Please enable JavaScript.
Coggle requires JavaScript to display documents.
Respiratory - Diseases (*Chronic Respiratory Diseases
obstructive vs.…
Respiratory - Diseases
-
*Chronic Respiratory Diseases
- obstructive vs. restrictive (on PFTs)
- others
*PFTs
- obstructive vs. restrictive
-
*PAH = Pulmonary Arterial HTN
- can be primary or secondary
- primary PAH is from genetic mutation of BMPR gene
--> endothelin receptor increases endothelial constriction and promotes growth of the pulmonary arteries
- Tx = bosentan = endothelin receptor antagonist
--> "BOTH SENTIN for PAH"
--> stops endoethial growth
"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 and Sarcoidosis
TB = Tuberculosis
-
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
-
-
-
-
*Sarcoidosis
- similar to TB
- NON-caseating granulomas
- can be systemic in the body
- Tx = wait and watch if no symptoms
--> symptoms + sarcoidosis = oral steroids (prednisone)
![dropped image link](https://production.coggleuserlinks.com/https%3A%2F%2Fi.paste.pics%2F674eb96ca7f195eccf93ecd2e86f81f7.png)
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
-
Sarcoidosis
-
-
-
Notes:
- note that any presentation with dyspnea that has imaging showing pulmonary infiltrates and hilar adenopathy
--> need to think of Sarcoidosis
-
Sarcoidosis granuloma
- have Shaumann inclusions int he granulomas
--> calcium deposits
--> due to the hyperCALCEMIA seen in sarcoidosis
-
*Pulmonary Hypertension HTN
- diagnosed through pulmonary artery cathederization
- measure all parts of right side of heart and left atrium by PCWP
- PCWP = pulmonary capillary wedge pressure
-
*Genetic Respiratory Diseases
- autosomal recessive respiratory diseases
- ezyme deficient diseases
*Respiratory genetic Autosomal recessive disorders
- cystic fibrosis
- Karategner Syndrome
--> imparied dynesin holding microtubules in cilia
--> classic triad of : dextrocardia / situs inversus, recurrent RTIs/sinusitis, bronchiectasis
*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
-
-
-
-
-
*Karategner Syndrome
--> imparied dynesin holding microtubules in cilia
--> classic triad of : dextrocardia / situs inversus, recurrent RTIs/sinusitis, bronchiectasis
-
*GCD = Chronic Granulomatous Disease
- deficient in NADPH oxidase complex
--> can't metabolize NADPH into oxides from the HMP shunt pathway
- constant infections from catalase positive organisms mix of bacteria fungi
-
*Pneumoconiosis
- coal mining, silicon, asbestos
- "Smoke rises in COPD, but in Pneumoconiosis --> asbestos from the roof is at the base and minerals = coal from the ground in the roof of lung"
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
-
-
-
Respiratory Diseases, Location and Anatomy
-
*Hypoxemia
- causes depend on the Alveolar-arteriole gradient = A-a gradient
*Normal A-a gradient Hypoxemia
- 2 causes
--> when there simple is less O2 available or able to get to the alveoli
- OHS = Obesity Hypoxemia syndrome
- high altitude
-
*Lower A-a gradient Hypoxemia
- right to left shunts = blood doesn't reach lungs enough to be oxygenated
--> ASD and VSD
- V/Q mismatch = PE
- impaired diffusion at alveoli = IPF
--> IPF fibrosis stops the exchange
-
Lung *Abscess
- air filled cavity in lung parenchyma
- caused by neutrophils trying to fight bacteria with their released granules
- usually from aspiration and bacteria in the lungs
- neutrophils releae myeloperoxidase
--> kills bacteria
--> but also causes damage to lung parenchyma and causes air to collect
- ALMOST all lung abscesses are caused by polymicrobial anarobes and aerobes
--> need wide coverage macrolides = clidamycin
- key = "foul smelling breath" in infected lungs
--> polymicrobial growth in lung abscess
-
-
Causes of Lung Abscesses
- most common = aspiration / polymicrobial
--> anaerobic gram - mouth flora and gram +
--> requires Clindamycin broad spectrum
--> caused by aspiration
--> people most risk for aspiration = alcoholics, elderly, epileptics (siezures)
- less common = single bacterial cause/ atypical pneumonia or bacteremia
--> atypical pneumonias , NOT strep pneumo
--> staph A, pseudomonas, EEKs
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
-
Common *RTIs in Children
- MOST RTIs are VIRAL caused
- 15 /30 rule for bacterial RTIs in children and adults
--> ONLY 5-15% of adult RTI pharyngitis are bacteria
--> ONLY 15-30% of child RTI pharyngitis are bacteria
- common cold = Rhyno RIC - rolled
--> no bacteria
- croup / stridor PARA = after initial common cold
--> PARAviruses
- Diptheria = tonsils DIP into the throat
--> pseudomembrane closure + lymphadenopathy
- Drooling and dysphagia = Esophagitis
- HIB - throat / ears / brain
croup / stridor PARA = after initial common cold
-
Diptheria / pseudomembrane closure + lymphadenopathy
- Diptheria - tonsils DIP into the throat
-
*Pulmonary Edema = Lung Consolidation
- can be caused by many different underlying issues
- pneumonia
left sided heart failure and volume overload
-