pulmonary medications

-NO: usually encourages guyanyl cyclase to convert GTP to cGMP... RIOCIGUAT (XLAbEL) that stabilizes this binding and encourages more NO to be used to promote for cGMP which blocks IP3 and reduced calcium release 

also phosphodiesterases involved with that above process: B label 

prostacyclins that bing to IP receptors that allow for more camp pka dilation 

endothelin inhibitors-- inhibit receptors ETa and b--this usually causes IP3 CA2+ release

• beclomethasone 
• fluticasone 
• budesonide 

oral: prednisone in severe acute cases

it blocks phosphodiesterase 3 and 4....3 is in the bronchus and 4 is the mast cells 

so in bronchus allows accumulation for cAMP which allows for bronchodilation

theophylline: narrow index-- so has to be given with access to constant and frequent BP checks bc can cause reduced blood pressure

rolumilast: not used for asthma, used in COPD

caffeine: in children

they are usually used in early stages of disease:

• -zileuton: inhibits the lipooxigenase inhibitor 
• -"lukasts" inhibit the LTD and E4. B PREGNANCY LABEL

inhaled corticosteroids are first line tx in persistent cases--they reduce the inflammation but they also prevent internalization of the beta receptors 

leukotriene inhibitors-- they usually cause for mucus hypersecretion, eosinophil migration, and bronchoconstriction 

methylxanthine--block the phosphodiesterase-- so that camp builds up.. and PKA is activated to allow for bronchodilation

indacaterol- lasts for longer than 24 hours

• ipratropium: antimuscarinic short acting 
• montelukast

• albuterol 
• salbutamol
• terbutaline 
• isoethanine

Ipratropium is the short acting and should be given in conjunction with short acting beta agonist 

Tiotropium is the long acting and should be given with other long acting beta agonists when steroids are not being given

there are short term and long term ones as well--they inhibit the muscarinic receptor M3 which causes decreased IP3 induced calcium release---vasoconstriction and mucus secretions are limited with these drugs

SABAS

selective ETA receptor antagonist which decreases endothelin activation

antagonists at both ETA and ETB receptors

ETA and ETB stimulate IP3 to produce Ca2+which causes vasoconstriction

is a selective IP receptor agonist.

**the ones that are synthetic copies of the prostacyclin have "prost" in their name 

**selexipag: looks similar and finds to and binds IP3 and stimulates camp production which allows PKA

phosphodiesterase inhibitor-- cGMP remains elevated-so it can activate PKA and continue to allow for vasodilation which decreases resistance and so blood pressure

has a B box label

• -Medication that stabilizes the interaction bw GC to facilitate the conversion of GTP to cGMP. 
• and can bind and directly stimulate this 

X box label for pregnant people

antifibrotic medication 

• intracellular inhibitor of receptor and non-receptor tyrosine kinases.

• Blocks intracellular signaling needed for proliferation, migration and transformation of fibroblasts

anti fibrotic medication acts by blocking TGF B

slow down the rate of fibrosis:

• Pirfenidone (Esbritet TM)
• • Anti-inflammatory: a TGF-beta synthesis inhibitor

• Nintedanib (Ofev TM)
• • intracellular inhibitor of receptor and non-receptor
• tyrosine kinases.
• • Blocks intracellular signaling needed for
• proliferation, migration and transformation of
• fibroblasts

primary cause of cancer related deaths in both males and females

mucin stain

• morphology
•  
• immunohistochemistry 

molecular testing--certain drugs target certain genetic mutations--next generation sequencing for adenocarcinoma does exist 

malignant mesothelioma

signature disease of asbestos exposure

tumor sitting on top of the lungs can compress the brachial plexus, the sympathetic trunk (horner syndrome)

secondary to cancer: compression causes limited return to the heart: collaterals form to increase blood flow back to the heart 

• T:tumor size 
• N: lymph node involvement 
• M: metastatic disease  

this score can be translated to clinical stage

this is the pattern for metastasis

cancer that came from somewhere else

large cell carcinoma--cancer that cannot be placed into any of the other groups

they cannot be categorized into either squamous cell nor glandular cell differentiation

seratonin release

carcinoid tumor

also derived from neuroendocrine cells

inside the lumen of larger bronchi 

really slow growing and so they do not metastasize that much, and you can remove it 

may produce serotonin 

small cell carcinoma

Small cell carcinoma

the pink stuff is necrosis-- the necrosis is very common in small cell carcinoma

because it grows so fast, by the time you diagnose it, it is too late to surgically do anything about it

derived from neuroendocrine cells-- it is very poorly differentiated, associated with rapid growth and mets, paraneoplastic syndrome, central location

when you see keratin pearls, you can say it is well differentiated SCC

SCC in the lung with central cavity formation probably because the tumor grew so large it cut off its own blood supply and became necrotic

there are squamous cells in the lung-- and are more likely to be centrally located-- and with keratin pearls on histology 

may produce PTH like substances

adenocarcinoma that has spread into interstitial tissue--  mucin stain can be used to identify.... although not all adenocarcinomas retain mucus producing ability

adenocarcinoma

adenocarcinoma

derived from gland cells and is often found on the periphery--

nonmet adenocarcinoma can be surgically removed

--adenocarcinoma is the largest lung cancer cause and nonsmokers get it too

in the other cancers, the nonsmoker category is very low 

small cell carcinoma IS NOT surgically resectable and are much more aggressive than the non-small cell carcinoma

even some non-small cell carcinoma  surgery is not possible if mets

• 
• after smoking cessation, your risk of developing cancer does reduce over the course of time--this reduction is not immediate it is over the course of several years and it won't ever go down all the way to 0

• is proportional to the amount of cigarette packs that you smoke 
•  
• cigarettes have a lot of chemicals and carcinogens: NNK, CO, and benzopyrine (found in car exhaust)

small cell lung cancer

5 year survival is dependent on lung cancer type and stage

localized cancer, no lymph node involvement--- 5 year survival rate is higher 56%

and if you have distant mets, your five year survival is 5%

overall, on average it is 20% 

because men started smoking earlier than females (smoking habits, social acceptance of women smoking came later)

as you age your chances of lung cancer increases....only 20% of the people survive five years after being diagnosed lung cancer

lung cancer is cancer that originates in the lung-- does not include mets to the lung 

carcinoma: epithelial lung tissue cancer

carcinoid

carcinoid

enophthalmos (posterior displacement of the eye)

ptosis (drooping) of the upper eyelid

miosis(constriction) of the pupil

anhidrosis (absence of sweating)

on the affected side.

SCC

they branch of at the mid axillary space to give the lateral cutaneous branch which then splits into the posterior and anterior

anterior is smaller and the anterior intercostal vein is a tributary to the internal mammary vein

External intercostal muscles: superior movement of the ribs: costal cartilage to the tubercle


internal intercostal muscles: sternum to the paravetebral line 

t1-t11...but there is subcostal nerve at T12

travels laterally to the vertebral bodies bilaterally and behind the pleura 

• Greater: T5-T9
• Lesser: T10-T11
• Least: T12

they function in the abdomen and pelvis though

• -the bronchial wall and the glands
• -visceral layer
• -lung parenchyma 
• -large vessel walls 

• the muscles and skin of the intercostal space 
• also the parietal pleura

T1-T4

sympathetic: T1-T6

parasympathetic: left vagus nerve sends branches that accumulate as the anterior vagal trunk and the right as the posterior

Starts at L1-L2 in the abdomen and enters via the aortic hiatus at t12 and then merges at the SVC 

hemizygous begins in the abdomen and enters the thorax cavity from the left crux of the diaphragm and merges with the azygous at T9.

accessory merges at T7-T8

• T8: caval: IVC
• T10: esophageal hiatus: esophagus and the vagus nerve 
• T12: aortic duct, descending aorta, and the azygous vein

• aorta: t5-t12
• esophagus: t5-t10

decreased ratio is indicative and then FEV1% is used to determine severity 

normal ratio does not ro disease and you have to get volume loops

VC-most reproducible

age sex and height

sandblasting, foundaries, mines 

TB reactivation is a risk 

asymptomatic condition where macrophages just ingest the coal and become black (anthracosis) --- but prolong exposure can lead to inflammation and fibrosis

aerospace association

asbestos

asbestos

white ivory plaques on the pleural border of the CT scan

plumbing, roofing, shipbuilding 

highly associated with cancer-- broncho cancers more likely than mesiolthiloma--but if there is a pleural effusion the latter is more likely

noncaseating granulomas and CD8/CD4 prominent response with increased ACE levels 

Schauman body seen in sarcoidosis-- DIAGNOSED WITH A TRANSBRONCHIAL BIOPSY THE OTHERS DONT REALLY REQUIRE BUT SARCOIDOSIS DOES

• Schaumann and Asteroid bodies 
• RA
• Calcium increase
• Occular involvement 
• Interstitial fibrosis 
• D vitamin
• Skin changes (if only skin changes-- then give hydroxycholorquine)

usually seen in farmers and bird fanciers-- secondary to aspergillus infection-- it is self resolving if stimulus is eliminated, but if not--irreversible noncaseating fibrosis with eosinophils 

although rare to do biopsy for this, type 2 pneumocytes will be increased, fibroblasts will be increased, type 1 pneumocytes will be decreased

because unable to ventilate it properly, you get hypoxia--and so the vessels nearby constrict

• -some stimulus is causing lung injury which leads to fibrosis 
• -affects subpleuraly, heterogeneously, and affects the bases more
• -honeycombing

• aspiration and intubated related pneumonias 
• likely to cause lung abscess that can rupture and leak into the pleural space

associated with comorbidities like DM chronic lung disease

is the most common and commonly affects asplenic patients

• Confusion 
• BUN>20
• Respiratory rate>30
• Hypotensive 
• hypothermia (less than 36)
• luekocytopenia
• thrombocytopenia
• multiple infiltrates

• 2: wards 
• 3: anything 3 and above send to the ICU

more than 2 weeks and it is usually caused by atypical (Mycoplasma pneumoniae, Chlamydia (Chlamydophila) pneumoniae, Chlamydia psittaci (Psittacosis), Legionella pneumophila, Coxiella burnetii (Q fever))

short acting bronchodilators-- they are beta agonists that activate camp which activates PKA which allows bronchodilation 

-albuterol and salbutamol