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485 Cards in this Set
- Front
- Back
Tell me all about Isoniacid
|
highly-effective
inexpensive eliminated by acetylation SE: liver, periph neuorpathy |
|
Tell me all about Rifampin
|
highly-effective
BUT expensive Eliminated by cytP450 SE: liver, inc. metabo of other drugs, like oral coags, contraceptives, skin rashes, and urine may go orange |
|
Tell me all about Pyrazinamide
|
highly-effective INTRACELLULARLY
SE: Liver, hyperuricemia |
|
Ethambutol
|
not active intracellularly
SE: RETROBULBAR NEURITIS |
|
Streptomycin
|
parenteral admin, so rarely used
aminoglycoside, affects ribosomal protein syn NOT active intracellularly SE: oto- and nephrotoxicity- ALL AMINOGLYCOSIDES have this, and must check with audiograms to make sure people are not losing their hearing by taking this drug |
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What percent of patients will have active TB?
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10%
|
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Of the active TB patients seen, how many will progress within the first 2 years? (Progress means to see caseating nectrotic airways, very sick people with cough and malaise. Defined as going from INFECTION to DISEASE because of an inability to contain the infection.)
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HALF will progress (50%)
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If you're HIV+, what's your risk of TB going infection --> disease?
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8-10% ANNUALLY
|
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Up to 20% of positive TST are FALSE POSITIVES, what are the possible causes?
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Ifx with mycobacteria other than TB
or BCG vaccine |
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Up to 20% of individuals with active TB may be FALSELY NEGATIVE, what are the most common causes?
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1) critically ill TB patient
2) Immunosuppressed person 3) Recent TB infection |
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What kind of testing do you want to do for TB?
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targeted testing, based on the idea that the accuracy oft he test depends on the prevalence of the disease in the population you're testing
|
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Goal of targeted testing in TB?
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identify persons at high risk for TB who would benefit by treatment of LTBI
|
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What are 2 things that put people at higher risk of TB disease?
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1) recent ifx with Mycobacterium Tuberculosis
2) presence of clinical conditions that are associated with an inc. risk of progression of LTBI to active TB |
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TST in positive if you're in the Risk group, and your induration is...
|
>/= 5mm
-HIV+ -recent contacts of TB case -fibrotic changes on chest radiograph consistent with old TB -patients with organ transplanta and other immunosuppressed patients receiving equiv of >15mg/day prednisone >1 month (corticosteroid >1month treatment increases the risk). |
|
What populations fall in the TST >/= 10mm induration as a positive test?
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-recent arrivals- <5yrs- from high prevalence countries
-IVDUs -residents and employees of high-risk congregate settings- i.e. prisons, jails, nursing homes, hospitals, residential facilities for AIDS patients, and homeless shelters -mycobacterial personnel -persons with clinical conditions increasing their risk -children under 4 and adolescents exposed to adults that are at HIGH risk |
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What populations fall in the TST >/= 15mm induration as a positive test?
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Persons with no risk factors for TB, but DO NOT TEST THIS POPULATION
|
|
STD of care for community in LTBI patient?
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Isoniazid daily for 9 months.
|
|
Signs/Sx's of TB DISEASE:
|
fatigue
malaise weight loss fever night sweats cough hemoptysis "Patients say they had it for weeks/months/years" |
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CXR in Dx of TB:
|
-95% of cases have abnormalities in apical/posterior segments of upper lobe, OR superior segments of lower lobe
-poss. unusual appearance in HIV+ pt. -CANNOT confirm Dx of TB |
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How many HIV+ patients have normal CXR?
|
30%!!!
|
|
How do you Dx TB?
|
-AFB smear
PROBLEM: not sensitive OR specific Instead, do MTB test! |
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What do you do to TREAT TB Disease patients?
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4 drugs:
INH Rifampin Pyrazinamide Ethambutol |
|
Summary of XDR-TB Conclusions:
|
1) HIGHLY lethal
2) resistance in most cases due to transmission of XDR 3) suspect nosocomial spread |
|
3 key enzymes to HIV
|
1) integrase
2) reverse transcriptase 3) protease |
|
Discuss the copathogenicity of TB and HIV
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1) TB causes IFN-gamma release from T cells, TB-activated macrophages release TNF and IL-1, BOTH of which enhance viral replication (TB ACCELERATES HIV)
2) one year mortality rate for treated HIV-related TV: 20-35%, 4X higher than HIVnegative patients |
|
How do you treat pulmonary complications of HIV, ideally?
|
via a DEFINITIVE microbio/patho diagnosis, over empiric therapy, whenever possible
|
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What are the 4 Influences on Risk of Developed HIV-Assoc Pul Disorders?
|
1) severity of immunosuppression
-CD4 count 2) patient's demographic charac -how you catch your HIV helps w/ prognosis of assoc disease 3) place of current/prior residence -What bugs are THERE???? 4) Wherther using prophylaxis against common HIV-associated infections and HAART -MOST IMPORTANT |
|
HIV-Assoc Pul Disorders:
|
Gay HIV+ men less likely to devo TB and bacterial pneumonia
-blacks, hispanics, and IVDUs more likely to get TB -Whites more likely to get PCP, KS, CMV |
|
Where do you most often see histoplasmosis?
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Ohio and Mississippi River Valleys
|
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Where do you most often see coccidiomycosis?
|
Southwest
|
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Prophylaxis and HAART have helped to decrease what two HIV-Pul associated diseases?
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PCP and TB
-NOTE: HAART reduces the incidence of ALL opportunistic infections |
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What is one indication of doing an HIV test because it might be the first presentation?
|
recurrence of bacterial pnemonias
|
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Despite the availability of an effective prophylaxis and HAART this DISEASE is still the most common AIDS-indicator infection and an important cause of respiratory illness and death among HIV infected individuals?
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PCP!!!
|
|
PCP Presentation
|
-insidious
-gradual progression of SOB, fever, dry cough over weeks, but could also be seen as a rapid development over days -MOST COMMON CAUSE of ARDS in patients with HIV |
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What's the test used to rule out PCP, for the most part?
|
LDH test, if it's not high, it's UNlikely to be PCP
|
|
Agent of choice for Tx of PCP?
|
Bactrim
-may need to start steroids too to calm down inflammation they're seeing |
|
HIV+, CD4 <200, what is something you do?
|
prophylaxis with Bactrim to hopefully prevent PCP
|
|
What is the key to a CMV diagnosis?
|
Owl-eye appearance of the cells
|
|
What would you like to see to Dx as CMV?
|
-it can be seen in a non-pathogenic situation, so to confirm it as the culprit, would prefer to see tissue invasion and inclusion bodies
|
|
How do you treat CMV?
|
-HAART to restore immune fucntion
-ganciclovir or foscarnet, too |
|
Most common site of infx for cryptococcus neoformans?
|
meninges
-Dx est. by seeing organisms on lung specimens but HIGH cryptococcal Ag titer on BAL may be suggestive; thick-walled organisms on an india ink stain |
|
Histoplasmosis
|
-endemic areas, so see people from those areas in order to consider this
-may see miliary pattern on CXR TREAT: amphotercin B, if more localized seen, then you may use itraconazole |
|
Aspergillosis
|
-VERY immunosupressed to see it there
-rare in AIDS, but it's dreaded again, wanna see tissue invasion to Dx, and tissue inflammation as a result is as bad as, if not worse, than the fungus itself |
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Key to aspergillosus Dx?
|
45-degree branching hyphae on the slides
|
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Where do you see blastomycosis endemic?
|
midwest US, sotuhwest US, and Canada
-Dx with organism isolation -treat with Amphotercin B -SAME AS coccidiomycosis |
|
Kaposi's
|
-most ocmmon malignancy in patients with HIV
-skin most common presentation |
|
What usually causes an ACUTE pneumonia?
|
bacterial in origin
manifests intraalveolar exudate |
|
What usually causes a CHRONIC pneumonia?
|
-viral, "atypical", intracellular bacteria, nocardia, actinomyces
-manifests as interstitial or granulomatous |
|
Pneumonitis, usually not infectious. What are they?
|
Usually toxins or sometimes "atypicals"
|
|
4 stages of pneumonia, assuming all goes well:
|
1) congestion
2) red hepatization 3) grey hepatization 4) resolution |
|
CHARAC of Congestion Stage of Pneumonia
|
heavy- red and boggy, airless, with vascular congestion
-see proteinacious exudate, few neutrophils, and intraalveolar bacteria |
|
CHARAC of Red Hepatization Stage of Pneumonia
|
-firm, red, airless
-feels like a liver |
|
Define Bronchiectasis:
|
PERMANENT dilatation of bronchi and bronchioles due to destruction of muscular layer and supporting connective tissue resulting from CHRONIC NECROTIZING INFECTIONS
-Clinically presents as a severe persistent cough and production of copious amounts of purulent sputum |
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Define an abscess:
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localized collection of supprative necrosis within pulmonary parenchyma--> 1 or more LARGE cavities
|
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How does necrotizing pneumonia differ from an abscess?
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-nectrotizing pneumonia is a SIMILAR PROCESS TO AN ABSCESS, with multiple small cavitations
|
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Abscess is usually often a result of acute bacterial pneumonia, often caused by one of what 3 organisms?
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1) K. pneumonia
2) P. aeruginosa 3) S. aureus |
|
Atypical or Chronic Pneumonia CHARAC:
|
Bugs:
-MYCOPLASMA -legionella -viruses -chlamydia -fungi Gross: red-blue AND congested, patchy OR lobar Complications: Diffuse alveolar damage, which is also seen in ARDS -see thickened/edematous interstitial infiltrates that are lymphocyte rich (VARIES from typical/acute because those are alveolar in nature) -difficulty breathing because of very poor air exchange |
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What is is Histoplasmosis similar to clinically?
|
it mimics TB
-fibrotic granulomas, veyr lamellar lookings see epithelioid histiocytes to define it as a granuloma -lamellar-ness is JUST A CLUE, need to find the bug! |
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ANYTHING GRANULOMATOUS, what tests do you definitely do?
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AFB (acid-fast), GMS/PAS (fungi) stains
|
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Aspergillous is highly invasive, especially in...
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LUNGS
|
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What is CHARAC of PCP on an H&E?
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-see the fluffy, cotton-candy like intraalveolar eosinophilic exudate
-with silver stain, see TONS of organisms |
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CMV CHARAC on a slide...
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-interstitial pneumonia, owl-like inclusions within the cell
|
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Why are the upper part of the lower lobes OR the lower part of the upper lobes the main locales for TB ifx?
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thought to be because of the oxygen tension in those areas
|
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Ghon focus
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area of caseating necrosis within the lung
|
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Ghon complex
|
area of caseating necrosis PLUS hilar adenopathy
|
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Secondary TB affects what part of the lungs?
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usually the apices
HIGHLY-CONTAGIOUS now |
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If pneumonia is acute, what's its cause and what pathology do you see?
|
bacterial
AND intraalveolar exudates |
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If pneumonia is chronic, what's its cause and what pathology do you see?
|
viral, "atypical", fungal, intracellular bacteria, Nocardia, Actinomyces
AND interstitial OR granulomatous |
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Pnumonitis is caused by...
|
a toxin
OR "Atypical"- interstitial findings; usually it's not infections though |
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Bronchopnemonia means
|
more than one lobe and it's patchy
|
|
Lovar pneumonia involves...
|
part of whole of one lobe, and that's how you see >90% of Strep. Pneumonia
|
|
What kind of pathology do you see with Histoplasmosis?
|
noncaseating/fibrotic granulomas with a lamellar arrangement
|
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What stain is used on aspergillosis?
|
GMS or silver stain
|
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What kind of histological finding do you see with PCP that is somewhat unique?
|
cotton-candy appearance
-using the GMS stain there to visualize the bugs |
|
CMV has what unique histo finding?
|
owl-eye intranuclear inclusions
|
|
Ghon focus is a...
|
primary lesion caused by mycobacterium bacilli (tuberculosis) developed in the lung of a previously uninfected individual.
|
|
What do you use to stain for Mycobacterium Avium Intracellulare
|
Acid-Fast Stain
-it's uncommon if you're immunocompentent, BUT in AIDS patients it causes disseminated ifx's |
|
What are the 5 causes of hypoxemia?
|
1) V/Q mismatch
2) low FiO2 3) diffusion barrier (almost never a cause at rest) 4) shunt 5) hypOventilation |
|
If you are talking about a suspected COPD patient, but they lack obstructive disease, what do you make as the diagnosis?
|
chronic bronchitis SOLELY is the diagnosis.
|
|
What are the main drugs used in obstructive lung disease?
|
bronchodilators
anti-inflammatory agents, ESPECIALLY glucocorticosteroids mucoavtive agents and antimicrobials |
|
Distinguish between Asthma AND COPD:
|
Obstruction:
Asthma- REVERSIBLE COPD- Poorly reversible Inflammation: Asthma- CD4s and Eosinophils COPD- CD8s, neutrophils, and macrophages |
|
In COPD describe the mechanism of destruction of lung tissue:
|
inflammatory cells, mainly neutrophils and macrophages, act via proteases and ROS to:
1) destroy lung tissue 2) create mucus cell hyperplasia and hypersecretion |
|
In asthma, what's the mechanistic basis of constriction?
|
ROS and eosinophils are acting on the epithelium and smooth muscle.
-vagus nerve is affected too |
|
What do methylxanthines do for asthmatics?
|
they can help to improve diaphragmatic breathing functions
|
|
What do you use leukotriene antagonists?
|
the substances are very potent SM constrictors normally, so wanna BLOCK their action.
|
|
Why would you give anticholinergics to an asthmatic?
|
they act to decrease the mucous hypersecretion
-perhaps they may relax the smooth muscle as well |
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What are the major group of drugs used in COPD?
|
ANTICHOLINERGICS
|
|
What's the most important target of drug therapy in obstructive lung diseases?
|
Inflammatory cells and their products
|
|
What's bad about using GCsteroids in a patient?
|
-they are systemically active!
-lots of SEs -want to avoid oral/systemic prolonged steroids |
|
Major effects of GCsteroids:
|
-bronchial hyperreactivity (no direct dilation)
-increase airway caliber -reduce freq. of asthma exacerbations |
|
What is the major class of drugs used for asthmatics?
|
beta-agonists
|
|
What is the major class of drugs used for COPD?
|
anticholinergics!
|
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How do we make the diagnosis of asthma?
|
it's a reversibility issue, so when you give bronchodilators, i.e. Beta-agonists, you see an increase in the %FEV, and that shows that it's an asthma patient because their exacerbation is reversible, as opposed to COPD which wouldn't respond very much to the Beta-agonists
|
|
What's a good chronic drug of choice for asthmatics?
|
salmeterol, it's a long-acting, with a slow onset and longer half-life, so don't use in acute exacerbation, but good for management of asthma
|
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What is most commonly used to potently dilate the bronchi in a short-term scenario of asthma attack?
|
albuterol
|
|
Leukotrien receptor antagonists act on which subtypes?
|
C4
D4 E4 NOT B4, that's done by LOX inhibitors, but those drugs are much more toxic |
|
Which drugs might you nebulize?
|
1) beta-agonists
2) anti-cholinergics 3) glucocorticosteroids |
|
How do you diagnose BPD?
|
-positive pressure ventilation during the 1st 2 weeks of life for a minimum of 3 days
-clinical signs- abnormal resp. function -KEY: requirements for supplemental O2 longer than 28 days of age to maintain pO2 above 50mmHg -CXR w/ diffuse abnormal findings charac of BPD "Chronic oxygen dependency with certain radiologic features at 28 days of age" |
|
What radiologic findings do you see in BPD?
|
Stage I:
ground-glass appearance, similar to HMD Stage II: Whiteout BUT IT'S SELDOM SEEN Stage III: Same patient at 1 month of age shows the development of small cystic lucencies in the lungs. Stage IV: 7 mo of age shows small cystic lucencies have coalesced into larger lucencies with interspersed fibrotic stranding. Hyperinflation. |
|
Oxygen facts in a BPD baby:
|
-O2 sat needs to be >/=90-92%
-wean daytime b4 nighttime- need O2 at night due to underventilation -hypoxia associated with failure to gain weight -chronic hypoxia will lead to pul HTN |
|
What can you say about fluids in BPD babies?
|
fluid intake and calories are related, they need 110-140 CC/KG/day necessary to get the needed calories, but you have to monitor closely so you're not giving them too much fluid and causing that now rarely-seen Stage II whiteout due to pulmonary edema
|
|
What are 2 electrolyte imbalances you must consider in a BPD baby?
|
hyponatremia
AND hypokalemia -also think of volume depletion with alkalosis -lasix could cause some issues, too |
|
Would you use bronchodilators in a BPD baby?
|
-quite possibly, YES
-Tx occurs with inhaled albuterol and atrovent, and they've shown beneficial short-term effects in lung mechanics |
|
What charac. an exacerbation of Chronic Lung disease?
|
rales
retractions tachypnea desaturations CO2 retention increasing oxygen requirement |
|
How do you manage an exacerbation of CLD?
|
oxygen
bronchodilators diuretics MAY need vent. support |
|
What is the most common cause of hospital admission in the 1st year of life?
|
RSV-based bronchiolitis
|
|
Define & describe bronchiolitis:
|
-acute LRI w/ inflamm of small airways of infants
-in winter see SPIKE in RSV ifxs -may also be caused by parainfluenza and influenza virus |
|
Risk factors of an RSV ifx
|
LBW
prematurity Low SES crodwed living coniditions parental smoking day care absence of breast feeding |
|
RSV infectivity CHARAC:
|
-incubation of 2-5 days
-nasal viral shedding of 6-21 days -secondary ifxs from fam members 46% of the time, 98% due to other kids in day care and 42% hospital staff |
|
RSV Presentation in infants/toddlers up to age 2
|
fever
cough dyspnea wheeze cyanosis: bronchiolitis, pneumonia |
|
RSV Presentation in children >2y/o
|
febrile rhinitis
pharyngitis |
|
RSV Presentation in older children and adulta
|
COMMON COLD
|
|
With RSV, when greater than 2 years old, we don't get bronchiolitis, but...
|
we have it in our nose and can easily spread it.
|
|
RSV clinical features
|
-profuse coryza (cold in the head)
-congestion -low-grade fever 40% go to be an LRI w/in 2-5 days cough dyspnea wheezing feeding difficulties usually fever has resolved severe: FLARING, retractions, cyanosis |
|
RSV course is mild, and what do you see?
|
func recovery- 5-7days
cough usually <2 weeks CXR clear w/in 9 days temporary immunity for THAT SUBTYPE |
|
What's the other virus, that's similar to RSV?
|
hMPV, aka Human Metapneumovirus
-no good test for it! -usually mild RTI, perhaps slightly milder than those caused by RSV -sevrere RTI not uncommon in young children and IC pts. -risk groups: children, elderly, Immunocomp people |
|
Babies in first 2-3 months of life with RSV are particularly at risk to develop...
|
apnea
-typically premie -<44weeks postconceptual age -central, but not obstructive -may be presenting symptom -lasts for a few days, as they get over the acute ifx, it tends to resolve |
|
RSV Bronchiolitis has what indications for admission?
|
HYPOXIA IS THE MOST IMPORTANT ONE!!!
-sustained O2 sat less than 90 or 92% in room air -<6 months of age ESPECIALLY -cannot maintain oral hydration -markedly elevated resp rate -CLD Tx'ed with O2 -CongenHD with Pul HTN |
|
Bronchiolitis hospitalization
|
-median stay is 3-5 days
-vent for 5 days, O2 for 7, and discharge by the 9th day |
|
Bronchiolitis CXR
|
-bilat perihilar and patchy parenchymal infiltrates
-peribronchial cuffing -hyperinflations with flattened diaphragms -atelectasis esp RUL or RML |
|
When does Bronchiolitis pt. get admitted to ICU?
|
-O2 sat less than 92% when 50$ FiO2
-pCO2 >50mmHg -extrapul Sx's -arrythmia -Congen HF -Apnea |
|
SUPPORTIVE CARE/Tx of Bronchiolitis is treated how?
|
-admin humidified O2
-nasal suctioning to clear the upper airway -monitor for apnea, hypoxemia, and impending resp. failute -normalize the body temp -rehydrate orally or by IV -monitor hydration status |
|
How do you treat the baby airway obstruction?
|
-trial bronchodilator, and if clinical response, then use to treat
|
|
Are steroids indicated in uncomplicated simple bronchiolitis?
|
NO
|
|
What is synagis?
|
-reduced hospitaliztions by 55% in high-risk groups
-monthly admin necessary during RSV season but costs $1,000/dose for 4 months |
|
What are the JUSTIFIABLE RSV therapies:
|
-supportive Tx
-nebulized epi -mech vent -trial of Beta-adrenergics |
|
What are the RCT-necessary RSV therapies:
|
-physiotherapy
heliox exogenous surfactant |
|
Apnea baby definitions
|
>15 secs for full-term
>20 secs for preterm |
|
ALTEs CHARAC:
|
-high recurrence risk
-not predictive of SIDS -most common cause is idiopathic -see them in ER with relative frequency |
|
Define SIDS:
|
-sudden death of an infant under one year of age which remains unexplained after a thorough case investigation, including review of clinical history, performance of complete autopsy, and examination of the death scene
NEED ALL OF THESE!!! |
|
What's the big high-risk group for SIDS?
|
prematurity
-peak age range 2-4 months -males -expossure to cigarette smoke -hyperthermia |
|
Keys to Michael Light Infant Pul Death Lecture:
|
-incidence of SIDS has declined dramatically int he last 15 years since the intro of Back 2 Sleep campaign
-smoking and co-sleeping remain risk factors for SIDS -home monitors should NOT be prescribed to prevent SIDS |
|
Cystic Fibrosis lungs show..
|
-bronchitis
-bronchiectasis -pulmonary abscesses arising in the bronchi |
|
What's the incidence of CF?
|
Caucasians:
1/2500 get it, 1/25 carry gene AfrAmer: 1/15000 get it, 1/61 carry gene AsianAmer: 1/31000 get it, 1/88 carry gene |
|
Major CF Sx's:
|
-respiratory are HALF of all
-FTT/malnutirion -steatorrheal/abnl stool -meconium ileus/intestinal obstruction THOSE 3 together make up a lot of the GI and malnutrition problems MAIN FEATURES: malnutrition failure to thrive diarrhea-like disease |
|
What's the basis of the CF defect?
|
There's a deficient Cl' channel, and so you don't have Cl- REABSORPTION, and thus Cl- is on the outside, and keeps Na+ with it
Normal Cl- is 10-30mequiv/L Positive Test: 60+ Intermed: 30-60 |
|
Cl- Test is positive for CF when?
|
Positive Test: 60+
Intermed: 30-60 |
|
How many patients with CF present initially with meconium ileus?
|
10-15%
-but when they present this way, MUST DO SWEAT TEST ON ALL OF THEM |
|
If you see rectal prolapse, what do you do next?
|
SWEAT TEST!
-even if basal polyposis and they have allergies, do the sweat test there too |
|
What percent of infants with meconium ileus also have CF?
|
NINETY (90%) PERCENT!
|
|
If an infant has an intestinal obstruction or perforation in utero, do you do a sweat test?
|
YES!
|
|
Define Pancreatic insufficiency:
|
-severe exocrine pancreatic disease with documented nutrient maldigestion
-requires pancreatic enzymes with meals -supplement food with those enzyme, and the disease can start very early and be progressive with time |
|
Define Pancreatic Sufficiency:
|
-mild/moderate exocrine pancreatic disease
-not severe enough to produce nutrient maldigestion -do not require pancreatic enzymes with meals |
|
What's the basis of the pancreatic issues in a CF patient?
|
There is a concentrated acidic protein secretion that blocks the tubular region and prevents the enzymes from ever even having the chance to get out
|
|
DO a serum immunoreactive trypsinogen test in a patient with suspected CF, what do you look to see?
|
a HIGH serum-level
|
|
Describe height/weight of CF patients?
|
they're shorter and thinner than normal folks
|
|
If the CF patient has GI/pancreatic issues, what do you do to Tx?
|
-give pancreatic enzyme supplements
-vitamin supplments -high-calorie diet -emphasis on good bowel regimen |
|
Newborn screening for CF follows what steps?
|
-Measures the IRT- immunoreactive trypsinogen
-elevated levels get sent for genetics -follow-up with a sweat test |
|
What disease is related to CF in 8-15% of patients?
|
CFRD- CF-related diabetes
|
|
What causes CFRD?
|
-acinar atrophy
-fatty infiltration -fibrosis -dec. in # of pancreatic islets NOT an autoimmune process -diabetic ketoacidosis is an exception |
|
A small portion of CF patients see what other disease appear?
|
-cholestasis, duct obstruction in the liver, so it's an overt liver disease
|
|
CF liver disease accounts for how much mortality?
|
1-2% of CF mortality
|
|
Why do CF patients have airway problems?
|
the airway fluids are underhydrated and that creates constant cough, along with a gelatinous, tenacious fluid there, when you really need mucociliary clearance to be functioning, and it's just TOO thick
|
|
What is the major cause of morbidity and mortality in CF patients?
|
MAJOR PATHOGENS:
staph. aureus and haemophilus influenzae often lead to the ability to be Ifx'ed with pseudomonas which is the ultimate killer -also see: Burkholderia cepacia- can cause rapid and severe advanced disease, also even septicemia -atypical myco- can lead to more aggressive disease -aspergillus- and it's not the aspergillus that is so brutal, but RATHER the allergic response to it- called ABPA that causes all the damage, and the most common patient pop for ABPA is CF patients |
|
Most common people to get ABPA?
|
CF patients
|
|
Do a lot of CF patients get pseudomonas disease?
|
YES! Up to 80% over the course of the disease!!!
|
|
What is the issue with CFTR in CF patients?
|
it prevents the OUTFLOW of Cl- ions into the extracellular space when the channel is mutated
|
|
How do you Tx CF:
|
bronchodilators- albuteral
chest physiotherapy rhDNase Abx- Staph aureus and p. aeruginosa ESPECIALLY -inhaled ABX -macrolide Abx as a protection for anti-inflammation influenza vaccine corticosteroids ibuprofen |
|
Classes of CFTR Mutation
|
Class 1: no synthesis
Class 2: no maturation Class 3: blocked regulation Class 4: decreased conductance Class 5: decreased abundance class 3 and 4 may see various other mutations, but having the same degree of function |
|
Class 1,2, and 3 mutations give what grade of disease?
|
SEVERE
-PI -meconium ileus CFRD severe hepatobiliary disease |
|
Class 4 and 5 mutations give what grade of disease?
|
Mild
pancreatic sufficiency risk of: acute pancreatitis -recurrent pancreatitis -chronic pancreatitis |
|
What Tx do you give to try and fix the truncated proteins of CF?
|
Gentomycin!
-can bridge truncation and correct the protein, intervenes on the stop codons! |
|
What repro sys issues does CF deliver?
|
-obstructive azoospermia
-can't conduct through the vas deferens! |
|
2 aspects of breathing volumes affected by a restrictive lung disease?
|
1) decreased Vital Capacity, leading to:
2) DEC TLC Recall Vital Capacity = IRV + ERV + TV |
|
What are all the extrinsic restrictive diseases?
|
-pneumothorax
-pleural effusion -pleural thickening as in asbestosis -scoliosis -ankylosing spondylitis -polimyelitis -GBS -ALS -Myasthenia gravis -muscular dystrophies |
|
What are the disease of the lung parenchyma?
|
-idiopathic pulmonary fibrosis
-sarcoidosis -hypersensitivty penumonitis- extrinsic allergic alveolitis -radiation-induced fibrosis -collagen vacular-related fibrosis -lymphangitis carcinomatosis |
|
Which type of collagen do you see in restrictive lung disorders?
|
Collagen Type III
|
|
An indication of restrictive lung disease is...
|
preservation of the FEV1/FVC ratio!!!
|
|
What is the test you would do with a suspected restrictive lung disease patient to show really strong indications of it being present? Think oxygen.
|
6 minute walking test
-RLD patients OFTEN desaturate very early on in disease because of the disease's patchiness |
|
What do you see, in general, histologically with restrictive lung disease?
|
cast-like blue collagen and hyaline, which is a result of the chronic injury to the epithelial cells
|
|
Progressive fibrosis is seen in what part of the lungs?
|
it progresses at the BASES of the lungs
-see O2 saturation dropping -pul vasc resist INC, with co-existing or even primary vasc disease AND destruction of pul artieroles and capillaries -pul HTN develops leading to cor pulmonale -starts in the bases of the lungs and with exercise you'll really exacerbate the disease |
|
Where do you see honeycombing?
|
in Usual Interstitial Pneumonia
|
|
Distinguish the patterns of UIP and NSIP
|
UIP:
heterogeneous, patchy NSIP Fibrotic + Cellular: -homogenous, all looks the same -other samples of this would appear cellular and homogenous |
|
IPF Chief Complaint:
|
shortness of breath and/or cough for several months
|
|
Onset of IPF
|
-variable
-usually age 50-70 -familial disease, SO ASK FAM Hx |
|
Clinical Presentation of IPF:
|
-progressive dyspnea on exertion
-cough, usually nonproductive and dry -Clubbing in HALF OF PATIENTS -bibasilar end-inspiratory crackles -bibasilar, subpleural reicular opacities on CXR and HRCT -restrictive pul phys with reduced lung columes and DLCo and WIDENED AaPO2 |
|
What are the MAJOR criteria of IPF?
|
-no known other causes of interstitial lung disease
-abnorm pul func studies -abnorm CXR/HRCT scan -No histo or cytological features supporting another diagnosis- MOST COMMON: IFX! |
|
When you hear "velcro" sounds, and the duration of illness is >/= 3 months, think what disease?
|
after having ALL the major criteria, think IPF!
|
|
What are the 2 parts to the path of UIP?
|
1) periph accentuation of disease
2) transition into uninvolved lung |
|
In what part of the lung do you typically see UIP?
|
usually subpleural and more prominent in lower lobes
|
|
What does general anesthesia do to FRC?
|
DEC by about 16%/500ml
-also creates V/Q mismatch and hypoxemia |
|
Why do you see hypoxemia due to V/Q mismatch?
|
2 things:
1) INC dead space ventilation: more vent to NON-dependent areas of the lung 2) INC shuntlike- INC perfusion to POORLY VENTILATED dependent areas of the lung |
|
What happens to lung volumes after abdominal surgery?
|
DECREASES IN:
TLC FRC RV |
|
Which affects lung volumes more, Upper or Lower Abdo surgery?
|
UPPER
|
|
What's the normal closing volume and what happens to it with surgery?
|
it's normally about 30% of TLC and it's the vol at which flow from the dependent parts of the lungs stops during expiration due to airway closure, so it INCREASES with surgery
|
|
How do you predict post-op FEV1?
|
FEV1ppo = Actual pre-op FEV1 x %perfusion of the lung to remain, determined by an isotope scan
Equation 2: FEV1ppo as a % of the normal |
|
When trying to determine whether a patient is a candidate for a pneumonectomy, what is the required FEV1ppo?
|
>80%
if 40-80 then look at symptoms, and if <40% predicted, don't do the surgery if their Blood Gases don't look good. |
|
How do you treat post-cardiac injury syndrome?
|
NSAIDs and corticosteroids work well!
|
|
Esophageal surgery post-op pul complications:
|
25-50% incidence
BUT 40-60% of operative MORTALITY!!! -there is recurrent laryngeal nerve injury -pleural effusion is possible |
|
What do you measure with an incentive spirometer?
|
IC = IRV + VT
|
|
How does the expiatory curve get shifted in restrictive disorders?
|
TO THE RIGHT
|
|
Why does respiratory failure in chest bellows disorders show hypercapnia?
|
see increased work of breathing
leading to decreased Tidal Volume and thus INC dead space leading to alveolar hypOventilation leading to the Hypercapnia, and acidosis |
|
What is one of the major presenting features of Guillen-bairre Syndrome?
|
-see a RAPID progressive parethesias and muscle weakness initially in the legs, and then later on the arms, followed by dyspnea and weak cough, with an inability to clear secretions
|
|
What's the main cause of hypoxemia in chest bellows disorder patients experiencing respiratory failure?
|
V/Q mismatch
|
|
If you dip below what level of respiratory muscle strength do you see problems, and what is the problem?
|
if you drop under 50% and it's an issue with hypercarbia
|
|
Why do a sniff test, and what does it show if positive?
|
have the patient "sniff" the air, and the diaphragm should go DOWN, but with a hemidiaphragmatic paralysis, see the paralyzed side GO UP!!!
|
|
DIP shows what?
|
numerous macrophages in the alveolar spaces in a diffuse and uniform manner
-see type II pneumocyte hyperplasia and desquamation into the air spaces -mortality: <20% -smokers: 90% OF THE PATIENTS WITH THIS DISEASE |
|
Respiratory Bronchiolitis-Associated Interstitial Lung Disease is strongly associated with...
|
smoking cigarettes
-more affinity for airways -not as diffuse as DIP -see broncioles with a lymphocyte infiltrate extending into the interstitium creating the picture of an interstitial disease PROGNOSIS is much better than DIP and UIP |
|
Where do you see NSIP?
|
-patients suffering from connective tissue disease, hypersensitivity reactions, and even due to drug toxicity
-uniform pattern with mononuclear infiltrates and different grades of fibrosis |
|
lymphoid interstitial pneumonia is...
|
considered a lymphoproliferative disorder associated occasionally with immunsuppression
|
|
giant cell interstitial pneumonia is...
|
a hard metal pneumoncniosis assoc with exposure to cobalt
|
|
Reaction to the inhalation of organic dusts or biologic aerosolized particles int he environment
|
hypersensitivty pneumonitis/extrinsic allergic alveolitis
APPEARS AS A RESTRICTIVE PATTERN |
|
Farmer's lung is caused by...
|
thermophilic actinomycetes
|
|
bird fancier's lung is due to...
|
pigeon breeder's lung, Ag present in bird poop, feathers, or serum proteins
|
|
Chronic Hypersensitivty pneumonia presents with.,..
|
chronic bronchiolitis
NSIP pattern scattered granulomas |
|
What are the complications of asthma?
|
infection
bronchiectasis cor pulmonale emphysematous changes status asthmaticus |
|
Wegener's Granulomatosis
|
charac. by presence of nectrotizing granulomatous inflammation and vasculitis
-affects upper respiratory tract, causes: sinusitis otitis nasal disease ear pain oral lesions lower resp tract sees: multiple lesions kidneys get affected by glomerulonephritis PATIENTS HAVE ANTRINEUTROPHIL ANTIBODIES- ANCA- in serum |
|
lung hemorrhage, glomerulonephritis, antibodies against basement membrane, with Ag being collagen IV
|
Goodpasture's Syndrome
|
|
Rheumatoid Arthritis
|
Patient presents with pleuritis, pleural effusion, chronic interstitial pneumonia resembling UIP, bronchiolitis, vasculitis, and necrobiotic nodules
|
|
Charcot-Leyden Crystals and Eosinophils
|
Asthma!
-see basement membrane thickening, too |
|
pleuritis with pleural effusion, interstitial pneumonitis, DAD, hemorrhage, and vasculitis
|
Sys Lupus Erythematous
|
|
hypersensitive vasculopathy, chronic interstitial pneumonia with prominent fibrosis being the usual findings
|
Systemic Sclerosis or a scleroderma
-also think PUL HTN when you see this |
|
Histo findings of sarcoidosis:
|
presence of collections of histiocytes and multinucleated giant cells
-granulomas have a distribution along the bronchovascular bundles -rare in ppl <15 or >65 -blacks > whites -T-cells mediate the granulomatous inflamm and thought to be due to an inhaled Ag rxn |
|
Irreversible increase in size of air spaces distal to the terminal bronchioles
|
emphysema
|
|
2 types of emphysema:
|
1) centrilobular- proximal portion of term bronchiole is affected
ASSOC WITH CIG SMOKING -it's the func impairment that does, because of great damage to the alveolar-capillary wall and reduced elastic recoil 2) panacinar- ENTIRE resp bronchiole is effected seen in elderly patients also in A1A deficiency patients NEITHER OF THESE IS RESPONS FOR CLINCAL COURSE THOUGH |
|
What is the pathogenic basis of emphysema?
|
IMblanace of proteases and antiproteases like A1A
-the antiproteases are made in the liver and if there's low production that could lead to a problem, or if the oxidative effects of cig smoke affected them, the elastic arch of alveolar septae may be destroyed -emphysema occurs in ~15% of smokers |
|
What are the major clinical Sx's of acute interstitial pneumonia?
|
cyanosis and SEVERE hypoxemia
BUT there is no catasrophic event precipitating it, so it's called idiopathic ARDS |
|
What is the histologic pattern of ARDS?
|
diffuse alveolar damage with:
-fibrinous exudates -hyaline membranes -interstitial edema -type II pneumocyte hyperplasia HOMOGENEOUS APPEARANC |
|
What kind of ifx in an immunosuppressed person could lead to acute interstitial pneumonia?
|
VIRAL ifx
|
|
How does an IPF patient present?
|
insidious presentation and PROGRESSIVE course, which is fatal in 5-6years
|
|
What does HRCT shown in IPF?
|
a PERIPHERAL honeycombing pattern!
|
|
How do you treat UIP?
|
cyclophosphamide, if anything
|
|
-numerous macrophages in the air spaces in a diffuse and uniform manner
-thickening of the alveolar septae with mild pneumonitis -type II pneumocyte hyperplasia WHAT IS IT? |
desquamative interstitial pneumonia
-disease of mainly cig smokers -affects lung homogeneously |
|
-more affinity for airways
-less diffuse than other interstitial diseases -macrophages in alveoli and bronchioles |
respiratory bronchiolitis, associated with interstitial lung disease
-could be the same as DIP but in different stages -related to cig smoke, too! |
|
Interstitial lung disease with good prognosis and responsive to steroids
|
non-specific interstitial pneumonitis/fibrosis
|
|
Histology pattern is uniform w/ mononuclear infiltrates and different grades of fibrosis
|
NSIP
-homogeneous appearance |
|
Interstitial disease due to the exaggerated reaction to the inhalation of organic dusts or biologic aerosolized particles in the home or work environment
|
hypersensitivity pneuonitis
-may result in severe fibrosing disease with continuous chronic exposure to the antigens |
|
#1 treatment for hypersensitivty pneumonitis?
|
REMOVE THE ALLERGEN
|
|
What immune rxn is seen in hypersensitivty pneumonitis?
|
type II, sometimes some type IV with granulomas present
|
|
Chronic hypersensitivty pneumonitis presents how?
|
-acute exacerbations less frequent
-progressive respiratory insufficiency -dyspnea -cyanosis -hard to tell from other chronic interstitial pneumonitis because total pul capacity is reduced -may see: honeycombing, loss of volume, and ground-glass opacities |
|
See Charcot-leyden crystals, who makes em' and why?
|
ASTHMA!
-made by eosinophils |
|
Multisystemic disorder charac by:
-necrotizing granulomatous inflammation -vasculitis |
Wegener's granulomatosis
AFFECTS: URT-sinusitis, otitis, nasal disease, oral lesions LRT Kidneys |
|
What is the key finding that will tell you "IT'S WEGENER'S!!!"?
|
ANCA
antineutrophil cytoplasmic antibodies with either the cytoplasmic/classic or perinuclear presentation |
|
Autoimmune disorder consisting of the triad of:
1) glomeulonephritis 2) lung hemorrhage 3) anti-basement membrane antibody formation. |
Goodpasture's syndrome
Ab's are to collagen IV |
|
Pleuritis
pleural effusion chronic interstitial pneumonia resembles UIP bronchiolitis vasculitis and necrobiotic nodules |
Rheumatoid Arthritis
|
|
Sarcoidosis demographic
|
women > men
blacks > whites granulomatous disease world-wide dist. T-cells mediate the inflamm, which is thought to be due to an inhaled Ag |
|
What's a very possible diagnosis when seeing a presentation involving bilateral hilar adenopathy?
|
sarcoidosis, especially if a female and/or black ethnically.
|
|
What tumors are centrally located?
|
squamous cell
AND small cell |
|
Breath Sounds, Resonance, and Fremitus of:
Pleural Effusion |
Breath Sounds: DEC
Resonance: DULLNESS Fremitus : DEC |
|
Breath Sounds, Resonance, and Fremitus of:
Pneumonia- lobar |
Breath Sounds: might be bronchial
Resonance: DULLNESS Fremitus : INC!!! |
|
Breath Sounds, Resonance, and Fremitus of:
Pneumothorax |
Breath Sounds: DED
Resonance: HYPERRESONANT Fremitus : ABSENT |
|
How does the trachea displace when there's a collapse?
|
TOWARDS the lesion
|
|
Tension pneumothorax, which was does the trachea deviate?
|
AWAY from the lesion, you've put pressure on one side, so trachea will be pushed by that pressure.
|
|
What parts of the lung are usually involved in bronchiectasis?
|
lower lobes, extending from hila to periphery
|
|
How do you Dx bronchiectasis?
|
CT! Most likely, HRCT to see honeycombing. See those signet rings, too.
Side note: Histologically, see a heterogeneous pattern. |
|
3 bugs that are most common causes of acute sinusitis, otitis media, and chronic bronchitis?
|
S. pneumo
Morraxella Catarrhalis H. Influenza |
|
What's the leading causes of death in AIDS patients?
|
TB!
|
|
What are the more likely risk groups for HIV-associated TB?
|
blacks
hispanics IVDUs Gays are NOT more likely. |
|
Where in the lungs do you see reactivation TB?
|
Apical areas
-like Dr. Goljan says, they're strict aerobes, so need to go to the place with the most air to grow, thus the apical regions! |
|
Key findings to make you think TB:
|
-night sweats
-hemoptysis -cough >3 weeks -cough w/fever >3 days -weight loss |
|
Atypical pneumonia causes:
|
mycoplasma
viral legionella chlamydia, which presents more insidiuously |
|
Nosocomial pneumonia implies...
|
gram negative and resistant
|
|
The bugs of bronchopneumonia
|
by definition, involving more than 1 lobe:
-staph -strep -H. influenza -P. aeruginosa |
|
Bugs of lobar pneumonia
|
>90% due to strep. pneumonia
-also can see Klebsiella |
|
What are the physical exam findings of pneumonia?
|
INC:
fremitus dullness egophony bronchial breath sounds |
|
What's a key radiologic finding of atypical pneumonia?
|
widening of the interstitium
-interstitial infiltrate predominantly lymphocyte rich with proteinaceous exudates in the alveolar spaces -DON'T see many cells in the exudates |
|
What are the findings of mycoplasma pneumonia clinically/radiologically?
|
bronchial wall inflamm w/ non-purulent patchy interstitial infiltrates
-assoc. with cold agglutinins- IgM |
|
What are good drugs to treat mycoplasma pneumonia?
|
B-lactams DON'T work
fluroquinolones macrolides- watch GI issues tetracycline |
|
Most common cause of lobar pneumonia?
|
strep pneumonia
|
|
Where does strep pneumonia proliferate?
|
in the alveoli, causing an influx of PMNs with minimal structural damage
|
|
How do you Dx Step. Pneumonia?
|
Gram+
a-hemolysis on agar catalse negative sensitive to optochin |
|
How do you treat strep pneumonia?
|
B-Lactams
emergence of penicillin resistant strains is big probme, but use bigger doses, or different beta-lactams ALSO combine with macrolides |
|
What are macrolides used to treat?
|
mycoplasma
|
|
What is the empiric therapy of a pneumonia diagnosis?
|
B-lactam, possibly with a B-lactamase inhibirotr
OR 2nd-generation cephalosporin AND macrolide (for mycoplasma, in case it's an atypical presentation) |
|
What's special about 2nd-generation cephalosporins?
|
Have EXTENDED gram-NEGATIVE coverage
|
|
How do you treat MRSA staph?
|
vancomycin
|
|
Patient presents with acute onset of fever, chills, chest pain and rusty sputum?
|
strep. pneumonia!
-alveolar proliferation with purulent secretions and lobar consolidation |
|
H. influenza CHARAC
|
-gram neg
-needs factors V and X to grow- so grows well on choco agar |
|
Moraxella catarrhalis is charac as a
|
gram neg
diplococcus makes oxidase, catalase, DNase |
|
What is the 2nd most common cause of COPD exacerbations?
|
moraxella catarrhalis
|
|
Legionella can't be treated with which drugs?
|
Beta-lactams
it's a gram neg bacilli, hard to see in a gram stain, and easier to see in silver stain DIFFICULT to grow, so especially consider it if you see lots of WBCs but no bacteria...but do also consider the other atypicals MAY GIVE hyponatremia -failure to respond to Beta-lactam may give the diagnosis |
|
Chlamydia pneumonia components and Tx
|
elementary body is INFECTIOUS
Reticulate body is metabolically active, non-infectious. Tx: fluoroquinolones are good for it. macrolides and tetracyclines could be used too. |
|
Adenovirus is a common cause of...
|
pneumonia in AIDS patients.
-SMUDGE cell or ROUND-GLASS appearance histo-wise |
|
What are the bugs that often cause abscesses and empyema, especially in LRI...
|
S. aureus
Klebsiella Pseudomonas anaerobes also common in nosocomial pneumonia, as a side-note SEE: alveolar prolif and necrosis, with lobar consolidation and CAVITATION!! |
|
Most common causes of bacterial pneumonia in HIV (2)?
|
S. pneumonia
AND H. Influenza |
|
What prophylaxis do you deliver in an HIV+ pt. when worried about bacterial pneumonia?
|
trimethoprim (TMP)
|
|
What prophylaxis do you deliver in an HIV+ pt. when worried about PCP?
|
Bactrim, aka TMP-SMZ
use in HIV+ with CD4 <200 |
|
Where do you see a cotton candy appearance?
|
PCP histology, due to intraalveolar eosinophilic exudates
-lots of edema and eosin in the alveolar spaces, not much damage to the tissues -helmet-like or cup-shaped organisms |
|
What's the threshold for seeing CMV?
|
HIV+ with CD4 <50 typically
-IFX of alveolar macrophages, endo and epi cells -SEE RETINITIS, along with other GI issues -OWL-EYE INCLUSIONS are indicative of CMV |
|
How do you treat CMV?
|
HAART with IV ganciclovir or foscarnet
|
|
Most common fungus-based life-threatnening HIV+ illness?
|
cryptoccous
-meninges are most common ifx site -CD4<100 usually -FOAMY CELLS with big thick capsule on india ink Dx. by seeing via histo TREAT WITH AMPHOTERCIN B |
|
Treating with amphotercin B, what do I have?
|
HIV+, likely CD4<100, Cryptococcus neoformans
|
|
Mimics TB with peripheral pulmonary lesion and hilar adenopathy, certain parts of U.S. specific, what is the bug?
|
Histoplasmosis
-MILIARY infiltrates on CXR -NON-CASEATING fibrotic granulomas AMPHOTERCIN B treatment or Itraconazole in pts with milder disease |
|
CD4<30
brancing, septate organisms with 40 degree angles |
Aspergillosis!
|
|
How does aspergillosis present?
|
NECROTIZING pneumonia and propensity for blood vessels so CXR shows UL disease with CAVITATION AND HEMOPTYSIS
Tx with AMPHOTERCIN B |
|
What all do you treat with Amphotercin B?
|
1) Cryptococcus
2) Histoplasmosis 3) Aspergillosis 4) Coccidiomycosis 5) Blastomycosis |
|
Where do you see blastmycosis
|
patient is immunosuppressed and localized to Midwest US, Southwest US and Canada
|
|
What's the major mutation of CF and the associated complication?
|
Δf508
-associated with pancreatic insufficiency! |
|
Explain the CF mutation
|
Cl- channel is blocked and Cl- can't leave the bronchial cells, so Na+ goes inside and creates and extra-thick mucous that gets stuck and can't be moved by the mucociliary elevator
|
|
Do you see clubbing in CF?
|
yes, true.
|
|
Meconium ileus
|
CYSTIC FIBROSIS
|
|
What's the means of diagnosis of CF?
|
Sweat test with Cl- >60, intermediate if 30-60
|
|
Common organisms colonizing CF pt. airways?
|
P. AERUGINOSA
S. aureus H. Influenza |
|
BPD is characterized by...
|
INC vasc perm
-lungs are leaky and inflamm cells go where they're not supposed to, creating a significant inflammatory response |
|
Is RSV seasonal?
|
Yes, but in Florida it's not as pronounced in terms of spikes during certain months, but rather it's higher most of the time!
|
|
Clinical Sx's of bronchiolitis?
|
-profuse coryza, or runny nose
-low grade fever -LRI w/in 2-5 days -cough, dyspnea, wheezing, feeding issues, flaring, retractions, and cyanosis |
|
CXR of Bronchiolitis shows...
|
-bilateral perihilar and patchy parenchymal infiltrates with peribronchial cuffing
hyperinflation with flattened diaphragm atelectasis especially in the right upper and middle lobes |
|
What's the prophylaxis of Bronchiolitis?
|
synagis
1X/month, but $1,000/Tx |
|
What are the intrinsic restrictive lung diseases?
|
PARENCHYMAL RESTRICTIVE:
IPF sarcoidosis hypersensitivity pneumonitis radiation-induced fibrosis autiommune-related fibrosis or lymphangitic carcinomas OR AIR-SPACE FILLING DEFECTS: i.e. pneumonia, could result in diffusion problems |
|
What are the extrinsic restrictive lung diseases?
|
Pleura:
-pneumothorax -pleural effusion -pleural thickening- asbestosis Chest wall: -scoliosis -ankylosing spondylitis Neurmuscular disease: -polio -GBS -ALS -Myasthenia Gravis -Muscular dystrophies |
|
In diseases of the lung parenchyma, where do you see the fibrosis?
|
starts at the bottom of the lung and works its way up.
|
|
Diseases that may lead to IPF:
|
scleroderma
asbestosis amiodarone (lipid containing vesicles) methotexate drug-use |
|
Does IPF respond to steroids?
|
NO!
only tx if any is supplemental O2 |
|
How does IPF spread?
|
usually starts at the periphery and works its way inward, there is also scattered fibroblast foci, and representative areas of active fibrosis
|
|
How many IPF patients have clubbing?
|
HALF!
|
|
If you hear velcro crackles, think...
|
IPF
|
|
Clinical presentation of IPF shows 3 big things:
|
-clubbing in half of patients
-velcro crackles -reticular opacities, i.e. ground-glass appearance |
|
Clinical features of AIP?
|
diffuse infiltrates on CXR
hypoxemia cyanosis hyaline membranes interstitial edema type II hyperplasia fluid in the alveolar space organizing DAD DIFFUSE PROLIFERATION OF INTERSTITIAL FIBROBLASTS |
|
NSIP is what kind of process?
|
VERY CELLULAR, LOTS of inflammation
|
|
Does NSIP respond to steroids?
|
YES!
|
|
What 2 interstitial diseases are associated with smoking?
|
DIP and RB-ILD
|
|
What characterizes Wegener's Granulomatosis?
|
NECROTIZING granulomatous inflammation and vasculitis
|
|
Key diagnostic finding of Wegener's?
|
ANCA antibodies!!!
|
|
Key pathogenesis of Sarcoidosis?
|
T-cells mediate inflamm
bilat hilar lymphadenopathy RESEMBLES TB |
|
2 key clinical features of sarcoidosis?
|
skin nodules
eye irritation, i.e. uveitis |
|
What do lab tests show for sarcoidosis?
|
hypergammaglobulinemia
hypercalcemia INC ACE levels |
|
How do you Tx sarcoidosis?
|
cortisone or prednisone
|
|
Where do you see the fibrotic nodules of silicosis?
|
upper lobes
egg shell calcification in the hilar LNs NO CLUBBING |
|
What part of the lungs do you see involved in asbestosis?
|
peribronchiolar fibrosis involving the LOWER lobes
-alveolar spaces may have asbestos bodies and inflamm cells |
|
Coal workers pneumonia is seen in what part of the lungs?
|
usually UL zones, with nodular or rounded appearance
|
|
Rheumatoid arthritis has what finding similar to IPF, what is it?
|
Velcro crackles in the lower lobes
|
|
What organs does Sjorgen's syndrome affect?
|
eyes
salivary glands |
|
Bleomycin toxicity causes...
|
PMNs alveolitis and eosinophil proliferation in hypersensitivity reactions
causes nodular lesions mimicking metastasis due to BOOP |
|
Methotrexate toxicitiy shows...
|
T-cell alveolitis and eosinophil prolif
|
|
Patient presents with lamellar bodies on EM and lipid-containing vacuoles, what's the problem?
|
amiodarone toxicity
|
|
2 KEY histo findings of Squamous Cell Carcinoma?
|
1) Keratin pearls
2) Intracellular bridges via desmosomes |
|
What is the triad of pulmonary embolism?
|
1) dyspnea
2) pleuritic chest pain 3) hemoptysis- occurs later on |
|
Most common mutation leading to PE?
|
Factor V leiden
|
|
How do you treat PE?
|
heparin, then long-term use coumadin, elastic stokcings, pneumatic compression devices, an IVC filter, thrombolytics are RARE and so is a thromboendarterectomy
|
|
What is defined as Pul HTN?
|
mPAP >25mmHg at rest or >30mmHg during exercise
|
|
Define ARDS:
|
diffuse alveolar damage, specifically to th e alveolar capillary walls that results in the rapid onset of severe life-threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia that is refractory to O2 therapy and may progress to extrapulm organ failure
|
|
Findings of ARDS
|
Profound dyspnea and tachypnea herald ARDS, but the CXR is initially normal. Subsequently, there are increasing cyanosis & hypoxemia, respiratory failure, and appearance of diffuse bilateral infiltrates on CXR.
Looks like bilateral lung opacity (“white out”). They’re heavy, stiff, non-compliant lungs. |
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Describe ARDS pathogenesis:
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-Diffuse alveolar damage leads to:
-INC alveolar capillary perm leads to: -protein-rich leakage into alveoli leads to: -formation of intra-alveolar HYALINE MEMB leads to: -neutrophilic substances toxic to alveolar wall, activaiton of coag cascade, or oxygen-derived free radicals |
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When does the incidence of lung cancer peak?
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ages 55-65
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#1 risk factor for lung cancer?
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SMOKING
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#2 risk factor for lung cancer?
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Passive exposure to smoke
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#3 risk factor for lung cancer?
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Occupational exposures:
-asbestos ESPECIALLY -roofers exposed to coal tars -railroad workers -others |
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Local tumor clinical Px:
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-cough
-hemoptysis -wheezing due to tumor obstructing airway -atelectasis or postobstructive pneumonia--> dyspnea, signs of pneumonia |
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What are the Sx's of pancoast syndrome?
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see Horner's syndrome, which is ptosis and myosis, along with anhydrosis
"a droopy-eyed, constricted people in someone NOT sweating." |
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What are all the paraneoplastic syndromes you could see:
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-endocrine
-mskel: hypertrophic osteroarthropathy -neurlogic- Lambert-Eaton, peripheral neuropathy, dementia, cerebellar degen -hematologic: thrombophlebitis |
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What are the paraneoplastic issues seen with squamous cell carcinoma?
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PTH-syndrome giving:
-HYPERcalcemia -lethargy -polyuria -polydipsia (excessive thirst) -constipation -abdominal pain -possible coma |
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Why do you typically see SVC syndrome?
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due to mediastinal LN invasion of the tumor
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SIADH Sx's
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hyponatremia leading to:
-irritability -confusion -weakness -poss. seizures |
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Cushing's Sx's:
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-facial edema
-cachexia -hypokalemia -alkalosis - |
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Hypertrophic osteoarthropathy Sx's:
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overgrowth of cortical bone and presenting with pain in the lower joints
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What are the 2 options for Dx of a Small-Cell lung cancer?
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Limited (30%)
or Extensive (70%) |
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What are the options for a Non-Small-Cell Lung CA:
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Can the patient tolerate resection, determined by pul func test
and is the tumor possibly resected for a cure? |
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When a tumor is more periperal, how do you resect it?
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Use fluorscopy-assisted percutaneous needle aspiration
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What are the levels needed to permit a pneumonectomy?
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FEV1ppo and DLCO >/= 75% predicted
if less, do split pul func test to estimate post-resection FEV1 and DLCO... If they're greater than 40% then you can still do the pneumonectomy |
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What are the steps of lung CA staging?
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1) extent of Primary Tumor- T
2) presence and extent of regional metastasis to hilar and mediastinal LNs- N 3) presence/absence of distant mets- M |
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T of TNN:
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T1 </= 3CM
T2 >3CM T3 INVADES CHEST WALL T4 invades VITAL intrathoracic strucs |
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N of TNM:
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N0- no LNs
N1- ipsilateral peribronchial/hilar LNs N2- ipsilateral mediastinal/subcarinal LNs N3- CONTRAlateral mediastinal/hilar LNs and/or supraclav LNs |
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Small Cell Tx:
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Limited disease:
-do radiation port to Tx, confined to one hemithorax, and only regional LNs, Tx is chemo and radiation! Extensive disease: tumor beyond limited limits, Tx is chemo |
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How to be sure a Solitary Pulmonary Nodule is benign?
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1) No growth on X-ray for 2 years
2) pt. <35 yrs of age AND non-smoker 3) chest radiograph and/or CT shows it's calcified: through and through, target, laminar, or popcorn |
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Which tumor do you Tx with surgery and which is too bad already when Dx'ed?
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try to treat Non-Small cell with surgery, but small cell is considered already spread by the time the Dx is made so you do chemo and radiation if it's a limited disease, and just chemo if it's an extensive small-cell diagnosis
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Atypia, dysplasia, and DCIS of bronchial epi imply...
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invasive squamous cell CA likely assoc with heavy cig smoking.
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Scar carcinoma is...
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when pul fibrosis, such as IPF is present and then a tumor arises at the site of prev fibrosis
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Desmoplasia is when..
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fibrosis 2ndary to presence of a carcinoma.
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C-myc is a mutation found in...
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small cell CA
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K-ras is seen in...
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adenocarcinomas
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What 2 genes are often inactivated in lung CAs?
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p53 and retinoblastoma
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Adenocarcinoma definition:
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malignant epi tumor with GLANDULAR DIFFERENTIATION
-see gland formation or see intracytu mucins! -usually periph location -equally frequent in men and women, but most frequent type in the non-smoker population -sometimes assoc with areas of scarring |
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4 sub-types of adenocarcinoma
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tubular/acinar
papillary solid bronchioloaveolar |
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Squa cell CA definition:
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-malignant epi tumor charac by presence of keratin prod AND/OR intracellular bridges
-closely assoc with smoking history |
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Large Cell CA is...
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malignant epi neoplasm undifferentiated
-cells large/polygonal -nucleolus is prominent and cell borders are well-defined -see giant cell CA and clear cell CA in this group |
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Adenosquamous carcinoma is...
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at least 10% of each of the two tumor types combined
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Small cell definition
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highly-defined neuroendocrine tumor strongly assoc with cig smoking
-usually close to hilum -originated in the Kulchitsky cells -composed of smallc ells with scant cytoplasm and ill-defined cellular borders -salt and pepper chromatin -nuclei molding is CHARACTERISTIC |
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Typical carcinoid tumors:
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-low-grade neuroendocrine tumors
-great survival rate >90% at 10yrs -salt and pepper chromatin appearance -mitotic figures scant and necrosis absent MOST COMMON LUNG TUMOR IN CHILDREN |
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Atypical Carcinoid tumors:
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-10-yr survival around 55%
-more mitotic figures -necrosis present -nuclei tend to be more pleomorphic and nucleoli are conspicuous slightly more agressive |
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What's the best way to Dx as an adenocarcinoma?
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mucin-stains!
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What's clearly indicative of a Squamous cell carcinoma diagnosis?
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KERTAIN!!!
-also see intracellular bridges |
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Where do you see the Azzopardi effect?
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in small cell carcinoma, it's a liberation of nucleic acids from the cells
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Which tumors have APUD?
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neuroendocrine tumors, which are Typical and Atypical Carcinoid and Small cell
APUD: Amine Precursor Uptake and Decarboxiylation These cells take up amino acids and modify them into amines and peptides. APUD cells synthesize most of the hormones in the body. |
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Carcinoid tumor CHARAC:
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Low grade malignant tumors demonstrating endocrine microscopic pattern admixed with abundant blood vessels
It usually involves large bronchi with an endobronchial growth pattern. Affects patients under 45 years of age. It is the most common lung tumor in children |
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Where do you see lamellar bodies in an interstitial lung disease?
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amiodarone toxicity
"lipid-containing vacuoles" |
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What is amiodarone used for?
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treat tachyarrhythmias
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Bleomycin can cause...
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BOOP
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NSAIDs can cause...
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pulmonary eosinophilia
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Ara C and Aspirin can be associated with which disease?
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ARDS
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What's a key hallmark of cancer chem agent drug-induced lung disease?
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-almost always assoc with fever, but they are a Dx of exclusion
-Tx limited to discontinuing the drug and considering ADDITION OF CORTICOSTEROIDS |
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Changes as a result of drug-induced lung disease?
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-vascular damage- endo swelling with exudation of fluid
-type I destruction and type II prolif |
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What are some possible findings from a BALF?
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-T-lymphocytes alveolitis- methtrxate
-PMNs alveolitis- bleomycin -eosinophils in hypersensitivty rxns- MTX, Bleomycin, Procarbazine |
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Bleomycin toxicity increases with...
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age
and dosage |
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Bleomycin facts:
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-DLCO predicted subsequent disease
-toxicity reversible if changes only minimal -anticancer drug -synergistic toxicity with cyclophosphamide -if O2 and radiation included, plus the drug, mortality is 50-75% -up to 20% mortality after cisplatin infusion -see nodular lesions mimicking metastases due to BOOP |
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What's the cardinal symptom of radiation pneumonitis?
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-2-3 months post-Tx
-see 93% dyspnea, but also dry cough and/or less-so fever -due to local cytokine prod -usually confined to field of irradiation -generally self-limited, but may become progressive fibrosis CAN ACCEL REPAIR PROCESS WITH CORTICOSTEROIDS |
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Malar rash, polyarthritis, rapid onset of a cough, fever, and some rapidly progressive dyspnea
-see also lung crackles and severe hypoxemia Diagnosis? |
Systemic Lupus, it was a black female, but I left that out.
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What's a hallmark of diagnosing lung disease as a result of rheumatoid arthritis?
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-pleurisy with effusion, an exudate that shows SUPER LOW SUGAR content, like less than 10
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Rheumatoid arthritis lung effects may be seen as what in the bronchioles:
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-bronchiolitis obliterans organizing pneumonia (BOOP)
-bronchiolitis obliterans |
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2 possible manifestations of rheum arthritis intrathoracically?
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Poly/Dermatomyositis:
-fibrosing alveolitis or BOOP -pul vasculitis or HTN -aspiration pneumonia -respiratory muscle weakness Systemic Sclerosis -fibrosing alveolitis -BOOP -pul HTN aspiration pneumonia CHEST WALL RESTRICTION Sjorgen's Syndrome: LYMPHOCYTIC infiltration, esp. in lungs Pul Fibrosis and Autoimmune DIsease -Myasthenia gravis -chronic active hepatitis -thrombocytopenic purpure -hemolytic anemia primary biliary cirrhosis |
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LNK- what disease?
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Lungs, Nose, and Kidneys
Wegener's Granulomatosis |
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Saddle-nose deformity, what disease?
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Wegener's!
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What are 2 major presentations in blacks > whites for sarcoidosis?
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skin sarcaoidosis
and ocular Sx's, i.e. uveitis |
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Inherited coagulopathies involve...
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Protein C and S
Factor V Leiden antithrombin III deficiency |
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Where do you get the majority of PEs from?
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DVTs
-with most coming from the popliteal fossa to the pelvis -start as platelet aggs on valves in the venous sytem |
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If you see infarcts from PE, what type will they be?
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red infarcts
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What's the classic triad of Sx's in PE?
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hemoptysis
pleuritic chest pain dyspnea |
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What is in Virchow's triad?
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1) stasis
2) hypercoaguability 3) venous injury |
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4 Signs of PE:
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tachypnea
tachycardia accentuated 2nd heart sound fever- due to infarct |
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With a PE, what vent/perfusion do you expect to see?
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It will create more deadspace, so if anything you would expect an elevated pCO2, but the person hyperventilates, so it's normal or low if anything
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What happens to the pO2 in PE?
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V/Q mismatch with hypoxemia due 2 bronchoconstriction
-DEC alveolar PCO2, and there's mediators giving clinical wheezing and bronchoconstriction |
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What are the expected pO2 and pCO2 VALUES in PE?
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hypoxemia
AND hypOcarbia |
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What would be an ECHO finding indicative of PE?
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right vent dilation due to quick onset of INC press
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Westermark's sign...
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shows area of poor perfusion in a PE, but Salathe has never even seen one!
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What happens on a V/Q scan when you have a PE?
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see bronchoconstriction, so the radioisotopes have delayed washout in those areas, so there will be an area of no mottling, and an area of prolonged washout
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What's diagnostic for PE when using a V/Q scan to examine the patient?
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2 or more segmental deficits that are MISMATCHED, i.e. no perfusion, BUT ventilation
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What 2 things can duplex measure?
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1) compressibility, or in the case of a DVT, NON-compressibility
2) flow measurements can be done too |
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Cannot diagnose patients with Protein S and C deficiencies if they're on...
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coumadin
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What can cavitate in the lung?
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1) squamous cell carcinoma
2) Wegener's 3) Aspergillosiss |
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What is the most common cavitator in the lung?
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squamous cell carcinoma
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Popcorn lung is associated with what disease?
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BOOP
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Where do you see the Golden S-sign?
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-simple collapse of a lung/lobe would give a straight line
here, collapsing AROUND A MASS -not a straight line b/c this mass is seeing lung drape over the mass |
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When do you see the air bronchgram sign?
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When you have consolidation in the alveoli so it outlines the bronchi which are the only spots left with air in them
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Where do 95% of pul thromboembo come from?
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DVT from popliteal or larger
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How many PEs affect the lower lobes?
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75%
>50% are multiple and 30% recurrence rate |
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Small emboli account for what % of PE?
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70-95%
-60-80% are clinically silent. -they're in a patient with adequate cardiorespiratory function -10-15% lead to infarction, which means there was some sort of cardiorespiratory compromise |
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Steps of SMall Emboli in the Lungs:
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1) ischemia of endothelial cells
-see pul hemorrhage with adequate cardioresp status and dual blood supply 2) Once there's compromised cardiorespiratory status, you'll get red infarct, which is coagulative necrosis of the parenchyma PLUS hemorrhage 3) RBCs will lyse and see red/brown hemosiderin deposits -wedge shape formation, apex will be at the occluded vessel, the base will be at the pleural aspect 4) org of embolus, gray/white shrunken peripheral scar, so now it's FIBROTIC |
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What are the other conditions associated with having a PE?
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pul HTN
chronic cor pulmonale vascular sclerosis |
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3 Ways to get pul HTN
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1) DEC cross-sectional area of pul vasc bed leading to inc vasc resistance
2) INC pul BFlow 3) INC in left heart resistance |
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How do you get secondary pul HTN?
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-chronic obstructive or interstitial lung disease- destroying the parenchyma and there will be fewer alveolar capillaries
-recurrent pul emboli reduce the cross-sectional area -heart disease with a Right --> Left shunt will INC flow across the lungs |
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What grades of pul HTN are reversible?
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Grades 1-3
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Grades IV/V of Pul HTN look like...
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an organizing thrombus with re-canalization
-can't tell the diff b/n the 2!! |
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Grade VI Pul HTN presents as...
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Necrotizing arteritis
AND fibrinoid necrosis (vessel wall is now acellular, amorphous material) |
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Classic sign of pleural effusion?
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meniscus sign
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As you go down a lateral CXR, the spine should....
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get DARKER, but if it gets lighter at all, then there is something there, some infiltrate is present.
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How do distinguish between pleural effusion and pleural thickening on CT?
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pleural thickening has an irregular border, whereas pleural effusion will appear pretty smooth. This was especially discussed in reference to a CT.
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How distinguish a DDx of pleural effusion and pleural thickening?
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POSITIONAL CHANGES
-put patient in the lateral decubitus position |
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Does the trachea deviate with pleural effusion?
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if there's a large amount of fluid it'll get pushed away from the side with the effusion
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What are 2 possible consequences of pleural effusion?
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1) diaphragm can do gown
2) lung can get compressed even to point of atelectasis -excess fluid in pleural space can compress lungs |
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If you see an opacity with a straight line, what do you think?
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without the meniscus, think of a HYDROPNEUMOTHORAX, where the air-water interface ends up being a straight line!
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If the pleural effusion is a transudate, what are the possible problems?
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1) CHF
2) liver problem 3) renal problem pleural fluid protein >3g/dl to be exudate |
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When is pneumothorax more apparent?
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during expiration because the lung retracts more from the chest wall, so ORDER CXR at EXPIRATION
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Bloody pleural effusion, think...
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possible malignancy
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What are the 3 most common causes of pleural effusion?
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1) CHF
2) pneumonia- bacterial 3) malignant disease |
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Usually what gives only transudate will not give exudate, but...
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what gives exudate may also give transudate
-part of why exudate is a more complicated DDx |
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Meig syndrome is the triad of...
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1) right-sided hydrothorax
2) ascites 3) ovarian fibroma |
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What could cause serofibrinous pleuritis?
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it's serous fluid plus fibrinous exudates
-inflamm in adjacent lung due to pneumonia, TB, an infarct, or abscess -collagen vasc diseases like rheum arthritis or lupus -uremia -radiaiton -systemic ifxs |
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Which is more common, metastases or primary PLEURAL TUMORS?
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metastases
-coming from LUNG, BREAST, ovary, and GI tract -see desquamated tumor cells in serosanguineous fluid |
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Solitary Fibrous Tumor, aka pleural fibroma:
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CD34+Keratin-
-attached to pleural surface by a pedicle -white, filmy mass |
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How often is malignant mesothelioma related to asbestos exposure?
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90% of the time!
-25-45yr latency -GROSS- diffuse grayish pink tumor, spreads widely in pleural space CD34-Keratin+ -epithelial mesotheliomas may be difficult to DDx from mets of adenocarcinoma to the pleura |
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How to disting b/n Adenocarcinoma and mesothelioma
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Adeno:
EMA + in CYTO, CEA+, Calretinin- Mesothelioma: EMA+membrane, CEA-, Calretinin- |
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How do you Dx diffuse pul interstitial fibrosis?
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see "asbestos bodies"- golden brown rods containing asbestos fibers coated with iron-containing proteinaceous material
-pul macrophages attempt ti ingest asbestos fibers and are activated to release chemotactic factors and fibrogenic mediators that lead to a diffuse interstitial fibrosis |
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serpentine/chrysotile asbestos looks like...
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curly and flexible
BOTH FORMS ARE FIBROGENIC |
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amphibole asbestos looks like...
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straight and stiff
BOTH FORMS ARE FIBROGENIC |
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Asbestos inc. risk of bronchogenic CA...
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5-fold
smoke too, see 55-fold increase in the risk of it!!! |
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How do you Tx mesothelioma?
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pneumonectomy, radiation, and chemo
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90% of mesotheliomas are related to asbestos exposure, BUT...
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asbestos workers have GREATER chance of getting bronchogenic CA
-remember Goljan said Bronchogenic CA develops faster, so it's gonna come before mesothelioma has a chance to develop, that's why it's more prevalent |
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If see a malignant cytopathology, what's the DDx?
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mesothelioma vs. adeno, so need IHC
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If malignant cytopath, and determine by IHC it's adenocarcinoma...
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use IHC cell markers like estrogen receptor for 70% of breast carcinomas, or TTF-1 for 70% of lung adenocarcinomas
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Hypoxic respiratory failure:
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Low paO2 (<50-60mmHg)
Normal/low pCO2 |
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Hypercapnic hypoxic respiratory failure:
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Low paO2 (<50-60mmHg)
PLUS Elevated PaCO2 (>49mmHg) |
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Kussmaul breathing is...
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very deep breathing that is used to correct for acidosis
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paCO2 is NOT affected by...
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age
OR position |
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CO2 ventilation equation
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VCO2 = paCO2 * Valv * k
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What are the ALI criteria?
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paO2/FiO2 < 300mmHg
only difference from ARDS is that ARDS is <200 |
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ARDS is NOT a homogeneous disease. Giving PEEP will...
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affect parts of the lung differently.
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4 Causes of Type I Respiratory Failure:
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This is hypoxic failure:
1) R-->L Shunt 2) V/Q MISMATCH 3) low piO2 4) diffusion problem, which almost never occurs at rest |
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Causes of Type II Respiratory Failure:
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Alveolar ventilation insufficiency, leading to HYPOXIC-HYPERCAPNIC Resp Failure
-central resp drive is low -INC work of breathing -resp. muscle dysfunction -hypOventilation -can be combined with INC CO2 production |
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Does shunting respond to supplemental O2?
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NO!
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Shunting can be caused by...
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-alveolar collapse- atelectasis
-intra-alveolar filling process, pneumonia or edema -intracardiac- platypnea possible (Difficulty in breathing when erect, relieved by lying down.) -vasc shunt w/in lung- AVmalformation When seeing air bronchograms, MOST CONSISTENT with alevolar filling process and likely pneumonia |
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In a situation where you hypOventilate because of a drug overdose/neuro or muscle disease or injury/excessive load on resp. sys, then...
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can see abnormal lungs WITH V/Q mismatch, and since patient can't INC alveolar vent sufficiently, then have hypoxia PLUS INC dead space, leading in total to HYPERCAPNIA
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Hypoventilation is defined as...
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HYPOXEMIA with a NORMAL A-a gradient.
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Does hypoxemia respond to supplemental O2?
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YES!
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What happens to the body with an acute rise in acidosis?
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1) DEC cardiac contractility
2) DEC resp muscle contractility 3) INC arterial vasodilation to compensate for cerebral BFlow 4) loss of conciousness |
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In a depressed drive patient, such as one with sedative and a prev. present resp. insufficiency, see that there is an increase...
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in paCO2 with oxygen therapy
-due to V/Q mismatch and -depressed drive |
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Aminoglycoside SE leading to poss. resp. effects:
|
curare-like effects--> could paralyze resp. centers
also consider procainamide |
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Assist-Control Ventilation
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-ventilator delivers set tidal volume when triggered by patient's inspiratory effort or independently if not patient effort occurs within a certain amount of time
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Intermittent mandatory vent:
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mandatory # of fixed volume breaths, pt. could also do own breaths in between
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Pressure support:
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graded assistance, physicians sets the level of pressure to augment every spontaneous resp effort
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Controlled mech vent:
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completely dependent upon rate and tidal volume set
-patients resp efforts have no effect |
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Peak Inspiratory pressure depends on...
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compliance
|
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Anosmia top 2 causes:
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1) Viral URI
2) Trauma RULE OUT: brain tumor/other neoplasm |
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Rhinosinusitis top 2 causes:
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1) Viral URI
2) Allergic Rhinitis |
|
Nodule
vs. Polyp vs. Cyst |
fix with speech therapy and it'll go away
vs. so big it won't resorb vs. usually won't go away, esp. fluid-filled issues |
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Who gets pulmonary venous hypertension?
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-left-sided atrial or vent. disease
-left-sided valvular heart disease |
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Definitive pul HTN dx?
|
Use right heart catheterization to measure right vent press
|
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Idiopathic pul HTN typically seen in what age population?
|
age 30-50
progressive disease- survival is 2.8 years w/o therapy |
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What disorder is most commonly associated with pul HTN?
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Systemic sclerosis
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What's the other HTN assoc with pulmonary HTN?
|
PORTAL
|
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When seeing PoPH, which presents first?
|
portal HTN
|
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What happens to cardiac output when the pulHTN gets SEVERE?
|
starts dropping, a BIG problem
|
|
epoprostenol
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IV med given through central line, and needs specialized pump and to be given on continuous basis due to a short half-life
-w/o the med see rebound and the pul art press shoots way up |
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What is Bosentan?
|
-aka tracleer
-oral endothelin dual receptor antagonist -oral twice daily metabo by liver -teratogenic DOES IMPROVE SURVIVALS |
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3 main pathways to impact in pul HTN?
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1) endothelin pathway
2) NO pathway 3) prostacyclin pathway |
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Acute exacerbation of COPD, what do you do?
|
give ABx and Glucocorticosteroids (IV/oral) for FOURTEEN (14) days
|
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Do you give steroids in hypersensitivity pneumonitis?
|
-DO NOT prevent the development of fibrosis
-they DO, however, reduce the time to recovery after exacerbation MOST IMPT: Allergen Avoidance |