Pulmonology Flashcards
Interpreting DLCO: decreased DLCO and reduced lung volumes
pulmonary fibrosis
Interpreting DLCO: decreased DLCO and normal LV
pulm vasc disease and anemia
Interpreting DLCO: decreased DLCO and airflow obstruction
COPD, bronchiectasis
Interpreting DLCO: increased or normal DLCO and airflow obstruction
asthma
Interpreting DLCO: increased DLCO
pulmonary hemmorrhage, polycythemia, or left to right shunt
Interpreting DLCO: normal dlco and decreased LV
obesity or extrapulmonary cause
Airway reversibility with improvement of bronchodilator signs
A ≥12% increase in either FEV1 or FVC and an increase ≥200 mL
Reversible airway disease with improvement of bronchodilator signs
A ≥12% increase in either FEV1 or FVC and an increase ≥200 mL from baseline
Restrictive airway disease ratio of FEV1 and FVC
Equal reductions in FEV1
and FVC
consider any cough that is nocturnal, seasonal, or related to a workplace
or activity as…
asthma
Bronchoprovocation testing is indicated for
patients with a suggestive clinical history for asthma but normal spirometry.
Bronchoprovocation testing with exercise is indicated to diagnose exercise-induced asthma in patients who have dyspnea following exercise but normal spirometry
does normal spirometry rule out asthma
does normal bronchoprovocation test rule out asthma
no
yes
alternative ddx for wheezing
HF, COPD, vocal cord dysfunction, and upper airway obstruction
xray in chronic eosinophilic pneumonia
“photographic-negative” pulmonary edema (peripheral pulmonary edema)
clinical findings in chronic eosinophilic pna
striking peripheral blood eosinophilia, fever, and weight loss in a long-term smoker
dx chronic eosinophilic pna
by bronchoscopy with biopsy or bronchoalveolar lavage showing a high eosinophil count
clinical findings of Allergic bronchopulmonary
aspergillosis
Asthma manifests with eosinophilia, markedly high serum IgE levels, and intermittent pulmonary infiltrates
dx of Allergic bronchopulmonary aspergillosis
positive skin test for Aspergillus and IgG and IgE antibodies to Aspergillus
xray of Allergic bronchopulmonary aspergillosis
radiographic opacities in the upper lobes
overlooked until advaced Allergic bronchopulmonary aspergillosis for
fixed obstruction and bronchiectasis
clinical findings of Eosinophilic granulomatosis
with polyangiitis
Upper airway and sinus disease precedes difficult-to-treat asthma
red flag sign of Eosinophilic granulomatosis
with polyangiitis
flares associated with use of
leukotriene inhibitors and glucocorticoid tapers
dx of Eosinophilic granulomatosis
with polyangiitis
Serum p-ANCA may be elevated
Hallmark diagnostic finding is eosinophilic tissue infiltrates
difficult to control asthma you should get what further testing
echo and cxr. Obtaining flow-volume loops and direct visualization of the larynx during an acute episode may be helpful in diagnosing tracheal obstruction
and vocal cord dysfunction
asthma is an extrapharyngeal manifestation of
gerd
symptom frequency asthma intermittent
<2 per week or <2 per month
symptom frequency asthma: mild persistent
Symptoms >2 per week but <1 per day or
nocturnal sx >2 per month
symptom frequency asthma: moderate persistent
Need for daily use of short-acting β-agonist ≥1 per week
nocturnal: Acute exacerbations ≥2 per week
symptom frequency asthma: severe persistent
Continual symptoms that limit physical activity nocturnal: Frequent
Step 1: Intermittent asthma tx
Select a short-acting β-agonist as needed
Step 2: Mild persistent ASTHMA TX
Add a low-dose inhaled glucocorticoid
Step 3: Moderate persistent asthma tx
Add one of the following:
1. Low to medium doses of an inhaled glucocorticoid and a LABA (preferred)
2. Medium doses of an inhaled glucocorticoid
3. Low to medium doses of an inhaled glucocorticoid and a single long-term controller medication
(leukotriene modifier or theophylline)
step 4: : Severe persistent asthma tx
Add high doses of an inhaled glucocorticoid plus a LABA or LAMA and possibly oral glucocorticoids
Omalizumab indications
- moderate to severe asthma
- inadequate control of symptoms with inhaled glucocorticoids
• evidence of allergies to perennial aeroallergen
• IgE levels between 30 and 700 kU/L
Anti–interleukin-5 monoclonal antibodies (mepolizumab, reslizumab) indications
r patients with an absolute eosinophil count >150 cells/µL and severe asthma
not controlled with standard therapy.
risk of theophylline and macrolide or fluoroquinolone
toxicity
risk of using laba isolated for asthma
increase mortality risk
diagnosis with patient with suspected asthma but improves immediately with intubation
vocal cord dx
COPD includes the following diseases
emphysema, chronic bronchitis, obliterative bronchiolitis, and asthmatic bronchitis
what to test in pts with COPD <45 years who have a strong family history of COPD or without identifiable COPD risk
factors
alpha antitrypsin dx
Bronchiectasis is usually associated with
inciting event (childhood pna, tb,
bronchiectasis symptoms
Large-volume sputum production with purulent exacerbations; hemoptysis
bronchiectaisis xray finding
tram lines diagnose with HRCT
adult CF characteristics
Obstructive pulmonary disease is most common presentation in adult patients; other symptoms may include
recurrent respiratory infections, infertility
Positive sweat chloride test result
Adult bronchiolitis characteristics
Found in current or former smokers; may be idiopathic or associated with other diseases such as RA
Poorly responsive to bronchodilators; responds to smoking cessation and glucocorticoids
Bronchiolitis obliterans characteristics
Presents with dyspnea without improvement following bronchodilators, normal or hyperinflated lungs on chest
x-ray; associated with injury to small airways; consider in patients after lung or stem cell transplantation
bacterial infections most common in CF pts>
Pseudomonas aeruginosa, Staphylococcus aureus, Haemophilus influenzae, or Burkholderia cepacia
• In patients with CF and acute abdominal pain consider
intussusception
supression of chronic pulm infections in cf
aerosolized tobramycin
tx for persistent secretions in cf
aerosolized recombinant human DNase (dornase alfa) or hypertonic saline
DPLD HRCT finding hilar lymphadenopathy
sarcoidosis
DPLD HRCT finding pleural effusion
connected tissue related disease
DPLD HRCT finding pleural placques
asbestosis
drugs causing dpld
: amiodarone, methotrexate, nitrofurantoin, chemotherapeutic
smoking relate dpld
X-ray shows ground-glass opacities and thickened interstitium
radiation dpld duration of onset
May occur 6 weeks to months after radiation therapy
hypersensitivity pneumonitis HRCT
ground-glass opacities on high resolution CT scan
IPF xray
honeycombing, bibasilar infiltrates with fibrosis
cryptogenic organizing pneumonia
x-ray shows focal areas of consolidation that may migrate from one
location to another
Pulmonary alveolar
proteinosis
Diagnosed via bronchoalveolar lavage, which shows abundant protein in the airspaces; chest CT shows
“crazy paving” pattern
pna/HF vs dpld Patients with dyspnea for days or weeks
PNA or HF
alternatiive dx: dyspnea and pulmonary crackles but no other findings of HF
dpld
characteristic findings of IPF
Characteristic findings
are the gradual onset of a nonproductive cough and dyspnea over approximately 3 months in older adults
PE in IPF
normal temperature
• bibasilar crackles (“dry,” end-inspiratory, and “Velcro-like” in quality)
• late-phase cor pulmonale
• clubbing (25% of patients)
IPF xray, CT scan and PFTs
Chest x-ray shows peripheral reticular opacities and honeycomb
changes at the lung bases. HRCT scan reveals subpleural cystic
changes and traction bronchiectasis.
Shoud you intubate or ventilate patient’s with resp failure in IPF
No
lofgren syndrome
fever, bilateral hilar lymphadenopathy, EN, and often ankle arthritis
uveoparotid fever
featuring anterior uveitis, parotid gland enlargement, facial palsy, and fever)
hypercalcemia in sarcoid cause
extrarenal production of calcitriol by granuloma cells a
occupation with exposure to berrylium
light bulb or semiconductor factories)
patients with silicosis, fever, and cough should be tested for
tb
occupations at risk for asbestosis
construction industry, the automotive servicing industry, and the
shipbuilding and repair industry.
the latent period for asbestosis is
10-15 years
what should also be excluded when finding pleural effusion in nephronic syndrome
PE and renal artery thrombosis
who should be screened for PH
- SSc
2.liver transplantation candidates with portal hypertension
3, first-degree relatives of patients with familial PAH - patients with congenital heart disease
with systemic-to-pulmonary shunts.
PH cut off
resting mean pulmonary arterial pressure of ≥25 mm Hg
PH 1-5
- small pulmonary arterioles resulting in high pulmonary vascular resistance (PAH)
- left sided CHF
- Respiratory illness
- CTEPH
- unknown causes
drugs associated with PH
fenfluramine, amphetamines, and cocaine
4 types of testing for PH
- echocardiography as the initial study; a systolic pulmonary artery pressure >40 mm Hg is suggestive of PH
- bubble contrast echocardiography or TEE is indicated to evaluate for intracardiac shunts (e.g., ASD)
- right heart catheterization to confirm the diagnosis and quantify the degree of PH
- left heart catheterization and coronary angiography exclude LV dysfunction as a cause of PH
testing for cteph
- pulmonary arterial pressure ≥25 mm Hg in the absence of left-sided HF
- compatible imaging evidence of chronic thromboembolism by V/Q scanning
most common cause of PH
left-sided heart disease and hypoxic respiratory disorders
Tx for group 1 PH
CCB for those with vasodilator resp on rh cath
Lung or heart-lung transplantation should be considered for patients in whom drug treatment is unsuccessful.
CTEPH tx
Life-long anticoagulant therapy is indicated in all patients with CTEPH. Pulmonary thromboendarterectomy is the only definitive therapy for CTEPH
3 most common causes of hemoptsysis
Bronchitis, bronchogenic carcinoma, and bronchiectasis
SOLID lung nodule: No (low-risk patient)
<6 mm
6-8 mm >8 mm
- No follow-up
- CT at 6-12 months, then consider CT at 18-24 months
- Consider CT at 3 months, PET/CT, or tissue sampling
SOLID lung nodule: High risk
<6 mm
6-8 mm
>8 mm
- Optional CT at 12 months
- CT at 6-12 months, then CT at 18-24 months
- Consider CT at 3 months, PET/CT, or tissue sampling
Pure Ground Glass Lung nodule
<6 mm
≥6 mm
- No follow-up
2. CT at 6-12 months to confirm persistence, then CT every 2 years until 5 years
Subsolid lung nodule
<6 mm
≥6 mm
- No follow-up
- CT at 3-6 months to confirm persistence. If unchanged and solid component
remains <6 mm, annual CT should be performed for 5 years
common medialstinal masses
- anterior
- middle
- posterior
- thymus, teratoma, lymphoma and thyroid
- lymph nodes and cysts
- neurogenic (schwannomma)
what AHI is positive on sleep study for osa
AHI of >5/h during a sleep study
High-altitude periodic breathing (HAPB) pathophys and signs
Hypoxia-induced hyperventilation lowers Pco2 toward the apneic threshold, decreasing respiratory rate, which raises Pco2 and results in recurrent hyperventilation
Repetitive arousals from sleep, often with
paroxysms of dyspnea
Acute mountain sickness (AMS) pathophys and signs
Hypoxia and hypocarbia-induced
alterations in cerebral blood flow
Headache, fatigue, nausea, and vomiting,
in addition to disturbed sleep related to
HAPB
High-altitude cerebral edema (HACE) pathophys and signs
Brain edema at altitudes typically above
10,000-13,000 feet
Confusion, irritability, ataxia, coma, and
death
High-altitude pulmonary edema (HAPE) pathophys and signs
PH and pulmonary edema
Cough, dyspnea at rest, pink frothy
sputum, hemoptysis, and pulmonary
crackles
prevention and tx of altitude illness
Prevention- ascend slowly
- Acetazolamide accelerates the acclimatization.
Acetazolamide, dexamethasone, and
supplemental oxygen are used to treat AMS.
Definitive treatment for HACE is immediate descent from altitude; dexamethasone,
supplemental oxygen, and hyperbaric therapy may also be used.
The HAPE treatment of choice is supplemental oxygen and rest.
PFTs in neuromuscular disorders
pulmonary function tests show restriction on spirometry and lung volume measurement but normal diffusing capacity
mild moderare severe ards cut off
Mild ARDS Arterial Po2/Fio2 ratio of 201-300 mm Hg, measured with PEEP ≥5 cm H2O
Moderate ARDS Arterial Po2/Fio2 ratio of 101-200 mm Hg, measured with PEEP ≥5 cm H2O
Severe ARDS Arterial Po2/Fio2 ratio of ≤100 mm Hg, measured with PEEP ≥5 cm H2o
Diffuse alveolar
hemorrhage characteristics
Acute kidney injury with microscopic or gross hematuria or other evidence of vasculitis present
Associated with stem cell transplantation
Hemosiderin-laden macrophages in bronchoalveolar lavage fluid
acute eosinophilic pneumonia
Cough, fever, pleuritic chest pain, and myalgia; may be precipitated by initiation of smoking
>15% eosinophils in bronchoalveolar lavage fluid
Hypersensitivity
pneumonitis characteristics
slower onset than ards
mimicks ards
exposure farmers, birds, hot tubs
Cryptogenic organizing
pneumonia
May be precipitated by viral syndrome
Slower onset than ARDS (>2 weeks) with progressive course; however, may present in an advanced stage,
mimicking ARDS
when starting nppv how do you know if tx is working
Improvements in blood gas values and clinical condition should occur within 2 hours of starting NPPV. If not, intubation should
be considered to avoid undue delay and prevent respiratory arrest
how to tell auto peep on ventalator
flow tracing on the ventilator shows continuous expiratory flow until the start of inspiratory flow
causes and findings in auto peep
COPD or acute asthma, ARDS (increased flow resistance), and a high minute ventilation
(>12-15 L/min). Characteristic findings are wheezing and marked expiratory prolongation, drop in BP, and patient restlessnes
how to improve auto peep
- treat airway obstruction (e.g., bronchodilators in COPD or asthma)
- decrease the respiratory rate or tidal volume
- increase the inspiratory flow rate (shorten inspiratory time)
- prolong the expiratory time
- allow permissive hypercapnia
- sedate and/or paralyze the patient
how to improve respiratory
acidosis on vent
↓ Arterial Pco2
Increasing respiratory rate
Increasing tidal volume:
in volume control mode, directly choose the tidal volume;
in pressure control mode, increase the
inspiratory support pressure to increase
tidal volume
Improve respiratory
alkalosis on vent
↑ Arterial Pco2
Decreasing respiratory rate
Decreasing tidal volume
Improve tissue
oxygenation on vent
↑ O2 saturation, arterial Po2
Increasing Fio2
Increasing PEEP
when can you extubate
When a patient can maintain an arterial O2 saturation >90% breathing Fio2 ≤0.5, PEEP <5 cm H2O, and pH >7.30, it is reasonable
to consider extubation
. Paired daily spontaneous awakening trials (withdrawal of sedatives) with daily spontaneous breathing
trials result in a reduction in mechanical ventilation time, ICU and hospital length of stay, and 1-year mortality rates.
Cardiogenic shock
Low cardiac output, elevated PCWP, and high SVR
Hypovolemic shock
Low cardiac output, low PCWP, and high SVR
Obstructive shock
Low cardiac output, variable PCWP, and high SVR
Anaphylactic shock
High cardiac output, normal PCWP, and low SVR
Septic shock
High cardiac output (early) that can become depressed (late) and low SVR
Malignant hyperthermia suggestive history, signs and treatment
Exposure to volatile anesthetic (halothane
isoflurane, succinylcholine, or
decamethonium)
Masseter muscle
rigidity; ↑ arterial Pco2
Stop the inciting drug
Dantrolene
neuroleptic malignant syndrome suggestive history, signs and tx
Haloperidol, olanzapine, quetiapine, and
risperidone or withdrawal from L-dopa;
onset over days to weeks
Altered mentation,
severe rigidity, ↑ HR, ↑
BP, no clonus, ↓ reflexes
Stop the inciting drug
Dantrolene
Bromocriptine
serotonin syndrome
Onset within 24 h of
initiation or increasing
dose
Agitation, rigidity,
clonus, ↑ reflexes
Stop the inciting drug
Benzodiazepines
Cyproheptadine
what sbp should you aim for in severe preeclampsia or eclampsia, or pheochromocytoma htn crisis in first hour
140
what sbp should you aim for in aortic dissection in the first hour
120
dosing of epi in anaphalaxis vs anaphalactic shock
• IM or subcutaneous epinephrine (0.3-0.5 mg of 1:1000) is first-line treatment for classic anaphylaxis. IV epinephrine
(1:10,000) is reserved for anaphylactic shock or refractory symptoms
how can you tell apart bradykinin angioedema from mast cell or allergic cause
bradykinin angioedema doesnt normally cause uticaria
lab studies to differentiate
Hereditary angioedema
Acquired C1 inhibitor deficiency
ACE inhibitor effect Medication history
Low C1 inhibitor and C4 levels (fam hx)
Low C1q levels (in addition to low C4 and
C1 inhibitor levels) (lymphoma,sle, mgus)
Low C1 inhibitor and C4 levels (med hx)
tx for mast cell mediated angioedema
Select epinephrine, antihistamines, and glucocorticoids for
acute episodes of mast cell–mediated (allergic) angioedema with
airway compromise or hypotension. Patients should carry an
epinephrine autoinjector
tx for c1 deficiency angioedema
bradykinin mediated angioedema (hereditary or acquired angioedema); use
FFP in an emergency. For long-term management of hereditary
angioedema, select danazol and stanozolol to elevate hepatic
synthesis of C1 esterase inhibitor protein.
along with co exposure during fires what else can patient be at risk for
cyanide poisoning coexposure
what normal lab finding would exclude cyonide exposure
a normal ldh
tx for cyanide tox
hydroxocobalamin
Toxic tx for the following
- Acetaminophen
- Benzodiazepines
- β-Adrenergic blockers
- Calcium channel blockers
- Digoxin
- Heparin
- Narcotics
- Salicylates
- Tricyclic antidepressants-
- N-acetylcysteine
- Observation; flumazenil
- Glucagon, calcium chloride, pacing
- Atropine, calcium, glucagon, pacing
- Digoxin-immune fab
- Protamine sulfate
- Naloxone
- Urine alkalinization, hemodialysis
- Blood alkalinization, α-agonist
level to diagnose sever acute carbon monoxide poisoning
A carboxyhemoglobin level >25% in any patient is diagnostic of severe acute carbon monoxide poisoning.
tx for co poisoning
Normobaric oxygen therapy is the treatment of choice. Hyperbaric oxygen therapy is indicated for patients with severe carbon monoxide poisoning
Sympathomimetic tox symptoms
Tachycardia Hypertension Diaphoresis Agitation Seizures Mydriasis
examples of sympathomimetic
Cocaine Amphetamines Ephedrine Caffeine
tx for sympathomimetic tox
Benzodiazepines for agitation Avoid β-blockers for hypertension
Haloperidol may worsen hyperthermia
Cholinergic tox signs
“SLUDGE” Confusion Bronchorrhea Bradycardia Miosis
cholinergic examples
Organophosphates (insecticides, sarin)
Carbamates Physostigmine Edrophonium Nicotine
cholinergic tox tx
Organophosphates poisoning requires external decontamination
Atropine
May require ventilatory support Add pralidoxime for CNS toxicity Benzodiazepines for convulsions
Anticholinergic tox signs
Hyperthermia
Dry skin and mucous membranes Agitation, delirium
Tachycardia, tachypnea Hypertension
Mydriasis
anticholinergic examples
Antihistamines
Tricyclic antidepressants Antiparkinson agents Atropine
Scopolamine
anticholinergic tx
Physostigmine for those with peripheral and CNS symptoms
Benzodiazepines for agitation May require ventilatory support
Opioid tox signs
Naloxone
Miosis
Respiratory depression
Lethargy, confusion Hypothermia Bradycardia Hypotension
tx for opiates
naloxone
