bodies
        
        Asbestosis can lead to malignancy / thickenning of the pleura
        --> Mesothelioma
        
        *Mesothelioma
        
        see oncology - lung CA notes
        
        CA of the lung pleura
        
        caused exclusively by asbestos exposure
        
        positive labs for cytokeratin and calretinin
        
        "asbestos is in the middle = MESO of work CYTES (nobody Kares...) and CALL centres"
        
        mesothelioma from asbestos
        
        work CYTES = cytokeratin
        
        CALL centres = calretinin
        
        Clinical Cases
        
        Clinical Case
        
        Notes:
        
        note that
        
        Clinical Case
- - - - OHS = Obesity Hypoxemia Syndrome
- - - - Clinical Case
        
        Notes:
        
        note that
        
        Clinical Case
    - - less common Abscess causes = single bacterial cause/ atypical pneumonia or bacteremia
        
        atypical pneumonias , NOT strep pneumo
        --> staph A, pseudomonas, EEKs
        
        Main cause of Abscesses = aspiration / Polymicrobial / broad spec Clindamycin treatment
        
        ALMOST all lung abscesses are caused by polymicrobial anarobes and aerobes
        --> need wide coverage macrolides = clidamycin
        
        Lung Abscesses are CLEAR in DA middle = Clindamycin
        
        special case of lung abscesses are Klebsiella can cause them