Pulmonary Exam: Clinical Flashcards
normal heart size on chest x-ray
smaller than half the width of the midline to the outside of the ribs
pulmonary edema on CXR
bilateral fluffy infiltrates, kerley B lines +/- cardiomegaly
pleural effusion on CXR
blunting of costophrenic angle (where diaphragm meets ribcage)
pneumothorax on CXR
absence of pulmonary markings on affected side with visibly deflated lung
lobar pneumonia on CXR
infiltrate in lobar pattern
interstitial lung disease on CXR
diffuse honeycombing
Normal FVC
5L
Normal FEV1
4L
normal FEV1/FVC
0.8
obstructive lung disease on CXR
hyperinflation with flattened diaphragms
obstructive lung disease on spirometry
reduced FEV1 and reduced FEV1/FVC ratio
restrictive lung disease on spirometry
Reduced FEV1 and FVC with normal ratio
chronic bronchitis criteria
productive cough 3 months per year for at least 2 years
chronic bronchitis pathophys
mucosal hypertrophy, inflammation, increased mucus leading to smaller airway diameter. Shunting from mucus plugs causes cyanosis
emphysema pathophys
smoke recruits macrophages and neutrophils into alveolar space; subsequent protease production destroys alveolar walls. Increased compliance and loss of elastic recoil
why use CO for DLCO
it’s diffusion-limited so it’s a good indicator of ability for gas exchange
decreased DLCO in COPD indicates
emphysema
emphysema characteristics
high respiratory rate can diminish cyanosis
pathophys of alpha-1 antitrypsin deficiency
deficiency of protease inhibitor leads to too much elastase that destroys alveoli. Misfolded proteins can occur in liver to cause cirrhosis
alpha-1 antitrypsan deficiency emphysema pattern
panacinar emphysema that is lower lobe predominant
smoking-associated emphysema pattern
centriacinar involvement that is upper lobe predominant
what is bronchiectasis
dilated and thickened airways due to repeated episodes of inflammation/infection
causes of bronchiectasis
cystic fibrosis, chronic infection, reflux, primary ciliary dyskinesia
primary ciliary dyskinesia
autosomal recessive, leads to cilia not being able to beat, coexists with infertility and situs inversus
2 categories of restrictive lung disease causes
poor breathing mechanics (neuromuscular, structural problems), interstitial lung disease
2 hallmarks of restrictive lung disease
low volumes and decreased DLCO
general pathophys of interstitial lung disease
inflammation in interstitium and alveoli
causes of interstitial lung disease
idiopathic pulmonary fibrosis, systemic autoimmune disease, pneumoconioses, drug toxicities
common presentation of ILD
insidious dyspnea, dry cough, fine “velcro” crackles in all lung fields, digital clubbing
ILD on CXR
diffuse, bilateral, small irregular opacities
idiopathic pulmonary fibrosis pathophys
repetitive epithelial injury with disordered repair leading to increased type II pneumocytes and fibroblasts and decreased type I pneumocytes
idiopathic pulmonary fibrosis presentation
insidious onset dry cough, dyspnea, ILD crackles, clubbing
idiopathic pulmonary fibrosis prognosis
average survival of 4 years (death due to pulmonary HTN, respiratory failure, lung cancer, arrhythmia)
idiopathic pulmonary fibrosis CXR/CT
honeycombing pattern
systemic diseases that can cause pulmonary fibrosis
scleroderma, RA, granulomatosis with polyangiitis, sarcoidosis
Sarcoidosis pathophys
activated macrophages cause widespread non-caseating granulomas
sarcoidosis lab findings
high serum ACE levels, hypercalcemia with elevated vitamin D activation
sarcoidosis clinical presentation
cough, dyspnea, fatigue, skin lesions, uveitis
sarcoidosis imaging
coarse reticular opacities with bilateral hilar adenopathy
sarcoidosis treatment
steroids
types of pneumoconioses
coal miner’s lung, silicosis, asbestosis, berylliosis, hypersensitivity pneumonitis
drug toxicities that can cause ILD
bleomycin, busulfan, amiodarone, methotrexate
tidal volume
amount of air moved in a quiet breath
inspiratory reserve volume
amount that can be inhaled after quiet inhalation
vital capacity
tidal volume plus expiratory reserve plus inspiratory reserve (total lung capacity minus residual volume)
functional residual capacity
expiratory reserve volume plus residual capacity (amount of air in lungs at the end of quiet exhalation)
total lung capacity
quantity of air in lungs at maximum inspiration
inspiratory capacity
tidal volume plus inspiratory reserve volume
forced vital capacity
total amount of air exhaled from total lung capacity down to residual volume in a forced maneuver
flow-volume loop for obstructive lung disease
wider than normal
flow-volume loop for restrictive lung disease
narrower than normal
bronchodilator response
increase in FEV1 of 12% and greater than 0.2L
main lung volumes measured
TLC and RV
definition of restrictive lung disease in lung volumes
TLC below lower limit of normal with reduced FEV1 and FVC but normal ratio
a decreased vital capacity in the presence of a normal FEV1/FVC ratio suggests
restriction
what might need to be corrected for when measuring DLCO
blood hemoglobin level
causes of decreased DLCO
emphysema, interstitial lung disease, lung damage from radiation or drugs, pulmonary embolism, pulmonary HTN
basic definition of pneumonia
infection of alveoli
basic def of pneumonitis
immune-mediated inflammation of alveoli
what is an empyema
purulent exudate in pleural cavity
what is a lung abscess
circumscribed collection of pus within the parenchyma
pulmonary physiology of pneumonia
impaired alveolar ventilation causes V/Q mismatch with shunting and causes hypoxia due to increased A-a gradient
pneumonia risk factors
old age, immobility, immunosuppression, impaired airway protection, chronic diseases, environmental factors (crowded conditions, toxins)
which pathogen is associated with ETOH abuse in pneumonia
klebsiella
foul-smelling sputum in pneumonia is associated with
aspiration pneumonia
most common pathogens in typical community-acquired pneumonia
strep pneumoniae, haemophilus influenzae, moraxella
what pathogen is usually responsible for bacterial superinfection in pneumonia
staph aureus
CXR CAP (typical)
lobar poorly defined patchy infiltrates with or without effusion
definition of community-acquired pneumonia
occurs outside of healthcare setting
atypical bacteria causing pneumonia
chlamydophila, mycoplasma, legionella
atypical pneumonia viruses
influenza, RSV, adenovirus, COVID
atypical pneumonia chest xray
diffuse reticular pattern concentrated in perihilar region
pathogens in hospital acquired pneumonia
pseudomonas, enterobacteriaceae, acinetobacter, staph aureus, strep pneumoniae
definition of hospital acquired pneumonia
onset >48 hours after admission
aspiration pneumonia pathogens
anaerobes and gram negeatives
ssx of aspiration pneumonia
immediate: bronchospasms, crackles. Late (24 hours): fever, dyspnea, cough with foul-smelling sputum
aspiration pneumonia CXR
depends on position on aspiration
bronchopneumonia on CXR
patchy areas spread throughout
cryptogenic organizing pneumonia definition
a non-infectious pneumonia of unknown etiology characterized by involvement of the bronchioles, alveoli, and surrounding tissue without response to abx. Supportive treatment only
outpatient pneumonia treatment
amoxicillin+azithromycin/clarithromycin or doxycycline
inpatient pneumonia treatment
ceftriaxone + azithromycin or doxycycline OR levofloxacin
hospital-acquired pneumonia treatment if gram negative
pip-taz or cefepime or ceftazidime+levofloxacin
hospital-acquired pneumonia treatment if gram-positive
add vancomycin to gram negative treatment
aspiration pneumonia treatment
ampicillin sulbactam or clindamycin
etiologies of syncope
vasovagal (psychogenic, stimulation of visceral organs/carotid bodies), orthostatics (dehydration, ANS dysfunction), cardiac valve dysfunction, arrhythmia, neurogenic
most common dvt location
popliteal
Homans sign
calf pain on dorsiflexion
superficial thrombophlebitis
pain ,tenderness, induration and erythema overlying a superficial vein with palpable cord (maybe)
superficial thrombophlebitis treatment
hot compress, nsaids, remove offending agent
superficial thrombophlebitis risk factors
same as DVT
when is indefinite anticoagulation
high-risk patients and those with 2 or more VTE events
what anticoagulant to give in case of renal insufficiency
unfractionated heparin
what anticoagulant to use in pregnancy
LMWH
anticoagulant duration for provoked VTE
3-6 months
anticoagulant duration for unprovoked VTE
6+ months and search for underlying cause such as cancer screening
part of coagulation cascade affected by enoxaparin
activates antithrombin III
part of coagulation cascade affected by heparin
inactivates thrombin and factor Xa
Large vessel vasculitis
giant cell, takayasu
Giant cell arteritis aka
temporal arteritis
Giant cell arteritis summary
involves branches of carotid artery, unilateral headache, associated polymyalgia rheumatica, can involve ophthalmic artery
Takayasu arteritis summary
commonly affects Asian women<40, involves aortic arch and proximal great vessels, fever, night sweats, skin nodules, arthritis, vision disturbances, weak upper extremity pulses
treatment for large vessel vasculitis
steroids
medium cell vasculitis
Buerger disease, Kawasaki disease, Polyarteritis nodosa
Buerger disease affects
young adult men, smokers
Buerger disease ssx
intermittent claudication of extremities leading to gangrene
Buerger disease treatment
smoking cessation
Kawasaki disease affects
Asian children <4 y/o
Kawasaki disease ssx
conjunctival injection, rash, adenopathy, strawberry tongue, hand/foot edema, fever, coronary artery aneurysms
Kawasaki disease treatment
IVIG, ASA
Polyarteritis nodosa affects
middle aged men who may be HepB positive
polyarteritis nodosa ssx
fever, weight loss, malaise, headache, abd pain, melena, HTN, kidney damage
polyarteritis nodosa treatment
steroids, cyclophosphomide
polyarterteritis nodosa affects what arteries
mesenteric, renal
Small vessel vasculitis - immune mediated
Behcet disease, immunoglobolin A, cutaneous small vessel, mixed cryoglobulinemia
Behcet disease is associated with what gene
HLA-B51
Behcet disease ssx
aphthous/genital ulcers, uveitis, erythema nodosum
Behcet disease precipitated by
HSV or parvo
Behcet disease treatment
none, self-resolving in 1-4 weeks
immunoglobulin A aka
HSP
immunoglobulin A follows
URI, IgA immune complex deposition
immunoglobulin A ssx
purpura of LE, arthralgia, GI pain
immunoglobulin A treatment
supportive, steroids
cutaneous small vessel vasculitis due to
response to certain meds or infections
cutaneous small vessel vasculitis ssx
palpable purpura
mixed cryoglobulinemia due to
viral infections (especially hep C), B cell malignancies
mixed cryoglobulinemia ssx
palpable purpura, weakness, arthralgias due to IgG and IgM immune complex deposition
small cell vasculitis ANCAs
Churg-strauss, Wegeners, microscopic polyangitis
Churg-strauss aka
eosinophilic granulomatosis with polyangiitis
Churg-strauss ssx
asthma, sinusitis, skin manifestations
Wegeners aka
Granulomatosis with polyangiitis
Wegeners ssx
upper respiratory, lower respiratory, renal
microscopic polyangiitis
like Wegeners but without nasopharyngeal involvement or granulomas
treatment for microscopic polyangiitis and Wegeners
cyclophosphamide, steroids
what is an ANCA
an IgG autoimmune reaction to neutrophils
other causes of vasculitis
infective endocarditis, syphilis, connective tissue diseases (SLE, RA), fungus
pediatric SBP should be
70+age*2
definition of shock
inability to remain aerobic metabolism
4 kinds of shock
hypovolemic, distributive, cardiogenic, obstructive
hallmark of hypovolemic shock
decreased preload
hallmark of distributive shock
decreased afterload
most common cause of distributive shock
septic shock
CO in shock means what kind
distributive
hallmark of cardiogenic shock
decreased CO
cardiogenic shock treatment
inotropes
hallmark of obstructive shock
normal contractility with decreased CO
distributive shock treatment
volume with or without pressors
low cardiac output and low filling pressures means
hypovolemic shock
low cardiac output and high filling pressures means
cardiogenic or obstructive shock
shock with low SVR means
distributive shock
neurogenic shock
vasodilation due to loss of sympathetic tone above T6 leading to bradycardia, hypotension, decreased SVR
neurogenic shock treatment
pressors
first sign of hypovolemic shock
narrowed pulse pressure with or without tachycardia
distributive shock skin findings
warm, moist
signs of obstructive shock
distended neck veins, muffled heart tones, possible tracheal deviation
what does a vasopressor do
increase SVR
what does an inotrope do
increase cardiac contractility
important principle of starting pressors
fill tank before starting pressors
goal MAP for septic shock
> 65
mainstay for inotropes
dobumatine (primarily B1 but also some B2, helps with decreasing SVR)
pure vasopressors
vasopressin and phenylephrine
when to use pure vasopressors
distributive shock
agents with both inotropic and vasopressor activity
norepi, epi, dopamine
norepi is primarily
vasopressor (alpha)
epi is primarily
inotrope (beta)
