Clin Med2 T3 Updated Lung dz

Histoplasmosis

"O" is ohio, midwest. granuloma, calcified, extrapulmonary sites: mediastiunum, CNS,adrenal, liver, CNS, Exposed dirt & soil, chicken house, cave, demolish homes S/s:can appear healthy & normal but have fever, chills, chest pain, headache, myalgia, cough-rales, blood in poop inflammaton. Enlarge liver or spleen. Lab: Disseminated: pancytopenia reduced in all rbc, CBC low Hgb&Hct), LFT: AST,ferritin, Lactate dehydrogenase eleveated Fungal Culture gold standard(but take a few days) Antigen testing- helpful if severe CXR: granuloma CT scan:coin lesions *************** txt: IV amphotericin followed then with Oral Itraconazole. ROSH:asymptomatic

PNA Outpatient/@home CAP txt:

1)Healthy person who not taken any meds in 3 months or S.pneumo resistant 1a)macrolide or doxycycline (5days) 2)MDR risk: duration 90 days. a)respiratory fluroquinolone (moxi,gemi,levo) EX: moxifloxacin, levofloxacin gemifloxaxin. b)macrolide & beta lactam beta lactam-> amoxillin Or ampicillin macrolide->clavunate older children or adults--> s/s: fever, SOB, cough with sometimes sputum. possible chills, sweats, blood cough, myalgia, headache, abdominal pain. ROSH: if a pt goes to the clinic feeling sick (that is outpatient), if a pt was sick while in hospital mentioned in exam then thats noscomial??? s/s:acute & severe, productive cough, Lung findings are focal (typical PNA) explained by "fine crackles in a specific upper lobe". recall atypical is diffuse. Secondary PNA atypical: constitutional symptoms (fever, malaise, headache) + NONproductive cough more likely to be Mycobacterium or chlamydia PNA. txt: Amoxicllin if first line txt for outpatient PNA in children

Thoracentesis for Pleural Effusion

1)diagnostic: when you want to know an unknown cause 2)Therapeutic:relieve SOB, remove fluid, medialstinal shift caused by Pleural effusion For both types-dont use: when their is coagulopathy dz, less than 1cm PE on lateral decubitis, infected skin area. Drained about 1000-1500ml, if drained more & fast then can develop edema, but usually nothing bad happens if you keep pressure 20cm constant

ARDS (acute respiratory distress syndrome) noncardiogenic pulmonary edema

ARDs are usually found in patients who already suffered from an illness/injury (ex:Super sick & hypoxemic, septic shock, Transfusion related acute lung injury (TRALI), near drowning). >There is a CXR that shows Pulmonary Edema**/fluid in lung. ARDS is a group of symptoms classification. Normally, the alveoli is near the blood so oxygen diffusion can occur readily. In an illness where the alveoli is affected such as an inflammation, there is a leakage of fluid. The water is surrounding and creating distance between the lung alveoli & the oxygenated blood, oxygen diffusion becomes more difficult. The liquid compresses the alveoli, which is basically making it smaller, increasing the diffusion distance aka "De-recruitment". Using PEEP, or small shallow breathes creates a counterforce inside the alveoli that pushes out against the water force that compresses the alveoli in. PEEP prevent alveoli collapse. Recall inflammation causes more gaps in cells making more leakage ((((blood clots" maybe))))The pt illness might also have decrease in surfactant causing alveoli collapse. Less gas exchange. compare ARDS vs. CHF. ARDs is a clinical diagnosis made by hypoxemic respitratory failure & Pulmonary Edema. ARDS measured with Pulmonary Wedge--> Data given 1)Left Ventricle Failure: 2) ****Pulmonary Capillary or Catether Wedge Pressure/Pulmonary BP: In CHF: 1A)Low, fluid backs up in veins (increase the vein size causing leakage) 2A) High ARDs: 1A) Normal or elevated, b/c ARDs 2A)Normal or Decrease Txt: >Intubation & treat the dz cause. >Diuresis: b/c dz is from pulmonary edema, but it is only a "try attempt" Co2: Tidal volume low & Respiratory rate high O2:Increase PEEP via small shallow fast breathes to help maintain Co2 levels. >Lying Prone: decreases the amount of area or volume of ARDs affected tissue is smaller. Reasoning: ARDS pt should receive low tidal volume b/c heterogenity & barotrauma. During ARDs, the affected lung is "concrete" due to the liquid impairment--> so air in an ARDs lung will choose the path of least resistance. Normally, if you put large air volume in, you Hyperinflate the good lung or stretch out areas where there is no resistance. Recall that ARDs is an illness already happening, so when the lungs are hyperinflated, the inflammation recruits more Interleukin (IL) immune responses that would worsen the alveoli area, making more leakage. S/S:SOB after injury or illness. Cyanosis due to hypoxemia in the blood. Edema-->Crackles. >CT or CXR: white out lungs from edema >PF ratio of partial pressure of arterial blood/fraction partial pressure of inspired oxygen (Pa02/Fi02) is less than 300mmHg. >Respiratory distress not caused by the heart. CHF has heart problems, making heart working inefficiently, causing the BP to increase since it needs to pump more. ARDs is caused by alveoli damage, meaning the heart is working normal, so Bp is normal.

Cystic Fibrosis.

Cystic: fluid filled sac Fibrosis: excess connective tissue autosomal recessive CFTR gene chromosome 7. Normally a CFTR protein pumps Cl- ions into thick secretions, like mucus, and thins it out (more particles in thick secretion causes osmosis water to come in). Mutation of F508 stops CFTR--> thus mucus is thick & epitheial cells on the lung is dry/dehydrated since water left. Infect LUNG & DIGESTIVE system. Stages: cascade of events 1) airway surface liquid abnormal (dehydration) 2) abnormal ciliary clearance 3) bacteria colonization 4) inflammation with Neutrophil WBC increase activity. Newborns: Meconium- baby first poop. "Meconium Ileus" in CF babies is an emergency b/c mucus causes poop get stuck in intestine requiring surgery. Early childhood: CF child has mucus blocking pancreas duct --> preventing the release of pancreatic enzymes "pancreatic insufficiency" into the small intestine that would help the intestine absorb fat & protein. --> 1)Causes Steatorrhea 2)CF is undersize/difficult to gain weight & fail to thrive. > Pancreas Insufficiency: has the mucus blockage causing a buildup of enzymes in the pancreas destroying the cells and causing inflammation aka "Pancreatitis". As damaged pancreas develop Cysts & Fibrosis at damaged areas, it impairs endocrine function of the pancreas (insulin-dependent DM-2) Later Childhood aka Chronic: Mucus increased in the mucocillary escalator causing colonization of bacteria stuck in bronchi lung area. Lungs can be infected by a variety of microbes not just bacteria. --> Chronic lung infection aka Bronchiectasis. If repeated CF infection in lungs aka Repeated CF exacerbations--> lead to respiratory failure (leading cause of death in CF) s/s: >infertile men b/c damage vas deferens >nasal polyps >finger clubbing >Allergic BronchoPulmonary Aspergillosus (ABPA) hypersenitivity rxn. *PPT:lung shape, undersized body, crackle/wheeze *MC: white ppl LABs: >Newborn screening: detect IRT (ImmunoReactive Trypsinogen) a Pancreatic enzyme that is found in blood when pancreas damaged. >Sweat test: detect high Cl- aka baby taste salty. *PPT: PFT FEV1 value monitor. *Txt ppt: 1)CPT or Chest PhysioTherapy: special vest percussion/aerobika or manual cup-hand percussion. 2)airway bronchodilator: SABA & SAAB 3)Mucolytic/Pulmozyme aka "Dornase Alpha" affects DNA to reduce mucus. 4)Hypertonic Saline (thins mucus) 5)Fight the infection that CF helped bring in different microbes. ex:Biofilm-->Macrolides (Erythromycin) ex:aminoglycosides alternate ex:Pseundomonas--> 2 drug classes. *PPT: Inflammation--> NSAIDs or Steroids *MC: White ppl CF management (3): 1)Lung dz:maintain lung health 2)Poor nutrition-must eat better to maintain lung f(x) (Vitamin deficy, Osteoporosis, Anemia) 3)CF causing diabetes: has reduced lung f(x) >Outpatient: quarterly regularly appointment. Collect Sputum & PFT each visit. >Inpatient: medicatipns for pathogen causing CF, airway enlargement, bronchoscopy

ICU- Community Acquired Pneumonia (CAP) txt:

Inpatient ICU txt: a) IV Azithromycin or b) Respiratory Fluoroquinolone + antipneumococcal beta-lactam (cefotaxime, ceftriaxone, ampicillin-sulbactam) if PCN allergy:Fluoroquinolone + aztreonam If CAP also @Pseudomonas risk: a)antipneumococcal, b) antipseudomonal beta-lactam (piperacillin-tazobactam, cefepime, imipenem, meropenem) + ciprofloxacin or levofloxacin a)antipneumococcal beta-lactam + aminoglycoside (gentamicin, tobramycin, amikacin) + azithromycin or a respiratory fluoroquinolone Pathogens: Strep pneumoniae, Legionella, H influenza, Enterobacteriaceae, Staph aureus, Pseudomonas MRSA infection: add Vancomycin or Linezolid

Coin Lesions X-ray

Internet picture

Sarcoidosis: ACE, Uveitis, nodules

Is a disorder in the immune response. Immune response happens over & over in the body many times even though there is no specific pathogen that stimulated the rxn. The immune cells go to healthy tissue & form small nodules/granuloma any where in the body since this immune response is a systemic disorder. If sarcoidosis is severe then there will be Fibrosis @ Hilar. Immune system cells aka Antigen Presenting Cells 1)most numerous Dendritic 2)B cells 3)macrophages -->Dendritic cell receptor "Major HistoCompatibility Complex (MHC class 2)" binds to a pathogen and brings it to a lymph node. At the lymph node where the dendrite cell brings the pathogen/antigen--> they go searching for a Naive Helper T-cells that can bind to the antigen. Once you find a compatible Helper T-cell, the dendrite cell releases cytokines to cause the T-cells activate by reproduce/divide into many cells.--> The new T-cells leave the lymph node & release their own cytokines--> cytokines recruits more immune cells (T-cells /macrophages). These immune cells aggregate @ healthy tissue and become a noncaseating/no necrosis granuloma. Sometimes these granulomas fuse together as a "Langhan Giant Cell". Inside the Langhan Giant Cell has 1) Asteroid Bodies 2)"Schaumann bodies" that retains calicum & protein. -->If immune cells accumlate at lymph nodes, most common is 1)"Bilateral Hilar Lymphadenopathy" 2) Erythema Nosdosum (inflammaton red/hard/painful) on lower legs. 3)Uveitis: inflammation of color iris 4)accumulation @ heart causes Arrhythmia. S/S: General:fever, fatigue, weight loss Specific depending body systems that are most affected: nodules location, SOB, cough, vision changes. > MC black females, hx of scaroidosis, exposed to Mycobacterium TB & Borrelia Burgdorferi *PPT: Lupus Pernio (nostril rim) enlared organs/glands LABs: >CXR & CT scan: mc bilateral hilar lymphadenopathy >Blood test: a)High value of Calcium-from macrophages b) Angiotensin Converting Enzyme (ACE)- T cells. >Bronchoavelolar lavage: elveated T-cells >BEST is Biopsy. Tx:Dz resolves by itself, but if severe symptoms--> Oral Corticosteroids/Prednisone.--> if steroid allergy then use immune system drugs "I-am" Infliximab, Azathioprine, Methotrexate ROSH: MC:black woman s/s: polyarthritis, fever, fatigue, weight loss, cough blood, SOB, Bell's palsy, HF, Uveitis/conjunctivitis., lucus perino (violaceous plauqe nodules on Cheek,nose,eyes). Labs: noncaseaing granuloma inflammation (T-cell & interleukin)*** bilateral Hilar lymph swelling High ACE serum pulmonary fibrosis TxT: Lung transplant is end stage (stage 4) when FVC below 50% & FEV1 below 40%

Inpatient CAP txt:

a)Respiratory Fluoroquinolone b)Macrolide + beta-lactam (ceftriaxone, cefotaxime, ampicillin) MC: S pneumoniae, Mycoplasma pneumoniae, Chlamydophila pneumoniae, H influenza, Legionella and respiratory viruses

acute bronchitis.

s/s: SOB, cough(dry&Nondry) wheeze & ronchi, inflammation of lower respiratory tract. 5 days self-limited means resolve by itself. URI occurs before acute bronchitis so can have commoncold symptoms (HA, Nasal congestion, sore throat). if involve lower respirartory (cough for sure primary symptom). chronic cough--> lead to chest way or substernal pain. If acute bronchitis have these different signs: require different txt: sudden paroxysm cough that has whooping or posttussive vomiting. Fever or systemic infection flu or pNA. **Parenchymal consolidation--> dullness or percussion, decreased bronchial breath sounds, rales, eggophony, plueral rub.** Labs: testing only if suspected PNA. Chest xray: unlikely to change in pts with chronic cough. sometimes you see thickening bronchial walls. tx:ANTibiotics increase more bad risks so....supportive,cough drops, hot tea/honey, stop smoking, antipyretics, good hydration humidified air, expectorants(mucus reducer) ROSH: inflammation of lower airway USUALLY VIRUS. s/s: most common complaint is cough. complains a mucus cough for more than 5 days (wheeze/ronchi). CSR: thick bronchial walls in lower lobes.

respirartory syncytial virus (RSV) bronchiolitis

the respiratory tract individual cells merge together called a Synctia. leading cause of hospitalization for babies (especially preamature)-grunting/wheeze. or older comorbid weaken immune system adults (transplants) cause of acute otitis media ROSH: confirmation lab is nasopharyngeal swabfor fluorescent antibody staining.

Types of lung cancer

1)adenocarinoma (invasive & mc) 2)Squamous cell carinoma 3)large cell carcinoma 4)Carcinoid (NeuroEndocrine Tumors aka NET) 5) small cell carcinoma (oat cell carcinoma)--> can secrete hormones (ADH or antibodies) osmosis what:

What am i suppose to see?

Hyaline RDS ppt

Lung Dz General groups

Restrictive Lung Dz:Decreased Total Lung Capacity (TLC) 2 Types A)Interstitial: lung tissue itself (lung parenchyma) is damaged so air cant really enter. All healthy lung tissue replaced by fibrosis. ( a1)Pneumoconiosis (occupation) a2)Sarcoidosis (unknown) a3)hypersensitivity pneumonitis (allergy) B)Extra-Pulmonary or Extrinsic: Structures around the lung is damaged so chest can't expand. (rib cage or diaphram) *PPT: ventilation disorder Kyphoscoliosis ex: Pectus Excavatum, obesity, Pleural effusion, Myasthenia Gravis air going out: FEV1/FEV air going in: TLC

Pneumothorax (PNX)

extra Air in the pleural spaces. Pleural cavity is a vacuum that absorbs air due to the balancing of opposing forces. The pleural space starts off as negative pressure compared to inbetween the chest wall & lung (as zero pressure). This negative pressure vacuum allows 2 forces stick to one another & counteract. 1)Muscle tension- the muscles of chest wall & diaphram pull out/expand. 2) Elastic recoil: lung pulls in & contract. PNX occurs when pleural space puncture, so no more negative pressure--> opposing forces dont cling to another. Chest muscle slightly expand up. Lungs recoils in aka collapse lung. Type 1) Spontaneous PNX: so no lung dz. alveoli has leak forming a Bullae/air pocket bubble bump on the lung. When the bullae pop, the air from aveloi enter the pleural cavity. Mc: thin, tall, male holding breath, adolescent younger ppl. no history of lung dz, Can be smoker or Autosomal dz. Type 2) Secondary Spontaneous PNX (SSP) come from lung dz. ex:marfan , Cystic fibrosis (young 20yo undersize), emphysema, lung cancer, COPD older 50 to 60yo, PNA pts. Hyperressoant & Michelin Man sign Type 3) Tension PNX: can be due to sponatenous or traumatic cause. A 1 way valve (tissue block air coming out) because air enters the pleural space from one side pushing organs. ex: Deviate trachea, compress lung & heart moves. Type 4 ) Traumatic PNX: gunshot, stab ruptures from outside. LABs: CXR or CT: Pleural space is black because PNX or air entering. Lung tissue partial black/grey. s/s: chest pain, SOB hypoxemia-SSP TxT: No admission: if smaller than 1cm, no symptoms, repeat xray 12-24hrs. Note:SSP always admit even simple? Observe & give 0xygen: Smaller than 2cm, live close by, repeat x-ray 12-24hrs, mild s/s. Larger than 2cm Admit: needle aspiration If severe: >use chest tube/tube thoracostomy or pigtail >Video assisted thoracic surgery (VATS): air leak wont go away, reoccuring PNX, special pressure pts like scuba & pilots

Tactile Fremitus

a vibration of the chest wall during speaking that is palpable/touch on physical examination. Depending on where the liquid or density is at-affects the sound. Increase tactile fremitus: denser lung tissue. Conditions cause lung to be more solid ex: inflammation, PNA Absent/Decrease tactile fremitus: air or fluid in pleural spaces that decrease lung density. ex: COPD,asthma, pleural effusion, PNX, increase fat Note:PNA has fluid within the lung so, the dense molecules of the lung help make sound travel louder & faster. PNX has air in the lung, so when sounds travel through, the molecules are so far apart it doesnt amplify. Pleural Effusion has liquid not in the lung but the barrier/lining of the lung called interstial cavity. The fluid on the cavity absorbs the lung instead of amplifying it, so sounds are decreased.

PNA This is one way of categorize the groupings

a)community acquired PNA >48hrs admission develop b)Noscomial hospital acquired (HAP)/health associated or ventilator associated PNA >usually extended care facility, clinic, nursing homes >dirty equipment or exposure to pharynx infection c)separate Anaerobic PNA (occur in both community or hospital acquired. ROSH: chest x rays are used to rule out PNA if there are abnormal vital signs including temperature greater than 38°C, pulse greater than 100/min, respirations greater than 24/min, or age greater than 75 years with more severe clinical symptoms

Traumatic PNX:

causes: a)Iatrogenic (from medical provider) central line internal jugular vein or subclavian vein b)Blunt Trauma (car accidents) c)Penetrating injuries (stab wounds vs. Gun shot) Types: a)PNX standard: can have large amount of crepitus due to subcutaneous emphysema or bronchopleural fistula b)hydroPNx: fluid(blood or stomach, chyle) within chest cavity c)Hemothorax: bleed into chest cavity d)chylothorax: injury in thoracic duct within chest cavity usually due to penetrating injury e)gastric contents: esophageal rupture & gastric rupture

Bronchiolitis

inflammation small airway in the lung.small children, Mainly caused by RSV, but can be caused by a variety & multiple microbes at one time such as viruses like adenovirus, human bocavirus, or bacteria like mycoplasma pneumonae osmosis what: type of pneumoviridae virus, contact but mostly sneeze/airborne. RSV targets Nasopharynx and goes down trachea & bronchi to bronchioles(main target). The respiratory epithelial cells are infected by RNA of RSV, causing destruction of other cells which stimulate an immune response of inflammation/swelling. The immune cells chemokines secrete mucus making the airway thicker and thus narrower (especially for kids). Mucus accumulation can form a 1 way mucus plug & 1) trap air overinflammation or 2) atelectasis (airway/alveoli collapse) ROSH: expiratory wheezing!

squamous cell carinoma

intercellular bridges keratin pearls osmosis what lung cancer s/s: & coin lesions on x ray

Miliary Infiltrates

internet. Miliary is a type under nodule.

signet ring

look up xray???? sign for bronchiectasis. cross section of bronchi & pulmonary artery.

tree in bud pattern

look up xray???? sign for bronchiectasis. they are the linear branch markings when small airways have infection.

Third Bacteria PNA CXR

ppt

Third viral PNA CXR

ppt

Tram track sign bronchioectasis

ppt

PNA pathogen microbes

1)Virus: flu 2)Fungi(rare):P-Bacch Pneumocystosis- PCP Blastomycosis-East-yeast Aspergillosis Coccidomycosis- "C" in cali/sw Cryptococcosis- hide any Histoplasmosis- O- ohio MW 3)Bacteria: a)Streptococci (mc) b)haemophilus c)staphlyococci (no cell wall & atypical- fatigue/walking PNA) d)chlamydophilla e)legionella f)mycoplasma g)Mycobacteria (slow grow like fungi) but actually bacteria aka TB. 1)bacteria that are antibiotic resistance 2)bacteria surrounded by biofilm(slime matrix) protection from Abx medication & Immune system.

PNA pathogen microbes

1)Virus: flu 2)Fungi(rare):P-Bacch Pneumocystosis- PCP Blastomycosis-East-yeast Aspergillosis Coccidomycosis- "C" in cali/sw Cryptococcosis- hide any Histoplasmosis- O- ohio MW 3)Bacteria: a)Streptococci (mc) b)haemophilus c)staphlyococci (aureus) (no cell wall & atypical- fatigue/walking PNA) d)chlamydophilla e)legionella f)mycoplasma g)Mycobacteria (slow grow like fungi) but actually bacteria aka TB. 1)bacteria that are antibiotic resistance 2)bacteria surrounded by biofilm(slime matrix) protection from Abx medication & Immune system.

Pulmonary HTN vs. Pulmonary Arterial HTN

Pulmonary HTN: elevation of pressure of the arteries of the lung. The umbrella term. Pulmonary Artery HTN (PAH) is a subgroup of Pulmonary HTN, the elevated BP of Pulmonary Artery is 25mmHg or larger @ rest.---> can Progression to Chronic Thromboembolic Pulmonary HTN (CTEPH). Multiple embolisms forming overtime causes an increase in BP thus Pulmonary HTN 5 group classifications based on WHO Chronic lower respiratory is most common cause of death since dz keeps on progressing & getting worse. MC:older than 50yo males, class 3 or 4, Right ventricle dysfunction. Echo:Right atrium is larger & has a higher BP. Also, see a heart septal shift TxT: Bosentan Prostacyclin Iloprost (PAH) ROSH: Pulmonary HTN txt: Theophyliline

COPD (chronic obstructive pulmonary disease)

1)Chronic Bronchitis: (min 3months-2years) inflammation of bronchi. Defined by clinical features like length of cough >narrowing of airway: causes WHeeze & crackles. When airway is blocked, there is a decrease of O2 in alveoli which in turn means more CO2. Since O2 cant be exchanged by the blood, the alveoli that is already full in co2 amount-->cant pick up co2 flood blood causing HyperCapnia (alot of co2 in blood)-->cyanosis or Blue Bloaters. If many areas of the lung are blocked off, increases pulmonary resistance causeing Pulmonary HTN. ROSH: s/s: mucus over produce & edema in the walls. 2)Emphysema: defined by structural changes. ex:enlarge air space >alveoli is damaged/destroyed due to permanent making it lose elasticity. When air leaves the lung, the alveoli deflates. When air enters the lung, the alveoli swells up and cant get rid of oxygen properly. Acinus (ending of airway). S/s: pts try to exhale slowly via "pursed lips" so the alveoli doesnt collapse suddenly. "Pink puffers" s/s:barrel chest, hyperressonant to percusion, cant walk to mailbox LABs:hyperinflation & flatten diaphram TXT: Tiotropium first line 3)COPD: airway obstructed in the bronchi lung, so some air is trapped in the lung & cant be expelled.

Anaerobic PNA & Lung abscess can occur in both hospital or community acquired.

Anaerobic bacteria multiple species causing: prevotella, melaninogenica, prepostreptococcus, fusobacterium nucleatum, bacteroides. S/s: start: when pt seeks help for symptoms, there is already necrosis PNA, lung abscess or empyema. Bad teeth later: fever, weight loss, cough sputum, dentition & malaise Lab: Culture: transthoracic aspiration, thoracentesis, bronchoscopy. CXR: a)lung abscess, thick walled solitary cavity surrounded by consolidation, air fluid level is present b) necrotizing PNA, multiple areas of cavity within an area of consolidation c)Empyema- purulent pleural fluid Tx: Clindamycin, amoxicillin-clavulanate PCN + Metronidazole therapy continue until chest x-ray improves. *tube thoracostomy--> for Empyema** pleural drainage

Nosocomial PNA txt

Empiric Txt: usually 8 days of IV antibiotic except if pseudomonas aeruginosa (longer therapy) >based on risk factors: MRSA, MDR, Pseudomoas gram (-) bacilli bacteria. When pathogens are Multiple Drug Resistant (MDR): Ceftriaxone Levofloxacin Moxifloxacin Gemifloxacin Ciprofloxacin Ampicillin-sub lactam piperacillin-tazobactam Ertrapenem I------I-----I Antipseudomonal coverage: CMP-T: a)ciefepime/ceftazidime (cephalop b)imipenem or meropnem c) piperacillin-tazobactam if PCN allergy give aztreonam A 2nd pseudomonal agent: a)levofloxacin or ciprofloxacin b)IV gentamicin, tobramycin, aamikacin c) meropenem d)colistin e)polymyxin B If MRSA--> IV vancomycin or Linezolid. s/s:fever, leukocytosis or high wbc #, sputum

PNA in ppl with Weak Immune Systems

If kids or ppl who get PNA outside of the hospital aka community acquired PNA, these are the likely sources. Cystic Fibrosis from babies: called Staph Aureus Pseudomonas Aeruginosa/ Burkholderia cepacia: in older kids.

PNA in kids

If kids or ppl who get PNA outside of the hospital aka community acquired PNA, these are the likely sources. 1)Neonates in hospital-->s/s: fever, hypoxia , SUBTLE [GBS or Group B streptococci PNA] 2) [RSV]--->infants---> s/s: Apnea & fever >mild elevated eosinophilia labs indicate C.trachomatis PNA. [From 3 weeks to 5yo can be RSV(mc) or C.trachomatis] 3)Mycoplasma PNA--->kids older than 5--> s/s: SOB/chest pain on breathing, cough, fatigue, fever, chills Streptococci PNA--> mc Bacteria type causing Lobes in xray & rust sputum Atypical PNA--> usually caused by Mycoplasma & Chlamydophila s/s:ear infecton ROSH: mc complication is Dehydration. s/s: SPO2: less than 92% hypoxia.

When admit PNA pt @ ICU

MC consider hospitalization: 1)infant under 6 months with bacterial PNA, 2)MRSA risk, difficult to monitor progression of symptoms, 3)pt with comorbiditis CURB-65 criteria (2pts or above can be considered admission) Confusion of new onset (defined as an AMTS of 8 or less) Blood Urea nitrogen greater than 7 mmol/l (19 mg/dL) Respiratory rate of 30 breaths per minute or greater Blood pressure less than 90 mmHg systolic or diastolic blood pressure 60 mmHg or less Age 65 or older

Lung Anatomy

Mouth- trachea- primary (main) bronchi--> Secondary (Lobar) bronchi--> Tertiary (Segmental) bronchi--> alveoli (gas exchange). Normally the bronchi walls are made of 1)elastin fibers(rubber band characteristics) 2)epithelial cells-cilia 3)epithelial cells- native body Mucus. All 3 of these components -Mucociliary Escalator- traps foreign particles & bacteria in order to remove out of body--> esophagus/pharynx-->stomach acid destroyed. Allows airway to pass through. If there is a problem such as an infection, then the progression goes like this. Bronchi can have 1) Cilia Dyskinesia- cilia dont move and transport foreign particles out, therefore an accumulation of bacteria causing an infection/PNA 2)Cystic Fibrosis: dz makes mucus extra sticky so cant remove thus accumulate particles for illness. If increase bacteria in lungs causes (COUGH & FEVER & change in CXR) aka Cystic Fibrosis Exacerbation 3) Damaged caused by obstruction 3a)foreign object stuck within the airway. 3b)Or tumor INSIDE that impedes that bronchi airway or OUTSIDE that pushes bronchi in from one side. >Overtime the Mucocilary escalator is destroyed causing chronic Inflammation. Inflammation causes Immune cells response to release cytokines--> cause damaged & dilated epithelial cells & destroys elastin. When tissue heals itself with collagen (the tissue becomes more stiff) so less able to get air in the body. If the inflammation/infection is localized in one area of the lungs (ex:bronchi) then the rbc around that area can have hypoxia (no lung & blood gas exchange). This causes arterioles @ infected area to vasoconstrict & divert/push blood out of damaged/ineffective areas. The vasoconstriction causes an increase in BP in the vessels within the lungs. If the inflammation/infection was widespread damage throughout the lungs --> more vasocontrictions--> Higher vascular resistance @ lung vessels--> "Pulmonary HTN". If the lung has high BP, then the place @ the heart that pushes blood too the lungs aka Right ventricle's Pulmonary Artery gets backflow. R. Ventricle Hypertrophy unable to push blood out of the heart to the lungs. This whole process of lung illness affecting heart function called "Cor Pulmonale" . Digit "clubbing" can occur, usually associated w/lung OR heart problems.

Pneumoconioses

Occupational exposure A) Coal worker: coal/dust (upper lung) a1)Simple/no symptoms but small opacities in CXR a2)Complicated/progressive masive fibrosis--> "Caplan Syndrome with RA lung peripheral. B)Silicosis: silicon/diamond & sand or stone cutting/ mining. (upper lung)increase risk of TB ROSH: CXR: hilar lymph node calicified into "egg shells" C)Asbestos: construction/ship workers (Lower lobes & pleural cavity--> CXR has pleural plaques @ lung base)

streptococcous staphyaureus

Outpatients CAP streptococci: works with doxycline & Inpatient you needto be careful of MRSA so--Vancomycin & Leukoizid. family tetracycline- doxycline, "cycline" staphylaureus:

Oxygen Delivery Notes

Oxygen: A)PEEP (positive end expiratory pressure) B)Fi02 >Oxygen is diffusion limited meaning bigger barrier,less 02 diffusion. Monitored by ABG or Sp02 pulse oximetery C02 A)Tidal Volume B)Respiratory rate C)Pressure Support over PEEP Ventilation >C02 not diffusion limited, but is perfusion limited, meaning faster breathing rate causes decrease co2 Monitored by only ABG--> pH, CO2, O2. Different types of oxygen deliver tools: A)On the Hospital Floor 1)Nasal Canula (deliver 1-6L) 2a)FaceMask(deliver 6-10L) 2b) Venti Mask 3)NRB (Non-Rebreather Mask) (deliver 10-15) B)ICU 1)NIPPV (nonInvasive positive pressure ventilation)-->comes in 3 different modes 1a) High flow nasal canula 1b)Bipap (Bilevel positive airway pressure) 1c)Cpap (continuous positive airway pressure) Cpap & Bipap pts need to cooperate with machine meaning they cannot have altered mental status. machine gives alot of pressure so if a pt vomits, it will get pushed down. Note:If a pt is already altered mental state/nausea vomiting where they would compromise their airway further--> might as well do ET tube. >Bipap=COPD, never asthma >Cpap= OSA >Asthma use Tubea-ation 2)ET (Endotracheal tube) >need to be mentally capable w/cough reflex >Assess BNP, need to be low & RsBi (rapid shallow breathing index). Theories: Oxygenation: goal is to increase 02. 2 methods A)Fi02 B)O2 >Increase Fi02 & O2 increases oxygenation. C)PEEP, increase in PEEP increases Surface area by increases more Alveoli, Increases oxygenation. Ventilation: goal is to decrease Co2. "Minute ventilation", is the more you breathe, the more you decrease CO2. A1)Tidal volume A2)Respiratory Rate TV & RR together is the calculated minute ventilation B2)Pressure support/ PEEP--> causes an increase in ventilation which decreases CO2. This involves lung compliance & elasticity. If emergency & on the floor you can start with NRB then descalate, but if NRB doesnt work, then ICU NIPPV or ETube.

Coal worker lung

PPT

Sarcoidosis Stage 1

PPT

Sarcoidosis Stage 2 or 3

PPT

Sarcoidosis Stage 4

PPT

Second Bacteria PNA CXR

PPT

Silicosis CT

PPT

Silicosis lung

PPT

"Millet-like" seeding of miliary Tb in lung.

PPT Mycoplasma Tuberculosis

Miliary infiltrates on chest x-ray.

PPT slide Mycoplasma PNA tend to be more reticular nodular patches, not defined in 1 large lobar consolidation.

Pleural Effusion

Pseudotumor: effusion in horizontal fissure a type of pleural dz (the lung is surrounded by 2 membranes Visceral-close to lung & Parietal-chest wall). There is a pleural space/cavity that has fluid/interstial or albumin which is lubrication for lungs to expand. Effusion=liquid. Make too much: Transudative or Exudative Cant remove enough: Lympatic effusion A1) Transudative effusion: too much fluid leaves the RBC capillaries and enter the pleural cavity via (hydrostatic pressure inc or oncotic pressure dec). Appear clear/no odor/ straw in color. sidenote: >hydrostatic pressure=Bp. Blood cant push out of the heart to the rest of the body due to heart failure so backs up in Pulmonary/lung cells. Increase in pressure force fluid into pleural space. >oncotic pressure=solutes cannot pass RBC capillary so there is more solute on lung side (a lot of albumin particles for example). By the process of osmosis, water leaves RBC & enter pleural cavity. ex: Cirrohsis (make fewer proteins) Nephrotic syndrome (more protein in urine). B1)exudative effusion: The RBC near the lung are inflammed. Inflammed RBC have larger openings hat allow more fluid/immune cells to enter the lung space. If infectious based source--> the lung space can be Fibrinous or form Lobes. ex: trauma, cancer, infection/inflammation: Lupus/PNA. Appear cloudy & smelly due to immune cells (bloody or viscous) C1)Lympathic Effusion/Chylothroax: The Thoracic duct near the lung cavity that normally removes unneccesary fluid gets disrupted (surgery/tumor). If not removing fluid, thoracic duct puts in LYMPH fluid in cavity. Appear milky lymph fats. Depending: fluid:homo/hetero, uni/bilateral, simple or multiloculated Size- small effusions may be hidden or blunting of Costophrenic Angle since fluid gravity to bottom. Large fluid effusions can cause pain/"Pleurisy" and become more obvious when lying down. Can push the lung and reduce breath or cause trachea deviation. Progression: Empyema aka pyothroax: is when effusion fluid can thicken into PUS making drainage difficult. Labs: CXR: appears "opaque/white" if standing fluid accumulates below to Costophrenic Angle or if lying down fluid is diffused- "layering effect" Thoracentesis is a diagnosis & txt. S/S: sharp stabbing pain that possibly radiate to 1 side of the chest/shoulder via phrenic nerve or the Back muscles. Pain worsens during inhale,cough, sneeze, laughing. Decrease breath sounds/ perccusion/tactile fremitus----> severe:--->: Pulmonary Embolism:SOB & fast breathing. Tactile fremitus: normally chest wall vibrate when pt talks, but effusion liquid dulls or create fewer vibration/sounds. Note: exudative Fluid Cholesterol over 45mg/dL (from osmosis) & LIGHT's Criteria: (need 1/3) distinguishes Transudative vs. exudative. All you need is 1 for it to be exudative. >Trans-ient/systemic: illnesses that often have overload fluid tend to end up in the lungs. >Ex-tra shit: extra cells & not just fluid like Abscess, cancer cells, inflammation mediator cells. Pleural:Serum ratio (P:S) 1)P:S LDH greater .6 2)P:S Protein > .5 3) Pleural LDH > 2/3 upper limit of normal. If you see a pt lab value is 2/3 close to whatever the standard range is. PS, in sex/6 you want the D, and up to 5 you hope your P. Tx: Remove fluid & treating the cause ex:HF-diuretic & reduce sodium ex: surgery & drainage from cancer or PNA bacterial /TB ROSH: Transient(lil protein): HF, cirrohsis, Nephrotic syndrome, embolism Exudate(a lot of protein): malignancy, Bacteria/viral PNA, TB, oancreatitis, esophageal rupture, collage vascular dz, chylothorax or hemothorax. S/s: decrease breath sounds, dull percussion, tactile fremitus down. Blunting of costophrenic angle

Obstructive Sleep Apnea (OSA)

Sleep Apnea: irregular breathing patterns--> apnea is when stop breathing for a moment.--> causes body to not get a full night's rest of sleep/exhaustion. 2 types of Apnea: 1) Central Sleep Apnea- Neurological (CNS) malfunction where the brain tells lung to stop breathing-->create imbalance in blood O2 & C02 levels. This is a cycle where the brain tells to stop breathing/apnea during sleep until low 02 levels which create a quick hyperventilation of rapid breathing to make up for apnea--> then goes back to apnea again. NO MIDDLE ground just Breathe fast or not breathing @ all. 2)Obstructive Sleep Apnea- Most common. There is blockage of the airway. >can be due to allergies or tonsils causing swelling >underbite pushing mouth in & narrow breathing >overweight & at night muscle relax so more pressure down on the airway. Upper airway obstruction occurs during sleep when the pharnyx muscle collpases during breathing in/ inspiration. s/s: >sleep deprivation/nocturia (need to pee at night). More episodes @ night means more severe. >cant concentrate, HA, fatigue, htn, BULL NECK, deviated septum worsen other conditions like arrhthmia. Lab: Erythrocytosis (more rbc), thyroid test-hypothyroid Best identifier: Otorhinolaryngologic exam Overnight polysomnography( eeg, electro-oculography, EMG, EGG, pulse ox, measurement of respirartory effort & airflow Diagnosis Definitive DX: 1)Sleep study monitor with "Polysomonogram" includes EEG,pulse oxy, measure respiratory effort 2)Otorhinolaryngologic exam TxT: >sleep sideways >avoid antidepressant drugs or alcohol: relax muscle mean closed off airway >Continous Positive Airway Pressure Device (CPAP) machine > Oral mouth piece >Surgery to clear airway. CAUTION b/c anaestheisa worsens when asleep. ROSH: history of allergies, snoring, LARGE TONSILS

Mesothelioma

caused by asbestos (ex:paint,roof). A rare cancer tumor in the lung pleura. Asbestos are jagged fibers inhaled stuck(forever) in layers of mesothelium causing inflammation & DNA damage creating a tumor due to uncontrolled growth. --> Mesothelial plaques. The mesothelial plaques start secreting "Calretinin" which regulate Calcium levels in cells. Lab: >Biopsy TISSUE Diagnosis for calretinin making cells--> "Fried egg shape" >CXR & ct scan: show pleural thick, Effusion or PNX. thoracenteisis, pleural biopsy s/s: Chest pain, SOB, Effusion or PNX, if mesothelia invade RBC (bloody sputum symptom) Txt: Mesothelioma very resilent so need to catch early depending on progression stage. Usually too late when detected. (surgery, chemo/radiation) 3 stage types: Epitheloid (operable), sarcomatoid, biphasic CAN APPEAR LIKE PLEURAL EFFUSION or PNX ROSH: Ferruginous bodies in asbestoes

Cor Pulmonale

change in right ventricle thickkness that causes malfunction of the lung. Can be caused by a variety of illnesses, but most common is COPD, middle age white men. This is usually a late stage of a serious dz. ROSH: s/s: peripheral edema, Dyspnea, fatigue, HTN chronic COPD can cause COr pulmonale acute Pulmonary Embolism can ccause Cor pilmonale Definitive Diagnosis DX: Right heart cathereization.

NeuroEndocrine Tumor (NET)

confused with PNA, so dx delayed higher chance in white women, cytoplasmic dense granules Types:Carcinoid,atypical carcinoid, large & small cell nueroendocrine tumor located on central bronchial air way, vascular.

extrapulmonary symptoms examples:

cough, headache, myalgia, skin rash, arthalgia, muscle aches, sweating, rhinorrhea, sore throat, lymphadenopathy

small cell carcinoma

dark cell stains, crowded tumor cells, lymphocute 2-3mm osmosis what:

Atypical PNA xray

osmosis

Hyperventilation syndrome

over breathing/rapid breathing to the point that levels of CO2 in arterial blood is excessive ; alkalosis. Also causes hypocapnia: less Co2 in blood. usually severe agitiation, anxiety or fright, hyperventilation, (light headedness dizziness, numbness, feeling of tightness, muscle twitching, carpal-pedal spasms, tetanus, seizures, loss of consciousness. Can be caused Voluntary or involuntary. Diagnosis DX Definitive: if symptoms are reproducable during voluntary hyperventilation then you can consider Chronic Hyperventilation. General causes: pregnancy, hypoxemia, obstructive infiltrate lung dz, sepsis, hepatic dysfunction, fever, pain a)acute hyperventilation: hyperpnea, paresthesisa, palpitation, dizziness b)chronic hyperventilation: nonspecific, fatigue, dyspnea, anxiety, palpitation or CHEST PAIN, dizziness. txt: 1) first exclude organic causes 2a)breathe through pursed lips or nose while PINCHINg 1 nostril. 2b) Can use a rebreather expired gas in paper bag. 3)anxiety/anxiolytic drugs

Atypical PNA CXR

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Hyperinflation and slightly flattened diaphram lungs of baby for RSv

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Viral PNA CXR

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second Atypical PNA CXR

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second viral PNA CXR

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steeple sign for croup or laryngotreacheobronchitis

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Croup (laryngotracheobronchitis)

swelling of windpipe that interferes with normal breathing causing Barking cough, stridor, hoarse voice. WORSE at night s/s: fever, harsh barking/brassy cough- Hoarseness. inspiration or biphasic(obstruction) stridor. Wheezing indicate lower airway involvement labored breathing- suprasternal, intercostal, subcostal retractions may occur. Labs: >Neck x-ray (AP)- steeple sign or subglottis narrowing >Dx labs arent useful b/c leukocytosis not common, so only clinical signs based on Physical exam. tx: Severe cases: EPINEPHRINE & aersol for severe children Dexamethasone (PO or IM) Prednisolone (PO) Complication: viral PNA, bacterial tracheitis superinfection via Staph aureus happens usually following a cold. In adolescent-laryngitis. Spasmodic croup: sudden onset: usu at night with no prodrome or allergy. Parainfluenza virus types 1-4 & RSV most common infection in middle respiratory. Fall or early winter- kids from 6 month to 3 years.

Blastomycosis

eastern beast- made out of yeast. need to rule out Acute Bacteria PNA malignant cancer skin/larnx FLU chest pain, SOB-tachypnea, cough (productive or nonproductive), fever, chills, body aches, Meningeal s/s Dysuria epididymitis, prostatisis wart lesions**** leukocytes anemia, wash bronchi culture, antigen detected in urine/blood. tx: non-meningeal/non severe: Itraconazole Severe dz/CNS involve: IV Amphotericin B

Chronic Thromboembolic Pulmonary HTN (CTEPH).

Pts who ever had a thromboembolytic event before is now at risk of CTEPH. Also the vessels have developed more resistance already from before. Pt with thrombophilia. Lab: V/Q or ventilation/perfusion lung scan performed. PHTN: if larger than 25mmHg@ rest or over 30mmHG during exercise. TXT: Pulmonary endarterectomy Ballon angipplasty, transplant, antiplatelet, surgery some drugs same when used for PAH

Tram-track

look up xray???? sign for bronchiectasis. Airway is dilated

Mycobacterium tuberculosis (TB) aka Pulmonary TB

Many ppl in the world are infected, but arent aware that they have it because "latent". MC in poor, overcrowding, HIV, healthcare workers, immigrants >Mycobateria Tubercuosois is a Slender bacteria rods that require oxygen to survive (Aerobes). It has no peptidoglycan but has a waxy cell wall/membrane made up of "mycolic acid". This cell membrane is considered acid fast since it wont wash away with alcohol, making it bacteria cells pink in a Zichlin test. Bacteria passes person to person by air which infects the airway of the alveoli. Machrophages in the alveoli normally eat outside microbes like TB, but TB has a special protein that doesn't let it be digested in the lysosome. TB can now intracellular proliferate/reproduce causing sickness resembling the flu. >Primary TB: after exposure , shows no signs of infection, most ppl show no symptoms. Latent TB cannot be transmitted. Latent TB Criteria: 1)Asymptomatic 2)+PPD test 3)no infection on CT/CXR --> The body's immune system uses cell-mediated immunity to encircle/surround the tissue that is infected (this forms a granuloma with the immunity cell macrophage). Once walled off, the bacteria inside circle dies via "caseous necrosis". These dead granuloma areas in the lung are called "Ghon Focus". If there is a hilar "Lymph node" due to a immune response or the TB infection infected the lynph node nearby-->These 2 parts are called "Ghon Complex". The granuloma & lymph tend to fibrosis & calcify which can bee seen on a CXR which is now refrerred as "Ranke Complex". TB can be now remain latent/killed off.... Or due to a weaken immune system, TB switches from latent to active phase (spread to upper lung lobes since likes oxygen). Now immune system respond by Memory T-cells to release cytokines in order to try and control infected cell areas.--> This time the "caseous necrosis" to progress differently by caviating/making holes within the lung for possible "TB dissemination" via blood/heme, airway, lymph ducts, vascular/vessels aka "Systemic Miliary TB" (can infect any area or organ). Milliary TB often seen in pts with weak immune systems. CXR: Milletlike seeding s/s:depends on the stage >pt LOOKS really SICK. extrapulmonary symptoms CHRONIC COUGH rales (dry to hemoptysis), malaise, WEIGHT loss, fever, NIGHT SWEATS, pleuritic chest pain. High Risk: >Drug use & weaken immune system >DM or HIV >Silicosis >Stomach surgery >contact /exposure to ACTIVE TB >TB on CXR Medium Risk: >any child or under 4yo exposed to a TB pts >Injection druggie >Travelers who visited TB countries >Healthcare workers or pts who live in medical facilities LABs: 1)PPD/purified protein dervivate test or Mantous test or Quantiferon.(+) induration or raised bump 1a)larger than 15mm is person has NO risk factors 1b) larger than 10mm with medium risk factors Diagnosis Definitive: positive skin ppd test then CXR(hilar lymph nodes large, granuloma, nodular infiltrates, MILLET SEEDS >Best Sputum culture for acid fast bacilli or DNA/RNA amplification. >depending on the TB infection. a)Urine culture-Renal TB b)Lumbar puncture-TB meningitis c)CT scan-disseminated or lung cavity TB d) MRI- TB in brain or spine TxT: Direct Observed Therapy: Regular doctor visits to check if medication course is good. A) STANDARD course: (active TB) 4 meds for 2 months: Rrifampin Isoniazid Pyrazinamide (stop at 2months probably b/c poison/mty guess) Ethambutol -->if culture shows sensitive to Isoniazid & Rifampin, dont use Ethambutol anymore. Continue for 6-9 months or 3 months if (-) sputum culture. If needed continue txt for additional 4 to 9 months with Rifampin & Isoniazid & Disseminated TB: same as above but for 9months B)Latent TB: 1)use 1 med to kill bacteria & prevent activating TB 1b)Isonizaid 9 months or use option 1a)Rifampin 4 months 2)2 drug therapy: 2a)Isoniazid & rifapentine weekly 3 mos 2b) Isoniazid & rifampin daily 3 mos C)Pregnant pts with TB:--> isoniazid tetraogenetic & need PYRIDOXINE/Vit B6 when taking isoniazid to prevent peripheral neuropathy C1) Rifampin, Isoniazid, Ethambutol (2months) C2) Isoniazd & rifambin (7months) Rifampin: orange secretion Isoniazid: hepatitis & PNS Pyrazinamide:hepatitis, uric acid in blood Ethambutol: optic neuritis. ROSH: LABs Definitive DX: PPD for latent TB or primary TB Sputum smear acid fast bacilli is gold standard for active/reactive TB. CXR: apical Cave or cavitation

Asbestos

PPT

Bacterial PNA xray

PPT

Infant Respirartory Distress Syndrome (RDS) aka Hyaline Membrane Dz different from Adult Respiratory Distress Syndrome (ARDS)

The alveloli of the lungs have epithelial cells called Pneumocytes with different functions. Pneumocyte Type 1: make large surface area & thin for gas exchange Type 2): make surfactant to reduce surface tension in order for alveoli to expand open. Cytokines responses (ex: lung injury or accident) has TNF-alpha or interleukin 1 responses cause inflammation response to alveoli. The damage alveoli impairs surfactant making alveoli leaking and forming blood clots that dead cells & protein fluid floating around develop into Hyaline Membrane. The blood flow around alveoli is working, but the damage alveoli cant expand to do gas exchange. If uncomplicated After alveoli heals itself, If complicated: >sometimes alveoli can develop fibrolin from fibroblast which can progress into "Restrictive Lung Dz" >babies with Patent Ductus Arterious are higher risk >Possible develop PNX >B1) If injury is caused by gastric contents (stomach), ACID causes inflamation aka "Pneumonitis"--> fever, tachypnea, cough/wheeze >C1)If caused by foreign artifact/object--> PNA, actelatasis, bronchiectasis, abscess in lungs. S/S: SOB Hypoxemia, Hypercapnia, hypoxia (no gas exchange) --> become blue/cyanosis. Since no breathing/apnea--> pT Trying to breathe (faster or tachypnea) with muscle retraction GRUNTing & nose flaring. The damage alveoli may develop pulmonary Edema since build up of cells inside alveoli. Labs: CXR: Sign1)atelecatasis or ground glass haze can be due to hyaline. Ground glass is a general term that encompasses a lot of different things. Sign2)if Severe progression shows Lung field White out (airless) b1)If caused by gastric acid: patchy capacities c1) you can see foreign object, MC right side (since straight shot)--> further bronchoscopy for DX. 4 criteria for DX: can choose 1 1)Acute (occuring less than 1 week) 2) White out in BOTH lungs (maybe caused by edema) 3) PFT less than 300mmHg Calculated by dividing O2 arterial/inspired air. (ex: Pa02/ Fi02) if less than 300 then (+ sign) 4) Check Respiratory stress source (RDS shouldnt be from heart since its caused by damaged Alveoli) Cathether Wedge measures BP in "pulmonary artery" to make sure Pulmonary BP should be normal. High pulmonary BP means caused by Heart Failure. ARDS pulmonary BP is normal in pulmonary artery and not due to Heart Failure. Tx: Premature babies can be given "Betamethaosone" to make surfactant & give 02 ROS: s/s:premature baby complains of breathing hours after birth. Labs: DX made clincial & radiograph CXR:ground glass appearance txt:02, intubation, CPAP, surfactant

Granulomatosis w/Polyangitis aka Wegener's Granulomatosis (WG)

2 types of host immune cells (Bcell vs. Neutrophils) attack each other. If cANCA present--> cause relapse. Neutrophil has released these granules called "anti-neutrophil cytoplasmic antibodies" aka ANCA (IgG). This causes Bcells to release "cytoplasmic anti-neutrophilic cytoplasmic antibodies" aka (cANCA). The cANCA binds to another neutrophil granule receptor called proteinase 3. cANCA bind to proteinase 3 to release oxygen free radicals. These radicals damage the endothelial cells (ex:lungs) causing vasculitis. (this inflammation damage can be seen as a granuloma on Xray). MC: middle age males' A)Nose&pharnyx (nose first sign usually) B)lungs C)kidneys s/s: A1) sinus inflammation & pain, bloody mucous, cruting, stuffy nose. A2)saddle nose deformity, cave in. A3)Mouth has strawberry gingivitis, loose teeth, mouth ulcers. trachea narrow/constrict B1)inflammation on blood veseels that pass through the lung & inflammation on the lung itself causes narrow airway. --> SOB B2)Ulcer-->blood cough B3)lung nodules "Coin Lesions" C1)Kidney no longer good at regulating blood volume because the blood is restricted in the Glomerulus. --> decrease urine output so more liquid in body increases BP. TxT: Corticosteroids & Cyclophospamide

No cell wall, peptidoglycan

>no gram stain >resistant to penicillin & Beta-lactam antibiotics: b/c they attack cell wall. >need tetracycline & erythromycin.

PNA labs

>urinary antigen test for S.Pneumonia legionella. >mild eosinophilia with infant C.trachomatis PNA >blood culture samples: if cold agglutin present in peripheral blood samples --> Mycoplasma PNA. WBC: slightly high for virus VS.. very high for bacteria (neutrophils over 20,000) >blood cultures are usually used to determine cause of PNA. Sputum culture can sometimes help. >Sputum gram stain & urinary antigen test for certain bacteria PNA like streptococci or Legionella, buttt Rapid Antigen test for Flu VIRUS. Definitive Diagnosis DX: physical exam signs & CHEST XRAY required. ****Above is CAP ****Below is Hospital AP all hospital pts need CBC & CMP ABG --> if pt has hypoxia CXR: used to assess severity & progression of dz. CT: more sensitive. CXR & CT can DX PNA, just not the type of pathogen. thoracentesis: if pleural effusion or empyema present--> for pleural fluid analysis. bacterial PNA: shows lobar consolidation or round pleural effusion????? Viral PNA: streaky & diffuse infiltrates of inflammation of bronchi. HYPERINFLATE Atypical PNA: interstitial marking or inflammation bronchi Hilar lymphadenopathy: signs of tb or histoplasmosis, UNCOMMON in bacteria PNA.

Kyphoscoliosis (type of restrictive lung dz)

A combo of kyphosis & scoliosis--> MSK disorder leads to under-ventilation/Reduced lung volumes Causes:anything that makes spine abnormal >most common cause for "secondary kyphoscoliosis is from a neuromuscular dz b/c it progresses to lung muscle weakness from the myalgia & quadriplegia OR cant control lungs properly due to infection or nerve damaged. (ex:polio, muscular dystrophy, CP) >other causes: a)fibrin in thorax b)Large effusion c)morbid obesity d)ankylosing spondylitis If Kyphoscoliosis appear in younger than 35 then asymptomatic. If Middle age pt--> SOB, decrease exercise tolerance, and respiratory infections. S/s: just check the spine curvature. Diagnosis DX definitive: Decrease tactile fremitus, dullness on percussion, decrease breathe sounds. >If Kyphoscoliosis caused by neuro problems--> accessory muscles, rapid shallow breathes, paradoxical breathing. TXT: surgery if Total lung capacity under 50%.

Mycoplasma pneumoniae aka walking PNA

Atypical- b/c no sputum & show extrapulmonary symptoms (things you can see like dry cough) OR ASYMPTOMATIC myco-fungi, but actually a bacteria pathogen causing PNA that happens really slowly- "hence the name myco", plus related to cold agglutin dz. Can resist antibiotic & survive INTRACELLULAR making it persistant. Free-living bacteria that passes person to person through respiratory droplets. No peptidoglycan cell wall. Instead has a cell membrane with sterols from the host intracellularly. This sterol means it requires special "Eaton agar" mc: adolescent & many ppl bunched into small areas. College students & military recruits.Often Community acquired PNA. Peak summer or late fall. if it has IgM antibodies attack rbc causing lysis/blow up--> Hemolytic anemia. s/s: headache, low fever, malaise, sore throat, cough (+/-) wheeze/rales, Chest pain on breathing, SOB, hypotension, hypoxemia. xray: bilateral patchy diffuse infiltrates localized in interstital areas. Reticular nodular or patchy instead of large nodes. Labs from Respirtatory ID ppt: blood culture samples: if cold agglutin present in peripheral blood samples & confirmed by PCR --> Mycoplasma PNA. tx: Empiric-what you think is best or most common for your specific pt ex:alcohol PNA. Not just most common bacteria PNA unless it is. A)First line: macrolidqe or fluorquinolones B)Pts in hospital, but not ICU: >fluorquinolone >Beta-lactam + Macrolide C)If specific M. pneumoniae strain--> macrolide & tetracycline &fluorquinolone ROSH: gradual increase in nonproductive symptoms & dry cough. LABs:Patchy infiltrates

Coccidioidomycosis

C in california, southwest. Rainy period bacteria is smaller in size so can get into upper respirtaroy tract & infect lower respirartory anatomy Grow spheres->segment->rupture--> form granuloma except with dissemination s/s:ereythema nodosum, fever, chills. HA, neckpain, arthalgia, CNS involvement Meningeal signs disseminated: filipino & pregnant women CBC: leukocytosis & eosinophila ELISA: IgM CSF: lymphocytsos, reduced glucose, complement fixing antibodies. CXR/CTscan: Right upper lung nodular infiltrate tx: do they have symptoms or not? a)yes progressing symptoms: Amphotericin B & Azoles(mild) Fix Titers

Antibiotic ladder onlinemed PNA

CAP: 1)(PO) Azithromycin if pt can walk & leave same day 2)(IV) Ceftriaxone & Azithromycin-->is the equivalent to moxifloxacin, so if pt needs IV meds you give them this. 3) Moxifloxacin: but can breed fluoroquinolone resistance if we dont use Ciprofloxacin first so we usually dont use Moxi. HCAP: worry for MRSA & Pseudomonas 1)Vancomycin & Piperacillin/Tazobactam Vancomycin is good for mrsa pseudomonas Pip/Tazo:has gram +, -, and anaerobic converage. Doesnt have MRSA & fungus. very broad spectrum aka Pseudomonas.

Rosh:PNA, Flu, bronchitis, PNX, PE

CAP: sudden cough-Rales, fatigue, FEVER. 1)Atypical PNA-mycoplasma: pt shows symptoms of cough, fever but vital signs are normal--> Azithromycin Pseudomonas: COPD, CF, alcoholics: FLu: Sudden Fever & Myalgia, cough sore throat, chills, HA heals by itself but 48hours oseltamivir. Bronchitis:Cough(more 5 days/week)-->wheeze/"Ronchi", lower lobe xray. PNA:tall & thin ppl, SOB & chest pain, Decrease BReATH sounds unilateral;hyperresonant percussion Pleural Effusion: decrease breath sounds & tactile fremitus. Dull percusion.----> severe:--->: Pulmonary Embolism:SOB & fast breathing COPD:all should have a SA broncho dilator chronic cough, long time smoker, --> LAAC (tiotropium) COPD exacerbation: azithromycin & oral predinosone 2 terms that use to be incorporated with COPD. 1) Chronic Bronchitis: productive cough for 3 months 2) Emphysema: enlarge terminal bronchiles & fibrosis Asthma exacerbation: oral prednisone Carcinoid Syndrome:skin flushing, wheezing cough, Diarrhea TB active:RIPE tx-Miliary xray pellets Tb latent: Isoniazid Pertussis: stuffy nose, cough, low fever, Bark cough-Azithromycin/macrolyde. Cystic Fibrosis:Recurring URI, LOW BODY WEIGHT SOB, cough/wheeze

Deep Vein Thrombosis (DVT) increase risk factors

Virchow's Triad 1)slowed blood flow (stasis)--> so areas where blood isnt moving but just coming in contact with the vein endothelial, the platelet/clotting factors form a clot to develop. 1a) normally blood flow is consistent, but if blood flow is turbulent, as in some places of blood goes fast then that means other spots are slower. 1b)during long inactivity: in bed, car trips, pregnancy kid pushes on vein 2)Hypercoagulation: is alter ammount of clotting factors (increase) 2a)genetics 2b)surgery- damage increase more clotting to form 2c)medications-Birth control increase clotting factors but decrease coagulation factors (protein C & antithrombin. 3)Damage to blood vessel endothelium 3a)infections, chronic inflammation 3b)tobacco

Hypersensitivity pneumonitis aka Extrinsic Allergic Alveolitis

When the immune system abnormally OVERreacts to an inhaled Antigen causing Inflammation in the lungs. (repeated inhale/exposure) An allergic bronchiolitis caused by multiple allergens. Antigen/foreign particle goes down the trachea airway to the lungs and end up in the alveoli where gas exchange occurs. At the alveoli, a "alveolar macrophage" picks up the antigen with a MHC Class 2 receptor & moves it to the nearest Lymph node. Inside the Lymph node, a Naive CD4+ "Helper T-cell" binds to the antigen becoming "mature". Once Helper T-cell is mature--> it can stimulate more a)T-cells b) B-cells c)Macrophages 1) Type 3 Hypersensitivity [hrs]: The B-cells can make IgG antibodies into the blood. The foreign antigen in the alveoli meets the IgG antibody in the blood as well and bind to form "rough immune complexes" and deposited @ basement membrane.--> A complement system (9 proteins pf C1-C9) create a enzyme cascade (multiplyer effect). The c3,c4,c5 fragments made at the end attract Neutrophils. Neutrophils degranulate (release lysosome & Reactive oxygen compunds aka "ROS")--> causes Alveoli & capillaries to inflammation & necrosis. 2) Type 4 Hypersensitivity [2-3 days]: Antigen/foreign particle attracts Helper T-cells(peripherally) & Macrophages (center) come together and surrounding foreign antigen, thus forming (aka granuloma). --> 2a)If antigen removed then the lung tissue heals itself & all is normal. 2b) If antigen not removed, so the antigen is still exposed to the body, then the alveoli becomes damaged overtime due to chronic inflammation. Chronic fibrin tries to heal alveoli when there is less elastin, thus alveoli becomes more stiff & less compliant. ---> Restrictive lung dz. S/S: >Acute (days-wks): Fever, SOB, chest pain, headache *PPT: After a couple of hours of exposure--sudden onset of malaise, fever, chills, SOB, cough, nausea. >Bibasilar crackles, fast heartbeat, cyanosis. B) Chronic (Months to Yrs) > symptoms get worse over time. for example long period of SOB Respiratory failure. LABS: >CXR: diffuse infiltrates >Abnormal PFT >Bronchoalveolar Lavage (fluid squirted from nose mouth into lungs) then analyzed for high values of WBC & Mast Cells. >Biopsy lung tissue: if type 4 Hypersensitivity have granuloma & lymphocyte in alveoli. >Inhalation challenge to try & Identify antigen *PPT Acute: CXR: small nodules not at Apices & Bases, High WBC, low blood oxygen, (+) hypersensitivity. >Subacute: No fever/chills. Longer time cough, SOB, weight loss & not hungry/anorexia. CXR:lung fibrosis white nodes in lower lungs Biopsy: fibrosis vs. noncaseating granuloma. >Chronic: No hx of acute symptoms????, slow onset??? partial recovery??? CXR:fibrosis & nodulars in lower lungs. Biopsy: fribrosis & noncaseating. txt: >can be reversed if Dx/identified early. Avoid the negative stimulus antigen by avoid/change environment or wear PPE. >Oral Steroids can help symptoms, but not txt issue. Taper doage 4-6 weeks. Caused by a variety of "organic antigens" aka fungal, bacteria, protozoan, & Reactive chemicals???? a)Farmer's Lung--> actinomycetes in Hay b)Bagassosis-->actinomycetes c)Grain handler lung d)Humidifer: e)Bird Breeder f)Cheese worker g)Malt worker h)paprika spliter i)wheat weevil j) Mollusk shell

Adenocarinoma

a malignant tumor that originates in glandular tissue lepidic growth pattern: grows along intact alveolar walls.

empyema, pyothorax

accumulation of pus in the pleural cavity Stage 1) Parapneumoia/exudative stage: increased permeability of inflammation & swollen pleural surface. Correspond to uncomplicated parapneumonia effusion Stage 2) Fibrinopurulent stage: True empyema or complicated effusion because fluid initally clear but then heavy firbin deposit in parietal pleura. Stage 3) Chronic/organizing stage: infection collagen buildsup & then mature/ turn into a peel . The thickening restricts lung movement & leads to trapped lung & fibrothorax tx:observe drainage-thoracentesis,pigtail catether,chest tube SUrgery: decortication/debridement, chronic drainage procedure.

Pneumocystosis (atypical) HIV

aka Pneumocystis carinii (PCP) Pneumocystis jirovecii (PCP) organ transplant, already sick pt, hiv, s/s: maybe weight loss, fever, SOB-tacypnea, dry cough- bibasiler crackles, spontaneous PNX *no culture, bronchoalveolar lavage, ABG (low O2 & Co2) hypoxemia & hypocapnia CXR: patchy heterogenous miliary infiltrates******** CT: coronal septal thickening (ARDs & bacterial PNA) tx: first line bactrim**** 2nd:Primaquine & Clindamycin ALternative: >Dapsone & Trimethoprim >Atovaquone, >Clindamycin + Pentamidine >Prednisone for AIDs pt ROSH: mc in HIV/weak immune system. s/s: sudden dry cough & unexplained fever for 2 weeks, chest pain fatigue. Lab: High LDL means dz is worsening CXR: Bilateral interstial infiltrates aka Bat Wing & ground glass CD4: under 200. >Diagnosis definitive; bronchoscopy-->bronchoalveolar lavage. IF severe PCP conditions: PaO2 less than 70mmHg = SPO2 under 93%--> txt with steroids before antibiotics. Dapsone side effect--> Hypoxia.

Pickwickian syndrome (OHS)

aka obesity hypoventilation syndrome (OHS) usually affect obesity ppl that has poor breathing due increased mechanical load on diaphram or neck (too fat for body to breathe). MC: sleep apnea Diagnosis DX Definitive Distinguishable: voluntarily breathing fast or hyperventilate can help normalize status sometimes. This technique does not work for COPD. TXT: 1)weight loss, 2)Non-invasive positive pressure ventilation (NIPPV), 3)respiratory stimulants drugs aka increase better breathing 3a) theophylline, 3b) acetazolamide, 3c) medroxyprogesterone acetate

Cryptococcsis

can be found anywhere crypts are sick-->give flu Pt originally goes in for granuloma and finds on xray--> identify cryptococcosis. a pt who has been through long term steroids, blood/organ transfer pt, cancer, hiv, poor. Pulmonary: SOB, chest pain, cough sputum CNS: meningeal signs (fever, HA, neck pain, memory change, lethargy) tx: host immune system & infection site 1a)If pt is healthy: pulmonary infection tx: fluconazole 1b)extrapulmonary infection: fluconazole mouth & amphotercin B IV 1c) CNS infection: IV amphotericin B & FluCYtosine mouth if pt is sick: a)Pulmonary & extrapulmonary: fluconazole begin & lifelong possible Flucytosine CNS:Fluconazole & IV Amphotericin B dead soon: intracranial pressure, older age, organ failure, decreased mental status, dz

"Eosinophilic" granulomatosis w/ Polyangiitis (EGPA) aka Churg- Strauss Syndrome

caused by P-ANCA "Peri-nuclear anti-neutrophil cytoplasmic antibodies Rare autoimmune dz that causes inflammation of small & medium blood vessels (vasculitis). Pt has a pmhx of allergic hypersensitivity of the AIRWAY. 3 stages:(no progression order) 1)Prodromal: has allergies (nose mc) & asthma --> possible systemic steroids. 2)HyperEosinophilia: a lot of eosinophil causes tissue damage in lung & GI. 3)Vasculitis that is life-threatening b/c reduced blood flow to organs, blood clots/infractions. shared s/s: >sinusitis, lung & kidney damage which can be mistaken for asthma or allergies. Nose can be runny or congested. >GI, skin, nerve & heart damage. **** Labs: High # of Eosinophils, thats why asthma/allergic pts have a inclination to develop Churg-Strauss. >Granulomas can form DX criteria (4 out of 6 needed): "Eh-pain" >Eosinophilia (high # blood) >Histology shows eosinophil >ParaNasal sinus abnormal >Asthma >Infiltrates in the lung >Neuropathy, nerve damage dz txt: usually rheumatologist but can involve pulmonologist. First line: Mepolizumab >Glucocorticoid steroids like prednisone >Azathioprine >Cyclophosphamide If in remission: >Azathioprine or Methotrexate

Pnuemonia (PNA)

normally the lung works by having air pathway down trachea, bronchi, then alveoli. Microbes/pathogens that enter body face obstacles like coughing, mucocilary escalator(lining of bronchi that traps and removes particles), and macrophages in alveoli. --> If microbe survives through all that and infect bronchi or alveoli then you have PNA. PNA microbes invade the lung tissue causing inflammation accumulate: proteins/WBC/rbc and Fluid. This infection in the lungs brings water--> breathe difficult.

Lung Cancer

early s/s: asymptomatic nodule or mass late s/s: symptoms present on mass Pulmonary s/s:SOB,cough, wheeze/stridor, hemoptysis PNA s/s: postobstructive PNAor atelectasis or lung abscess. Fever, chills, chest pain, sputum production s/s:endocrine, Metasis CNS, bone, liver/adrenal, skin, anorexia, weight loss Labs: 1)Nonivasive: >chest roentgenogram or chest x ray, CT/PET scan, MRI, bone scan ROSH: annual low dose chest CT scan for assessing smokers Lung cancer risk. 2) Invasive: >Sputum culture (3 samples needed for accuracy), >bronchoscopy good for central lesions not peripheral unless fluorescence >transthoracic needle aspiration/core biopsies (PNX risk) >Endoscopic bronchial ultrasound (EBUS)- balloon inflate/deflate >navigational bronchoscopy:locate lung nodule in 3D system >mediastinoscopy: transcervical mediastinoscopy, rigid scope in mediastinum anterior to trachea >Video assisted Thoracic surgery(VATS) Lung Cancer staging:TNM classifications aka classification of malignant tumors (slide 77 & slide 78 Nodes) 1)Non-small cell lung cancer (NSCLC) 2)Small cell lung cancer (SCLC) Simple Cancer stages: 1)Cancer confined to lung tissue with no involved lymph nodes 2)Cancer confined to lung tissue with involved surrounding tissue or lymph nodes 3)Cancer confined to lung tissue & involve adjacent structures & lymph node within mediastinum 4)any lung cancer spread to opposite lung, other organ, disseminated in pleural fluid. Difficult to stage b/c: lesions, nodules, enlarge lymph, false positive imaging. what are digit stations????? ROSH: s/s: cough most common, chest pain, sob, blood cough. Hip/back pain, Horner sydnrom, Hypotension with tachycardia. Labs : Exudative effusion (so protein stuff & malignancy) Hypercalcium

Goodpasture Syndrome GPS

is a rare autoimmune dz that affects lung & kidney (usually lung symptoms appear first). Eventually blood in lung & kidney. MC in White males 20-30yos. The Basement Membrane is the layer of protein that keeps the skin cells/epithelium in place in every organ. A component of the basement membrane is collagen. Collagen comes with many different types based on the differnet combination of DNA collagen chains (alpha 1 through 6). Collagen type 4 (most common in lungs & kidney basement membranes) is that is made up of alpha 3, 4, & 5 form a triple helix. GPS auto-antibodies (IgG) attack own cells alpha 3 part of the helix via Hypersensitivity 2 mechanism. --> The IgG antibodies are a immune response that normally fights off microbes, but in this case attack own's body collagen. IgG signals a complement system (a cascade), that brings in cascade protein (C1) to cleave alpha proteins 3,4,5 to serve as Chemotactic agents. Alpha protein 3,4,5 are chemotactic agents, meaning their cleaved bodies stimulate more neutrophils to arrive and fight infection. Neutrophils release peroxidase, myeloperoxidase, proteinase enzymes which are also Free Oxygen radicals that damage the basement membrane in Collagen type 4 specific alpha-3 collagen DNA portion of the helix. (kidney & lungs). S/S: Chest pain, cough, SOB, blood cougg/ HTN, blood & protein in urine., Edema swelling on face/limb LAB: diagnosis via Biopsy (especially kidney). positive for "anti-GBM antibodies"--> note Cytoplasmic AntiNeutrophils antibodies in bloodstream is an early indicator. txt: Long term dialysis or die from kidney failure/lung hemorrhage. Plasmapheresis ImmunoSuppressant drugs: CycloPhosPhamide Prednisone Rituximab Maintenance: Azathioprine

Pulmonary Embolism

is a type of blockage in the blood due to a clot. Clots happen all the time in the body, but usually large clots that form in large vessels/veins can form in important areas like the heart or lungs/bronchi. Pulmonary infarction is the death of tissue in an area of the lung due to a Pulmonary embolism clot. "Pulmonary embolism" is the blockage of the pulmonary artery in the heart that will send blood out of the right ventricle and into the lungs. Normally superficial veins drain into deep veins (DVT, popliteal, femoral, iliac) by muscles pushing blood forward pass 1-way valves to eventually reach the heart (inferior or superior vena cava). If a moving clot aka "Thromboembolus" is pushed along the bloodstream and eventually reaches the heart it can affect 1)pulmonary saddle/ middle portion of pulmonary artery that splits direction of R/L lung. aka Saddle Embolism is INSTANT DEATH or decrease cardiac output since oxygenated blood cant be pumped to the rest of the body via problem with R.ventricle, this is called "Car Pulmonale" and can progress into Heart failure. 2)cause stroke if a pt has "Atrial septal defect" (hole between R & L atrium so no need to go to the lungs via pulmonary artery but instead exits the left ventricle that pushes blood to other areas of the body aka brain. Embolic stroke Multiple embolisms (even small ones) forming over time increases BP aka Pulmonary HTN/R.venticle failure. Large embolism: sudden & severe chest pain, SOB, fatigue Small embolism: can have no symptoms LABs: D-dimer blood test- detects fibrin breakdown products that usually occur when there is a blood clot. SINUS TACHYCARDIA ROSH: Hampton's hump, wedge on the outside border of lung.,

large cell carinoma

no gland formation, large bizarre cells, no keratin pearls or intracellular bridges