UW Flashcards
Bone pain (pain in limbs) in SCD occurs when ___.
sickled RBCs occlude the small bone vasculature.
Acute chest syndrome can be precipitated by an acute skeletal vaso-occlusive crisis by which mechanisms?
- fat-embolism: inflammation, ischemia, and necrosis of the bone marrow –> breakdown of BM fat –> release into circulation –> trapping in the pulmonary vasculature –> acute chest syndrome.
- Hypoventilation:
-Splinting (holding the breath) from pain or use of opioids to control acute pain–> hypoventilation, atelectasis –> VQ mismatch –> hypoxemia –>further sickling.
Acute chest syndrome in SCD manifests with __.
Following an acute vaso-occlusive crisis–> sudden onset and progressively worsening dyspnea, chest pain, fever, hypoxemia, and new-onset pulmonary densities on CXR.
Other than a preceding vaso-occlusive crisis, acute chest syndrome in SCD patients can be triggered by which other conditions or states?
-Asthma exacerbation (in children)
-pulmonary infections (children).
Atelectasis usually presents on a CXR as a ___.
triangular opacity d/t volume loss and alveolar collapse (SEE ATTACHED IMAGE)
Patchy, perihilar opacities with peribronchial thickening and prominent pulmonary vascular markings on CXR are typically suggestive of ___.
pulmonary venous congestion d/t volume overload or HF (SEE ATTACHED IMAGE of bilateral pulmonary edema).
True/False? Aspirin exacerbated respiratory disease (AERD) is an immunologic reaction to aspirin and other NSAIDs.
False;
AERD is a non-immunologic reaction to aspirin and other NSAIDs.
Pathogenesis:
Aspirin/NSAIDS ↓ COX path-> ↓ PG synthesis, while the LOX pathway continues to make LTs –> IMBALANCE between the production of anti-inflammatory PGs and pro-inflammatory LTs; LTs –> B’constriction,↑ vascular permeability, and chemotaxis.
C/P: AERD p/w exacerbation of respiratory s/s (chest tightness and wheezing) after intake of OTC painkillers/aspirin in a pt. with h/o chronic rhinosinusitis, asthma, and nasal polyps.
AERD should be suspected in a patient who presents with s/s consistent with __ triad.
SAMTER TRIAD
-Asthma
-chronic rhinosinusitis with nasal polyps.
-exacerbation of s/s with NSAIDs/Aspirin use.
___ is the primary driver of pathogenesis in extrinsic allergic asthma (dust, pollen, etc) and allergic rhinitis with/without conjunctivitis (Hay fever) as compared to AERD in which the primary driver of pathogenesis is _____.
IgE–> extrinsic allergic asthma, allergic rhinitis, angioedema, anaphylaxis.
Leukotrienes -> AERD (non-immunologic reaction).
Under what conditions, do AERD patients not relate exacerbation of symptoms to NSAID/aspirin use?
If NSAIDs/Aspirin is/are taken habitually.
Some patients of AERD may p/w dramatic s/s such as facial flushing, urticarial hives, swelling of lips, angioedema, and anaphylactoid reaction (hypotension, bronchoconstriction) ____ (? minutes, hours) after NSAID ingestion.
30 minutes - 3 hours.
Treatment strategies for AERD include __.
-Avoid NSAIDS
-NSAID desensitization
-LOX Inhibitor: Zileuton
-LOX Receptor Inhibitor: Montelukast, Zafirlukast.
ANCA (p-ANCA > > > c-ANCA)) are a/w _____ that often p/w prodromal ___ and ____ years before the onset of overt systemic vasculitis.
Eosinophilic granulomatosis with polyangiitis (EGPA fka Churg-Strauss);
often p/w prodromal asthma and nasal polyposis years before the onset of overt systemic vasculitis.
____ is the mediator of extrinsic asthma (dust, pollen, etc) versus ___ which is a mediator of intrinsic asthma (exercise, weather, stress) with chronic rhinosinusitis and nasal polyposis.
IgE –> extrinsic asthma
IL-5 (Th2 cytokine) –> intrinsic asthma and/with chronic rhinosinusitis and nasal polyposis
How can chronic rhinosinusitis with nasal polyposis and asthma d/t intrinsic asthma be differentiated from AERD which also p/w asthma, chronic rhinosinusitis, and nasal polyps?
With intrinsic asthma, sinus, and pulmonary symptoms would not be aggravated by NSAIDs/Aspirin.
Peak airway pressure is ____.
Peak airway pr = (resistive pr) + (plateau pr)
= (flow x resistance) + (elastic pr + PEEP).
Explain Peak airway pressure.
Peak airway pressure is the maximum pressure measured as the tidal volume is being delivered in the lungs.
Resistive airway pressure is ___.
flow x resistance
Plateau pressure in mechanical ventilation is ___.
Plateau pressure is the pressure measured during an inspiratory hold maneuver when the pulmonary airflow and the resistive pressure are both zero.
Plateau pressure is __ + __.
elastic pressure + PEEP.
Elastic pressure is inversely proportional to ___.
lung compliance
eg. ↓↓ lung compliance (fibrosis)–> ↑↑ elastic pressure.
An increase in the peak pressure (resistive pr + plateau pr) without an increase in the plateau pressure suggests___.
Increased airway resistive pressure d/t any of the following:
-mucus plug
-bronchospasm
-biting/kinked ET tube
Elevation of both the peak (resistive pressure + plateau) pressure and the plateau pressure suggests___.
suggests d/t any of the following
- increased elastic pressure d/t ↓↓ compliance d/t
-pneumothorax
-pulmonary edema
-pneumonia
-atelectasis
-right mainstem intubation - Increased PEEP –> lung injury–> ↓↓ compliance
Why is it not possible to calculate the upper airway resistance in a mechanically ventilated patient?
Because the ET tube bypasses the upper airways.
Auto-PEEP is a marker of ___.
End-expiratory pressure;
measured by end-expiratory hold maneuver.
According to the guidelines published by the Infectious diseases society of America, community-acquired pneumonia (CAP) is defined as __.
pneumonia that develops in a non-hospitalized setting.
According to the guidelines published by the Infectious diseases society of America, hospital-acquired pneumonia is defined as __.
pneumonia that develops ≥ 48 hrs after hospital admission.
According to the guidelines published by the Infectious diseases society of America, ventilator-acquired pneumonia is defined as __.
pneumonia that develops ≥ 48 hrs after ET intubation.
What are some risk factors for CAP?
-Age > 65 years
-Immunocompromised state
What is the most common cause of CAP?
Strep. Pneumoniae (lancet-shaped GP diplococci)
A foul-smelling sputum and respiratory symptoms that progress over a period of 1-2 weeks in a patient with a risk of aspiration (alcoholics, dysphagia, bed-ridden state, etc.) are highly suggestive of pneumonia d/t ___ pathogens.
anaerobic bacteria.
___ is a common cause of hospital-acquired pneumonia.
Pseudomonas aeruginosa;
*can cause CAP in immunocompromised hosts or those with structural lung diseases such as cystic fibrosis.
What are the indications for long-term o2 therapy (LTOT) in patients with COPD?
Resting Pao2 ≤ 55 mmHg or resting Spo2 ≤ 88% on room air,
or
Resting Pao2 ≤ 59 mmHg or resting Spo2 ≤ 89% on room air in patients with cor pulmonale, e/o right HF, or Hct > 55%.
What is the target saturation goal in COPD patients prescribed LTOT?
Spo2 > 90% on LTOT during sleep, normal waking, or at rest.
Survival benefits of home o2 therapy are significant when used for ___ hrs a day.
> 15 hrs a day.
There is usually a latency period of ___ years between asbestos exposure and the development of pneumoconiosis (RLD).
≥ 20 years
Digital clubbing and/or bibasal fine inspiratory crackles each is seen in about ___ percent of patients with asbestos-associated pneumoconiosis.
~ 50%
The 3 most common causes of chronic cough (> 8 weeks) are __.
-upper airway cough syndrome (postnasal drip)
-Asthma
-GERD
The diagnosis of upper airway cough syndrome is confirmed by ___.
elimination of nasal discharge and cough following t/t with antihistaminic H1R blockers such as chlorpheniramine.
Quitting smoking ___ days/weeks prior to an elective surgery substantially reduces the risk of postoperative pulmonary complications (pneumonia, respiratory failure).
4-8 weeks prior to surgery
Proteinase-3 ANCA aka ____ antibodies are positive in which small/medium vessel vasculitis?
PR-3 ANCA aka c-ANCA is +ve in Granulomatosis with polyangiitis (fka Wegener’s granulomatosis).
MPO-ANCA aka p-ANCA may be positive in about __ % of cases of granulomatosis with polyangiitis (Wegener’s granulomatosis).
~20%
What major systems are involved in Granulomatosis with polyangiitis (Wegener’s granulomatosis)?
*GPA: c-ANCA > > > p-ANCA; C-ANCA (PR3 anca)
-URT: sinusitis/otitis/saddle nose with granulomatous lesions/ulcers
-LRT: lung nodules/cavitations, ILD, diffuse alveolar hemorrhage all d/t granulomatous vasculitis.
-Skin (leukoclastic vasculitis): Livedo reticularis, non-healing ulcers
-Renal (pauci-immune GN): RPGN
75% of malignant pleural effusions are caused by ___ cancers.
-lung carcinoma
-breast carcinoma
-lymphoma
What is the best initial step in the diagnosis and suggestive diagnosis in a patient who p/w episodic shortness of breath, throat tightness, and noisy breathing during exercise or when exposed to strong fragrances with no expiratory wheezing during the acute episode?
Paradoxical vocal fold motion (PVFM) aka vocal cord dysfunction.
The best diagnostic step is the demonstration of vocal cord adduction during inspiration during a laryngoscopic exam.
What are some risk factors for the development of acquired tracheomalacia?
-ET intubation
-recurrent pulmonary infections
-relapsing polychondritis.
How can PVFM be differentiated from acquired tracheomalacia both of which can present with noisy breathing during increased respiratory effort?
PVFM: inspiratory stridor
Tracheomalacia (acquired): expiratory stridor
dyspnea during exercise d/t PVFM can be differentiated from exercise-induced asthma by ___.
Absence of expiratory wheezing in PVFM.
What are Lights criteria for an exudative pleural effusion?
-Pleural protein/Sr. protein ratio > 0.5
-Pleural LDH/Sr. LDH ratio > 0.6
-Pleural LDH > 2/3rd upper limit of sr. LDH.
What are the characteristics that differentiate chylothorax from exudative pleural effusion?
Chylothorax
-appears milky white
-High triglyceride content
-Low LDH levels
pH decreases by ~ ___ for every 10 mmHg increase in PaCO2.
decreases by ~ 0.08 for every 10 mmHg increase in PaCO2.
Normal PaCO2 levels are 35-45 mmHg.
An HIV +ve patient is hospitalized and t/t for PCP with antibiotics and IVFs. On day 3rd, he develops confusion with normal vitals and hyponatremia. What is the most likely cause of his hyponatremia?
IV fluid administration against a background of pulmonary pathology-induced SIADH in HIV +ve patient.
PLEASE NOTE: Both HIV and pulmonary pathology can independently induce SIADH.
In Hodgkins Lymphoma patients cured with CT and RT, the lifetime risk of secondary malignancy is ___ percent.
> 30%
Most cases of secondary malignancy arise after ____ years of initial curative t/t of HL.
after 10 years of initial t/t.
Sequelae of untreated OSA include _____.
-Systemic HTN
-Pulmonary HTN –> Right-sided HF
_____ is the single greatest risk factor for life-threatening (fatal) asthma.
h/o any previous attack requiring intubation, NIPPV, or admission to ICU.
What are some other risk factors that indicate potential life-threatening asthma?
-increased nocturnal awakenings
-Increasing reliever use
-recent or frequent acute care visits
-multiple courses of systemic steroids
Acute asthma ___ (? increases, decreases) pH and PaCO2 due to ___.
Even though asthma is an obstructive type of lung disease with characteristic CO2 retention (respiratory acidosis), in acute asthma a respiratory alkalosis is induced (↑ pH & ↓PaCO2) due to the initial increased respiratory drive.
What are some signs of impending respiratory failure in acute asthma?
any of the following
-marked tachypnea (RR > 30/min)
-hypoxemia (SaO2 < 90%)
-accessory muscle use
-inability to complete sentences
-Silent chest (severe bronchoconstriction)
-AMS
-initial low PaCO2 is normalizing or ↑, relative to the work of breathing (indicates resp. muscle fatigue and impending resp. failure).
True/False? MTX-induced lung injury is a dose-dependent drug reaction.
False;
MTX lung injury is an idiosyncratic (not dose-dependent) hypersensitivity pneumonitis –> fibrosis.
The onset of MTX-induced lung injury is typically within ___ months/years of MTX initiation.
1-12 months.
MTX-induced lung injury is considered a hypersensitivity reaction because of ____.
the lymphocytic pleocytosis in the BAL fluid.
What is the m/m strategy in MTX-induced lung injury?
1st step: rule out infection
2nd: cessation of MTX (diagnostic and therapeutic)
3rd if no symptom improvement: systemic corticosteroids.
______ should be considered in a young patient (≤ 45 yrs) with COPD with minimal or no h/o smoking, and with family h/o lung disease/emphysema and/or liver disease (cirrhosis).
AAT deficiency.
Smokers with AAT deficiency present a decade earlier than non-smokers at around __ years of age.
~30 years of age.
Primary adrenal insufficiency (PAI) involves the destruction of __ layer of the adrenal cortex.
all layers of cortex leading to
1. ↓ aldosterone-> Na+ loss, K+ retention –> hyponetremia & hyperkalemia.
- ↓ cortisol -> ↓↓ BP, hypoglycemia
- +/- peripheral Eosinophilia (d/t loss of cortisol support in Eo migration into tissues.
____ is the second most common cause of adrenal insufficiency worldwide.
Tuberculous adrenalitis.
An upward displacement of the left main bronchus on CXR in an immigrant patient p/w sob on exertion and non-productive cough is highly suggestive of ____.
Rheumatic MS with LA dilation (dilated LA pushing up the left main bronchus).
____ is a sensitive early clinical exam marker for interstitial fibrosis.
Inspiratory “Velcro” crackles (fine, dry)
* typically present long before CXR findings emerge.
All patients suspected of ILD should undergo a _____ regardless of a normal CXR.
high-resolution CT scan (HRCT).
Asbestosis alone increases the r/o lung cancer by ___ -fold; smokers with asbestos exposure have a ___-fold increase in r/o bronchogenic cancer.
Asbestos alone –> 6-fold ↑ in r/o lung ca
Asbestos + smoking -> 59-fold ↑↑.. in r/o lung ca
Other than mesothelioma, ___ lung cancer is commonly a/w asbestos exposure.
bronchogenic ca
List the occupations commonly a/w asbestos exposure.
-Plumbers
-electricians
-carpenters
-construction workers
-Shipbuilders
-insulation workers
About __ percent of patients with asbestosis have pleural plaques, which helps differentiate the condition from other causes of pulmonary fibrosis.
~50%
The use of ____ medications in the elderly is a/w a much higher r/o CAP.
antipsychotic medications such as quetiapine.
*possibly d/t anti-cholinergic and anti-H1R effects that lead to oropharyngeal dryness (r/o CAP) and inability to form a food bolus (r/o aspiration pneumonia).
Patients with a h/o ____ are more likely to develop Hs Pneumonitis (HP) which is an exaggerated immune response to an inhaled antigen such as ___ (list all).
h/o atopy (asthma, eczema);
inhaled antigens such as mold, animal protein, certain bacteria, etc.
In acute HP, the symptom onset is usually within ___ hours of antigen exposure.
within 6 hours
Acute HP manifests with _____ s/s, d/t ____ (describe).
manifests acutely (within 6 hrs) mostly d/t high antigenic exposure;
with sudden onset fever, SOB, chest tightness, cough, and malaise.
Acute HP is ___ on PFT, unlike COPD/asthma/ exacerbation which is ___ on PFT.
acute HP–> restrictive pattern
COPD/asthma/ exacerbation –> obstructive pattern.
____decreases the r/o developing HP, possibly d/t ___.
smoking; d/t blunting of the immune response.
How can acute HP be differentiated from asthma exacerbation based on physical exam and CXR?
HP (restrictive PFT)
-bilateral fine inspiratory crackles; no wheezing;
CXR: Acute HP: scattered micronodular interstitial opacities-> patchy interstitial inflammation
Chronic HP: DIFFUSE RETICULAR interstitial opacities
Asthma (Obstructive PFT)
-expiratory wheezing.
-hyperinflated lungs.
Obesity hypoventilation syndrome (OHS) is defined by the presence of ____ and ____ in a patient with BMI ≥ _____.
daytime hypercapnia (PaCO2 > 45 mmHg) + alveolar hypoventilation in a patient with BMI > 30 kg/m2 (often > 40 kg/m2).
The PFT pattern in OHS is ___.
restrictive.
What are the t/t strategies for OHS?
1st line: Weight loss and NIPPV
-OHS + OSA: CPAP –> BiPAP
-OHS + hypoventilation –> BiPAP
-Avoid sedatives medications
-Bariatric surgery in select cases
-last resort: Acetazolamide (respiratory stimulant).
OHS patients “can’t breathe” d/t excess weight and altered lung mechanics, and “won’t breathe” d/t _____.
won’t breathe d/t reduced sensitivity of neural chemoreceptors to hypercapnia caused by persistent nocturnal hypoventilation.
In addition to fine bibasilar crackles during the early phase of idiopathic pulmonary fibrosis (IPF), patients with advanced disease will have ___ (list all) findings on clinical exam.
fine bibasilar crackles in early disease progress to
-end-inspiratory squeaks
-digital clubbing
-loud P2; fixed split S2 d/t pulmonary HTN.
_____ lung tumors account for only 1-2% of all lung cancers but they are the most common lung malignancy in non-smoking adolescents and young adults.
Bronchial carcinoid tumor
-tumor of NE cells
-Chromogranin A+ve
True/False?
Bronchial carcinoid tumors, the most common cause of lung cancer in non-smoking adolescents and young adults often p/w carcinoid syndrome d/t high release of serotonin/vasoactive amines.
False;
Bronchial carcinoid tumors are far less likely to produce/release serotonin/vasoactive amines as compared to GI carcinoid tumors.
Invasive aspergillosis primarily affects *ICH hosts (neutropenic, corticosteroids, HIV) and p/w a triad of _______, ______, and ______.
*ICH: immunocompromised hosts
triad of fever, chest pain, and hemoptysis.
During which respiratory cycle, is airflow reduced in a fixed upper airway stenosis?
both inspiration & expiration –> flattening of the FVL (see image).
