respiratory Flashcards
chronic bronchitis defination
chronic productive cough for
atleast 3mnths
in 1 year
for 2 consecutive years
effect of excess oxygen in COPD
In advanced chronic obstructive pulmonary disease (COPD), destruction of the terminal bronchioles and alveoli causes areas of physiologic dead space to develop. The affected regions have limited surface area available for gas exchange, which leads to ventilation/perfusion (V/Q) mismatch causing local hypoxia and hypercapnia.
Hypoxia induces selective vasoconstriction in these areas of the lung and redirects blood flow to better ventilated alveoli, reducing V/Q mismatch.
Supplemental oxygen improves hypoxia but can cause C02 retention by the following mechanisms:
• Loss of compensatory vasoconstriction in areas of ineffective gas exchange worsens V/Q mismatch
• Increase in oxyhemoglobin reduces the uptake of C02 from the tissues by the Haldane effect
• Decreased respiratory drive and slowing of the respiratory rate causes reduced minute ventilation The acidosis caused by an acute increase in C02 increases brain gamma-amino butyric acid and glutamine and decreases brain glutamate and aspartate, causing a change in level of consciousness. Hypercapnia also causes reflex cerebral vasodilation and may induce seizures, as seen in this patient
. Oxygen should be used cautiously with a goal Sa02 of 90%-93% or Pa02 60-70 mm Hg. Patients who develop significant acidosis or have severely reduced level of consciousness require mechanical ventilation.
bohr effect
⬆️ pco2》⬆️H+》⬇️hb affinity for o2》⬆️o2 unloading
occurs at tissue level
haldane effect
⬆️pO2⬆️unloading of CO2 at alveoli level
Oxygenation of blood in the lungs displaces carbon dioxide from hemoglobin which increases the removal of carbon dioxide. This property is the Haldane effect. Conversely, oxygenated blood has a reduced affinity for carbon dioxide.
cause of leukocytosis after treatment of aasthma exacerbation
patient being treated for an asthma exacerbation now has leukocytosis with
neutrophilic predominance, which is a common effect of systemic glucocorticoids (eg,
methylprednisolone).
Glucocorticoid use causes a leukocytosis due to the following:
• Mobilization of marginated neutrophils into the bloodstream (predominant
mechanism
): Marginated neutrophils are attached to the endothelium of blood
vessels: glucocorticoid-induced mobilization of these neutrophils leads to a higher
number of circulating neutrophils
• Stimulation of release of immature neutrophils from the bone marrow (as evidenced
by the 3% band forms in this patient)
• Inhibition of neutrophil apoptosis
In contrast, glucocorticoids decrease the number of circulating lymphocytes and
eosinophils through a combination of increased apoptosis, increased emigration into the
tissues, and decreased production
theophylline toxicity cause and symptoms
Theophylline has a
narrow therapeutic index, and toxicity can occur from accumulation by reduced clearance
or decreased metabolism due to saturation of metabolic pathways. Theophylline is
metabolized predominantly by the cytochrome oxidase system in the liver. Inhibition of
these enzymes by concurrent illness (eg, cirrhosis, cholestasis, respiratory infections with
fever) or drugs (eg, cimetidine, ciprofloxacin, erythromycin, clarithromycin, verapamil) can
raise serum concentration and cause toxicity.
Symptoms of toxicity usually manifest as central nervous system stimulation (eg,
headache, insomnia, seizures), gastrointestinal disturbances (eg, nausea, vomiting), and
cardiac toxicity (arrhythmia).
This patient recently began taking ciprofloxacin, a drug
known to decrease clearance of theophylline. Therefore, the best next step is to
measure serum theophylline levels to assess for toxicity.
uses of non invasuve positive pressure ventilation
Noninvasive positive-pressure ventilation (NPPV) is ventilatory support delivered by
facemask rather than endotracheal tube; it can be delivered in several different modes,
including continuous positive airway pressure and bilevel positive airway pressure.
NPPV decreases work of breathing, improves alveolar ventilation, and is the preferred
method of respiratory support in patients with AECOPD. Physiologic benefits include a
decrease in respiratory rate and arterial carbon dioxide tension (PaCOzl, with an increase
in tidal volume, minute ventilation, and arterial oxygen tension (PaOzl. NPPV in patients
with AECOPD is associated with a decrease in mortality, intubation rate, treatment
failure, length of hospital stay, and incidence of nosocomial infection.
if it fails then⬇️
Invasive mechanical ventilation may be required in hypercapnic patients with
poor mental status (eg, somnolence, lack of cooperation, inability to clear secretions),
hemodynamic instability, or profound acidemia (pH <7.1 ). This patient’s pH of 7.32 and
PaC02 of 60 mm Hg suggest a mild to moderate acute respiratory acidosis on an existing
chronic respiratory acidosis. A trial of NPPV is warranted prior to intubation, especially
as advanced COPD may make weaning and extubation more challenging. If this patient
fails a 2-hour trial of NPPV (eg, h
A-a pressure gradient
PE causes ventilation/perfusion (V/Q) mismatch, resulting in an increase from the expected alveolar-arterial (A-a) oxygen gradient.
Alveolar oxygen (PAOzl is calculated as follows:
PA02 = (Fi02 x [Patm-PH,Q))-(PaC0/0.8)
where Fi02 = fraction of inspired oxygen, Patm = atmospheric pressure, PH20 = water vapor pressure, and PaC02 = partial arterial pressure of carbon dioxide (obtained from arterial blood gas [ABG) results).
This simplifies to PA02 = 150-(PaC0/0.8) for patients breathing room air at sea level.
The A-a gradient is then calculated by subtracting PA02-Pa02, where Pa02 = partial arterial pressure of oxygen (also from ABG results). The A-a gradient is elevated if it is higher than the expected A-a gradient on room air, estimated by (2.5 + [0.21 x patient age)) or (patient age/4 + 4).
A-a gradient elevation occurs in processes that cause impaired gas exchange.
tram track sign is seen in
Tram-track signmay be used in chest radiography or CT to denote the thickened non-tapering (parallel) walls ofcylindrical bronchiectasis.
string of beads in radiology
String of beads in radiology- Fibromuscular dysplasia Chr. Pancreatitis (chain of lakes) Small bowel obstruction varicose bronchiectasis
clinical features of sarcodosis
systemic granulomatous ds characterised by noncaseating granulomas
constitutional symptoms of fever anorexia wht loss
organs involved
lungs
cough dyspnea
skin
erythema nodosum
lupus pernio
eyes
ant and post uveitis
heart
arrythmias
heart block
musculoskeletal
arthritis arthralgia
nervous
cn paralysisdiagnosis of sarcodosis
CXR - bilateral hilar adenopathy hallmark of sarcoidoisis
hypercalcemia
hypercalciuria
biopsy
noncaseating granulomas
PFT
dec lung volume
dec diffusing capacity
dec FEV1/FVC ratio
ace enzyme levels just to note ds progress
stages of sarcoidoisis on chest xray
Stage I
bilateral hilar adenopathy without parenchymal infiltrates (highest rate of remission)
.
StageII
hilar adenopathy with parenchymal infiltrates
StageIII
diffuse parenchymal infiltrates without hilar adenopathy (least favorable prognosis)
.StageIV
pulmonary fibrosis with honey combing and fibrocystic parenchymal changes
treatment of sarcoidoisis
corticosteroids
hallmark of sarcoidoisis
bilateral hilar lymphadenopathy
causes of egg shell calcification
silicosis
sarcoidoisis
treated lymphoma
amyloidosis
chest xray finding of asbestosis
typically involves lower lobes
pleural plaques
chest xray finding of silicosis
typically involves upper lobes
and causes pleural plaques
occupational increasing risk of silicosis
sandblasters
quartz
mining
most common cancer caused by asbestosis
bronchogenic carcinoma
then malignant mesothelioma
