pulm exam 1 Flashcards
what is inflammatory lung disease?
large group of heterogeneous disorders
inflammatory process involving alveolar wall that can lead to irreversible fibrosis, distortion of lung architecture and impaired gas exchange
are imaging studies useful for inflammatory lung disease?
they’re nonspecific, and do not point to a definitive diagnosis
-often need to obtain tissue biopsy
symptoms of interstitial lung disease
Cough – usually nonproductive
Dyspnea on exertion
Other symptoms possible secondary to another condition
signs of interstitial lung disease
Rales heard at lung bases Oxygen desaturation Digital Clubbing Signs of pulmonary HTN and Cyanosis in advanced disease JVD, LE Edema
Pneumoconiosis
chronic, fibrotic, occupation lung disease
caused by inhalation of a foreign particle which causes a reaction in the lung which results in fibrotic changes
when does pneumoconiosis appear?
20-30 years after constant exposure
what is the most common diagnosis among ILD patients?
idiopathic pulmonary fibrosis (increased frequency men and smokers)
typical age 50-70
onset of symptoms 1-2 years prior to diagnosis
prognosis of idiopathic pulmonary fibrosis
highly variable disease course
mean survival 3-7 years after initial diagnosis
*treatment is highly controversial, 70% do not improve with therapy and experience progressive disease
what is sarcoidosis?
multi-systemic granulomatous disease - inflammatory reaction to one of many possible triggers
where does sarcoidosis affect?
90% lung
eyes, skin, liver, spleen, heart, nodes
etiology of sarcoidosis
more common in AAs, women
typically 20-30 yo
how does a typical sarcoidosis patient present?
young, constitutional symptoms, resp complaints, blurred vision, erythema, nododsum
workup and hallmark of sarcoidosis
CXR: Bilateral Hilar and Right Paratracheal Adenopathy
- Potato nodes
hallmark: bilateral diffuse reticular infultrates
treatment of sarcoidosis
systemic corticosteroids (90% response) - most resolve/spontaneously improve within 2 years
where in the lung is ventilation higher?
lung bases (alveoli at the apex are stretched more at baseline, thus worse compliance)
-perfusion is also higher at the lung bases - due to gravity, arterial and venous pressure exceed alveolar pressure at the bases,but alveolar pressure exceeds these vascular pressures at the apices
what disorders decrease ventilation?
airway (COPD) and airspace (pneumonia) disorders
what disorders decrease perfusion?
pulmonary vascular disorders (PE)
what are the causes of hypoxemia?
low inspired partial pressure of oxygen
hypoventilation - alveolar to arterial oxygen difference will be normal (opioids)
ventilation-perfusion mismatch
shunt
diffusion abnormality
a low forced expiratory volume in 1 second/forced vital capacity ration indications what functional classification?
obstructive defect
a low FVC and low total lung capacity (TLC) suggests what functional classification?
restrictive defect
low FEV1/FVC and low TLC suggests what functional classification?
combined defects
low diffusing capacity of the lung for carbon monoxide (DLCO) and hypoxemia suggests what functional classification?
gas transfer defect
Rapid, deep respiration due to stimulation of the respiratory center of the brain by ↓ pH, normal during exercise, and common in patient with severe metabolic acidosis (DKA)
kussmaul
breath fast for a while then stop, and then breath fast for a while and then slow down. Brain disorders
cheyne-stokes
dyspnea when sitting up *liver disease
platypnea
dyspnea when supine (HF)
orthopnea
dullness in percussion indicates what?
decreased resonance noted with pleural effusion and other diseases
hyperresonance with percussion is indicative of what?
increased resonance either due to lung distention (COPD exacerbation) or focal air collections (bullous disease, pneumothorax)
are breath sounds increased or decreased in emphysema?
markedly decreased
if there is asymmetry in intensity, which side is abnormal?
the side where there is decreased intensity
with vesicular breath sounds, which component predominates?
inspiratory (turbulent airflow within the lobar and segmental bronchi) prdominates
Continuous musical sound lasting longer than 250 ms
Due to oscillation of opposing airway walls that are narrowed almost to the point of contact.
wheeze
clinically, wheezing indicates what?
airflow obstruction, though its absence does not exclude obstruction
long continuous adventitious sounds, generated by obstruction to airways
Low-pitched, continuous sounds that have a tonal, sonorous quality
rhonchi - may be due to excess mucus in the airway that’s moving around
localized rhonchi suggests what?
obstruction of any etiology (tumor, foreign body, mucus)
rhonchi due to respiratory secretions will often disappear with coughing
High-pitched continuous sound heard over the trachea
Due to turbulent flow generated in the upper airway during extrathoracic airway obstruction
stridor - generally inspiratory
this tests measures the total amount (volume) of air exhaled during forced expiration (forced vital capacity) and the volume of air exhaled during the first second
spirometry
Bronchoprovocation
using maneuver (exercise) or inhaled medication (methacholine) to detect bronchial hyperresponsiveness (one of the defining features of asthma)
how much methacholine is given during bronchoprovocation?
concentration required to decrease FEV1 by 20% (PC20) - then give albuteral
in a chest CT, what IV contrast useful for?
to help differentiate hilar lumph nodes from pulmonary arteries
what is bronchoscopy useful for?
evaluation of pulmonary infections, diagnosing and staging lung cancer, diagnosing sarcoidosis, excluding endobronchial lesions (stenosis or tumor) and therapeutic aspiration (mucus plugging)
what is an ultrasound useful for?
diagnosing pneumothorax and pleural effusion (cannot visualize normal lung as air reflects ultrasound waves)
what is pulmonary HTN?
elevated pulmonary pressure
- Pulmonary artery pressure greater than 25 mmHg at rest (normal is 12-16 mmHg)
- elevated PA pressure results in the R ventricle pumping against elevated pressure often resulting in RV failure
who should be screened for PAH?
pts with family history of PAH
pts with systemic sclerosis (scleroderma)
pts with portal HTN being evaluated for liver transplant
yearly screening
epidemiology of PH
prevalence not known - rare in gen population.
at risk groups (HIV, SCD, portal HTN, scleroderma)
hallmark symptom of PH
SOB (50%)
other clinical manifestations of PH
atypical/exertional CP, exertional dyspnea, fatigue, syncope
PE findings for PH
early disease- often unremarkable PE
loud pulmonic component of second heart sound, split second heart sound
increased JVP
signs of RHF (hepatomegaly, ascites, anasarca/edema)
diagnostic eval for PH
echocardiogram to start (non invasive, estimate PAP, assess both right and left heart)- better for screening than definitive dx
chest xray also good, often incidental findings when CXR ordered for another reason, not good for definitive diagnosis, only suggestive of PH
gold standard = lung biopsy
is EKG helpful to diagnose PH?
can show right heart hypertrophy or strain, right axis deviation, and RBBB.
- cannot make dx of PH with EKG, but helpful in the evaluation of R heart failure
what is the preferred imaging for CTEPH (chronic thromboembolic PH)?
V/Q scan ( can see clots very nicely)
if CTEPH on V/Q, pulmonary angiography is confirmatory test
why is exercise testing good for PH?
***establishes functional baseline - need to find out before tx (also need to know cause of PH)
detects PH that is only symptomatic during exercise
measures functional class
prognostic
what is given during a right heart cath (RHC) as a vasodilator to see if change in PAP?
nitric oxide
what is a positive response in pulmonary vasoreactivity testing?
decrease in mean PAP by >10 mmHg to an absolute value less than 40 mmHg without change in cardiac output
diagnostic criteria of class 1 PH
PAP> 25 mmHg at rest measured by RHC
PCWP less than 15 mmHg
elevated pulmonary vascular resistance
no thromboembolic disease, parenchymal lung disease, or systemic or metabolic disease associated with PH are present
diagnostic criteria of class 2
on a right heart cath, the following can confirm L heart disease is the cause of PH:
PAP > or equal to 25 mmHg
PCWP greater than or equal to 15 mmHg (indicating LHF)
reduced CO (can be normal)
L atrial enlargement
diagnostic criteria of class 3
elevated PAP on RHC
PFTs indicating hypoxia
CT scan indicating ILD
diagnostic criteria of class 4
elevated PAP on RHC
evidence of thrombus or thrombi on VQ scan
differential Dx for PH
angina MI/CAD valvular disease/stenosis COPD CHF
treatment of PH WHO class 1
no effective primary therapy and advanced therapy and combination therapy is usually called for (only after all causes are exhausted and RHC is done)
*treated differently bc therapy is directed at the PH itself not other causes
Oxygen therapy (POx > or equal to 90% at rest, with exertion and during sleep)
treat fluid overload diuretics (salt restriction, weight monitoring)
advanced therapies for PAH that target cellular pathways
endothelin - vasoconstrictor and mitogen
nitric oxide - vasodilator and antiproliferative
prostacyclin - vasodilator, antiproliferative, and inhibits platelet function
most efficacious combination therapy for PAH
combination of tadalafil and ambrisentan
treatment of group 2 PH
treat the underlying cause
- reduced EF with ACE/ARB, diuretics
- preserved EF- treat HTN with beta blockers
- valve correction may resolve PH due to valvular cause
treatment of group 4 PH
surgery
- pulmonary thromboendartectomy can be curative
- lifelong anticoagulation
T or F: pulmonary HTN is an contraindication to judicious exercise
F - it is important to avoid deconditioning
-mild breathlessness is acceptable, but pts should avoid exertional dizziness, near syncope or chest pain
prognosis of PH
can be fatal.
- those with RHF/RV dysfunction have a poor prognosis
- those with 6 min walk distance 150pg/mL
which PH group has the worst prognosis?
group 1
- epoprostanol improves survival
- advanced therapies improve survival
what is the most common cause of bacterial pneumonia?
strep pneumo
clinical presentation of CAP
fever chills rigor tachycardia pleuritic CP (hurts when breath in) mucopurulent sputum cough shortness of breath nausea, vomiting
**Older patients: malaise, confusion common
physical exam for CAP
80% are febrile respiratory rate above 24/min tachycardia crackles rales heard over involved SEGMENT increased tactile fremitus
gold standard to diagnose CAP
CXR
leukocytosis (15-30k) if you order a CBC
when should sputum culture be used for pneumonia?
IDSA/ATS guidlines : sputum culture for hospitalized patients with signs and sx of pneumonia and : ICU admission failure of outpt antibiotic therapy cavitary lesions ETOH abuse structural lung disease pleural effusion
- not first line test in a CAP outpatient
do you need to know of pneumonia is bacterial or viral?
in theory, no
usually treated empirically with antibiotics
outpatient tx of CAP
repeat CXR not indicated if patient clinically improving, although smokers and non responders may need another CXR to document resolution of pneumonia and assess presence of malignancy
smoking cessation!!
risk factors for drug resistance PNA
- age > 65
- recent use of beta-lactam, macrolide, or quinolone (3-6 mos)
- ETOH
- comorbidities
- immunosuppression
- exposure to children in daycare
inpatient treatment (non ICU) of CAP
respiratory fluoroquinolone alone
cephalasporin or carbipenem plus macrolide or doxycyline
inpatient ICU treatment of CAP
cover MRSA if admitted to ICU (add vancomycin)
empiric therapy - IV beta-lactam plus macrolide or quinolone
difference between HCAP and HAP
HCAP - healthcare associated pneumonia : non hospitalized patient exposed to IV therapy/wound therapy in the past 30 days, residents in a nursing facility, hospitalization for 2 or more days within 90 days prior to discharge, attendance at hospital or clinic within prior 30 days
HAP- hospitalized aquired pneumonia : pneumonia occurring > 48 hours after admission that was not present at time of admission
complications of pneumonia
destruction of lung tissue pleural effusion bronchectasis empyema lung abscess
transmission of legionnaires disease
aerosolization or aspiration of contaminated water (cooling tower, humidifiers, resp equipments) - usually linked to contaminated hot water supply. Not transmitted person to person
symptoms of legoinnaires disease
early: malaise, muscle aches, lethargy, and slight headaches. high fever, non-productive cough, abdominal pain, diarrhea
late: extreme lethargy, comatose state. impaired kidney and liver functioning, nervous system disorders
when to suspect legionnaires disease
when patient is hyponatremic
when patient has alot of extrapulmonary symptoms
antibiotic failure
gram stain shows PMNs with no organisms
white in lungs on CXR
blood
pus (pneumonia)
water (pulmonary edema)
cells (cancer)
protein or calcium - rare
what does a pleural effusion look like on an CXR?
dense white area, transitions through gray to black normal lung as you go higher
you will be able to see the other diaphram in the lateral view
most layer out in the lateral decubitus position
bilateral perihilar opacification (“bat-wing” patter) and cardiomegaly on a CXR is indicative of what?
heart failure
what would you see on a CXR for LLL pneumonia?
lose the left hemidiaphragm and descending aorta
