final exam Flashcards
abx for strep pneum, legionella, mycoplasma pneum and chlaymida
macrolide (azithromycin)
drug for DRSP, enterobacteria
3rd gen cephalosporin (ceftriaxone)
drug for staph aureus
vancomycin
drug for pseudomonas
cefepine
pneumonia outpatient
mycoplasma penumoniae, respiratory viruses, strep penum, chlamydia pneumoniae
pneumonia hospital
s. pneum, respiratory viruses, m. pneum, h. flu
pneumonia ICU
s. pneum, legionella, gram neg bacilli, s. aureus
influenza pneumonia
nonproductive bought, rtetroorbital headaches, myalgia; bilateral interstitial infiltrate
suspicion for tb
cough for more than two weeks and compatible epidemiological history
what defines ARDS?
acute in onset
bilateral disease present on chest radiography
hypoxemia
4 phases of ARDS
1) permeability pulmonary edema (the exudative phase)–diffuse alveolar damage (hyaline membranes)
2) proliferation and fibrosis (the fibroproliferative phase)
3) recovery of lung function
4) residual lung, physical, and neuropsychological impairment
pathology findings of permeability edema
diffuse alveolar damage (diffuse refers to all parts of the alveolus not to widespread lung injury)
etiology of diffuse alveolar damage
direct lung injury or systemic disorder (viral infection, septic shock, toxic lung damage)
2 phases of pathology of diffuse alveolar disease
1) exudation
2) regeneration/resolution or fibrosis
where is the initial injury in diffuse alveolar damage?
alveolar capillary endothelium but can also be to the alveolar epithelium (cytoplasmic blabbing in both but only really necrosis and denudation of basement membrane in the epithelial not the endothelial)
what do you see in the early (acute or exudative) phase of DAD?
edema and hyaline membranes
what do you see in the late (proliferative or organizing) phase of DAD?
occurs after 1 to 2 weeks; fibrosis predominate
cardinal symptoms of COPD?
dyspnea (primarily exertional)
cough
sputum production
is oxygen requirement a good indicator of COPD severity?
NO!!! FEV1 is how we classify
is COPD the only leading cause of death that has increased steadily since 1970?
yes
most common cells in COPD pathogenesis?
macrophage, CD8 lymphocyte and neutrophil
severe emphysema–> clinical picture
pink puffer–leaning over to improve breathing
clinical picture of chronic bronchitis?
the blue bloater (coughing up so much mucus)–blue b/c hypoxic
when are symptoms in asthma?
vary day to day and often worse at night or early am
major cells in asthma?
cd4+ (th2) and eosinophils and mast cells
type of breathing seen in copd?
dynamic hyperinflation (only way to increase minute ventilation os to the inc. the rate)
how do you diagnose copd?
NOT x-ray or CT; history and PE
what vaccines should copd patients get?
influenza and pneumococcal
theophylline
bronchodilator used less commonly; little added efficacy to other bronchodilators, narrow TI esp. in the elderly (nausea, vomiting, tremor, palpitations), requires monitoring of levels
when should you use glucocorticoids in copd?
systemic steroids should be used ONLY in acute exacerbations (can be added in addition to LABA/LAMA for pts with FEV1 < 50% predicted and repeated exacerbations)
when should you send pts to pulm rehab in copd?
when their fev1 is less than 50 and they are symptomatic; may consider in pts who are symptomatic and exercise-limited even if their fev1 is more than 50
surgery used for copd?
lung volume reduction surgery–the problems suppressed lungs! (removing dead space and relieving alveolar compression and improving elastic recoil)–only can do if emphysema and focal (upper lobe)
acute exacerbations of copd?
use bpap!
site of obstruction in bronchial asthma
bronchi but also bronchioles
histology of bronchial asthma
edema and chronic inflammation in the bronchial walls, many eosinophils and excess mucus, mucus plugs contain shed epithelium and charcot-leyden crystals, goblet cell metaplasia and thickening of basement membrane, submucosal gland hypertrophy, inc. in superficial blood vessels
what are charcot-leyden crystals
found in allergic diseases (asthma)–breakdown of eosinophils
gross pathology of fatal asthma
alveolar hyperinflation and alveolar collapse (atalectasis)–thick mucous plugs in airway
clinical definition of chronic bronchitis
productive cough with a specific duration of symptoms
site of obstruction in chronic bronchitis
bronchi and bronchioles
histology of chronic bronchitis
chronic inflammation within the respiratory epithelium and submucosa; inc. goblet cells; hypertrophy/hyperplasia of bronchial submucosal glands; SQUAMOUS METAPLASIA AND/OR DYSPLASIA OF BRONCHIAL EPITHELIUM
mechanism of obstruction in bronchiectasis
1) poor airway recoil due to structural airway alterations
2) mucous plugging
3) obliteration of airways (usually distal small airways)
what lobes are most often affected in post-infectious bronchiectasis
lower lobes
location of widespread bronchiectasis in CF
upper lobe predominance but diffuse
site of obstruction in emphysema
acinus
mechanism of obstruction in emphysema
1) loss of radial traction by alteration of tethering forces on airway lumen
2) contribution of small airway disease
3 types of emphysema:
1) centrilobular (centriacinar)
2) panlobular
3) paraseptal
centrilobular emphysema
proximal acinus around bronchiole destroyed; distal alveoli spared (upper lobe predominant-smoker)
?relative lack of serum alpha1-AT to this less perfused region of the lung
panlobular emphysema
who oceans uniformly involved; predominantly lower lobe involvement (alpha-1-antitrypsinase deficiency)
paraseptal emphysema
distal acinus along interlobular septa, upper peripheral lung; associated with spontaneous pneumothorax or bulla formation in young adults
gender demographics of asthma
before puberty: men>women
after puberty: woman>men
3 factors of asthma
- bronchospasm
- hyperresponsiveness
- inflammation
2 components of asthma pathophysiology
- smooth muscle dysfunction
2. airway inflammation
3 stages of asthma
- rapid, spasmogenic–> mast cell-antigen reaction (direct acting mediators such as histamine, leukotrienes, and prostaglandins on the smooth muscle)
- late, sustained–> neutrophils
- subacute/chronic inflammatory–> eosinophils, monocytes
what sound can you hear in ILD?
dry velcro crackles
most common form of interstitial lung disease?
idiopathic pulmonary fibrosis (aka cryptogenic fibrosis alveolitis)
risk factors for idiopathic pulmonary fibrosis
cigarette smoking, gerd
hrct results with idiopathic pulmonary fibrosis
basal and peripheral predominance, honeycombing, minimal ground glass opacities, reticular abnormalities
UIP pathology
architectural distortion, fibrosis with honeycombing, fibroblastic foci, patchy involvement, temporal heterogeneity
conventional treatment for IPF
corticosteroids, azathioprine, cyclophasphamide
new drugs for IPF
pirfenidone (inhibits tgf-beta induced collagen synthesis)–ppl still get worse but at a slower rate and also reduced death
nintedanib–triple tyrosine kinase inhibitor (slowed progression, didn’t show reduction in mortality)
demographics of sarcoidosis
bimodal distribution with greatest peak in late 20s and then again in 50s
hallmark on pathology of sarcoidosis
noncaseating granulomas
symptoms of sarcoidosis
most pts are asymptomatic
most common organ involvement of sarcoidosis
lung, skin, eyes, liver
cutaneous sarcoidosis
cutaneous granulomas erythema nodosum (IC deposition) lupus pernio (red to purple plaques on skin)
what are the stages of sarcoidosis and what do we use to determine?
chest x-ray!
- bilateral hilar adenopathy
- bilateral hilar adenopathy with parenchymal infiltrates
- parenchymal infiltrates alone
- advanced fibrosis
most common treatment for sarcoid
systemic corticosteroids
how do you diagnosis usual interstitial pneumonia (UIP)
diagnosis of exclusion
very unusual under the age of 45 unless family history
other entities with the same histologic appearance: asbestosis, radiation injury, connective tissue disease
histology of UIP
temporal heterogeneity and non-uniform patter of fibrosis that reflects chronicity; patches of normal lung and honeycomb change at the periphery
interstitium widened by dense collagen
minimal chronic interstitial inflammation
FIBROBLASTIC FOCI–suggest ongoing injury
honeycombing change is prominent at periphery and lower lobes!!!!!
sarcoidosis histology
non-random distribution of granulomas–primarily along lymphatics, around bronchi and blood vessels, as well as in the interstitium
where do you see fibrosis in sarcoid
upper and middle lobes (upper lobe bronchiectasis are common)
histology seen in chronic hypersensitivity pneumonitis
- diffuse chronic interstitial inflammation, temporally uniform
- bronchiolar inflammation often present
2/3 have small non-necrotizing usually interstitial granulomas
mineral dust penumoconioses
can cause interstitial fibrosis and present as progressive dyspnea (asbestosis, coal worker’s pneumoconiosis, silicosis)
what is the most common occupational disease in the world
silicosis
asbestos breaks into _______
fibers, rather than dust
ferruginous body
indigestible fibers phagocytes by macrophages and coated with iron and glycoprotein; have a translucent core
INDICATE ASBESTOS EXPOSURE NOT ASBESTOSIS!!!
histology of asbestosis
initially peribronchiolar fibrosis that eventually interstitial fibrosis that is most severe in the lower lobes (b/c you are inhaling stuff)
end-stage fibrosis similar to other forms but for presence of numerous asbestos bodies
associated lesions of asbestos exposure
pleural plaque on diaphragm
pleural effusion
malignant mesothelioma
bronchogenic carcioma
definition of asbestos
interstitial fibrosis with the identification of numerous asbestos bodies
bronchoalveolar lavage in sarcoidosis
inc. in activated T cells, cd4 cells, immunoglobulins, and igg-secreting cells, reduced number of cd8 cells, and an elevated Cd4-cd8 count!
copd inflammation is mediated by ______
NEUTROPHILS (cd8+ t cells and macrophages)
asthma inflammation is mediated by
HELPER T2 CELLS AND EOSINOPHILS
anticholinergics vs. beta agonists
what works best in what
copd: anticholinergics
asthma: beta agonists are better
two basic ways to promote airway smooth muscle relaxation and decrease airway constriction
- receptor blockade promotes relaxation: cysLTR and muscarinic receptor antagonists (inhibition of receptor that is coupled to a G protein that increases cytosolic calcium and promotes contraction)
- receptor stimulation promotes ASM relaxation: cAMP or cGMP (beta-2 agonists)–> activate PKA
anticholinergic of choice in copd
ipratroprium
methylxanthines
theophylline–causes bronchodilation by inhibiting phosphodiesterase thereby dec. cAMP hydrolysis
albuterol
short acting beta2 agonist
long acting beta2 agonists
indacaterol, salmeterol, formoterol
anticholinergic does or does noT dec. bronchial hyper responsiveness over time?
DOES NOT
what do leukotrienes do?
potent inflammatory mediators that promote smooth muscle contraction, induce vasopermeability, and enhance mucus secretion while decreasing mucus clearance and promoting eosinophil chemotaxis (leukotriene modifiers–have both bronchodilator and limited anti-inflammatory because they act on both beta receptor and also cysltrs)–but they are only really effective in 20-30% of pts
what are the most potent of the inhaled steroids?
fluticasone and budesonide
what is the best combination for copd?
ipratroprium (anticholinergic) and theophylline (phosphodiesterase inhibitor)
what is the only therapy proven to prolong life in copd?
o2 therapy!
most common pathogens in cf
s. aureus, p. aeruginosa, mrsa
what is the new drug for CF called
kalydeco
timing for acute sinusitis
less than 4 weeks
timing for chronic sinusitis
greater than 12 weeks
what is the first line tx for treating acute sinusitis
amoxicillin
microbiology of acute sinusitis
strep pneumo, h. influ, staph aureus
histopath for acute vs. chronic sinusitis
acute: exudative process, associated with hemorrhage and necrosis; NEUTROPHILS!!!
chronic: proliferative process, fibrosis of lamina propria, LYMPHOCYTES, PLASMA CELLS, EOSINOPHILS!!
complication of ethmoid sinusitis
orbital extension–> periorbital cellulitis, orbital cellulitis, sub-periosteal abscess, orbital abscess, cavernous sinus thrombosis
complication of frontal sinus
cranial extension (meningitis, epidural abscess, subdural abscess, frontal lobe abscess)--> POTT's puffy tumor inferior extension--orbital infection similar to ethmoid disease
complication of sphenoid sinus
cavernous sinus extension: visual loss, cranial neuropathies, ACUTE SPHENOID SINUSITIS IS AN EMERGENCY
protein e6 hpv
degrades tumor supressor gene p53
protein e7
causes loss of the tumor suppressor protein rb and overexertion of p16
monoclonal antibody against RSV
palivizumab
virchow’s triad
1) vascular injury
2) venous stasis
3) hypercoagulability
presence of PAH on PE?
loud p2 rv lift systolic murmur (TR) diastolic murmur (PR) RV S4
presence of RV failure on PE?
JVD with V wave RV S3 hepatomegaly edema ascites
what does S3 mean?
heart failure!!!
general medical management for PAH?
oxygen, diuretics, digoxin, warfarin and lifestyle adjustments
what factors have increased activity in PAH?
endothelin
what factors have reduced activity in PAH?
no and prostacyclin
drug name for the target of the egf pathway
erlotinib
geftinib
fusion gene that has been identified in non-small cell lung cancer
eml4/alk translocation (seen previously only lymphoma)
the normally silent anaplastic lymphoma kinase (ALK)–a tyrosine kinase is driven by the fusion with the eml4 gene
inhibition of alk in lung cancer cells carrying this fusion gene leads to apoptosis and cell death
oral inhibitor of ALK
crizotinib
what is the most common mutation seen in lung cancers?
kras
two molecules in the normal pathway of T cell inhibition
CTLA-4 and PD-1
anti-PD1 drug
nivolumab
which arrhythmia has been shown to most commonly recur in patients with untreated obstructive sleep apnea?
atrial fibrillation
the normal increase in pack during sleep is related to:
a decrease in the tidal volume NOT respiratory rate
central sleep apnea is most commonly associated with….
severe chronic heart failure
cheyne-stokes respiration typically occurs during which stage of sleep?
stages 1 and 2
the parietal pleura is supplied by which vascular supply?
intercostal arteries
hemoptysis is from which blood vessel usually?
bronchial arteries
primary source of fluid production in the pleural space
parietal pleura
how does the fluid in the pleural space get reabsorbed
stomata located in the parietal pleura (direct communication with lymphatics)
what is the usual first test to confirm presence of pleural effusion?
chest x-ray
what other imaging modality is used to evaluate pleural effusion after chest x-ray?
ultrasound
when does something become an exudate
lights criteria: protein in the fluid:serum has to be greater than 0.5; LDH ratio has to be greater than 0.6
when do you get decreased glucose levels in pleural fluid (<60 mg/dl)
infection–empyema, tb
malignancy
RA
esophageal rupture
when do you get low pH <7.2 in pleural fluid
infection–empyeme, tb
malignancy
ra
esophageal rupture
when do you get >10k cells in pleural fluid
infection, connective tissue dz, cancer
what do neutrophils in the pleural fluid mean?
infection
what do lymphocytes in the pleural fluid mean?
cancer, tb, chylothorax (high TG)
what do eosinophils in the pleural fluid mean?
blood–trauma/pe; air–pneumthorax asbestos exposure, drug reaction, parasitic infectio
different between a complicated parapneumonic effusion (CPE) and an empyema
both will have low ph and low glucose and high cell count with neutrophils but there will be NO bacteria in the CPE and YES BACTERIA IN THE EMPYEMA
major cause of exudative effusion globally?
tb
pleural effusions in RA
often painless, more often in males, subcutaneous nodules
tx: immunosuppression; occasional drainage and pleurodesis
pleural effusions in lupus
often pleuritic chest pain, arthralgia of lupus
tx: immunosuppression and occasional drainage and pleurodesis
