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step 2 ck pulmonology > p4 amboss > Flashcards

p4 amboss Flashcards

1
Q

classic presentation of BPD?

A

Persistent tachypnea
Labored breathing (intercostal and subcostal retractions)
FiO2 > 30% to maintain peripheral saturation > 90%
Diffuse granular densities with basal atelectasis on x-ray
Later in the disease course, interspersed cystic areas and diffuse hyperinflation of the lung can develop

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2
Q

Chronic cough not responsive to antihistamine?

A

GERD likely? Antacid

GERD unlikely: PFT–NC–BPCT

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3
Q

Acide base disorder in OSA?

A 
Near normal PH
Compensated respiratory acidosis
Low serum chloride
hypoxia (normal non apneic episode)
Chronic Co2 retention
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4
Q

treatment for sever sulpha allergy patient with PCP?

A

IV clindamycin and oral primaquine

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5
Q

OHS diagnosis?

A

in patients with BMI ≥ 30 kg/m2 with symptoms similar to OSA (excessive daytime sleepiness, restless sleep, snoring with apneic episodes) and evidence of daytime alveolar hypoventilation on arterial blood gas (ABG) analysis that cannot be otherwise explained.

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6
Q

APA sx?

A

In patients with bronchial asthma, there should be concern for ABPA if respiratory symptoms worsen despite treatment and features of bronchiectasis (e.g., productive cough with thick brown sputum, thickened airways with irregular cystic opacities on chest x-ray) develop along with an elevated ESR, eosinophilia, and very high concentrations of serum IgE.

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7
Q

management?

A

prednisolone

itraconazole

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8
Q

treatment of OSA?

A

Treat all patients with diagnosed OSA.
First-line treatment: positive airway pressure (PAP)
Consider alternative treatment in patients who are unable to tolerate or decline PAP:
Oral appliances
Positional therapy
Upper airway modifications
Supportive care should include management of risk factors, e.g., weight loss and sleep hygiene.
Nocturnal positive pressure t

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9
Q

Upper airway modifications?

A

Description: surgical dilatation of the upper airway or neurostimulation of upper airway muscles
Procedures
Uvulopalatopharyngoplasty: resection of the uvula and redundant retrolingual, soft palate, and tonsillar tissue
Other procedures include hypoglossal nerve stimulation, radiofrequency ablation of tongue and/or soft palate tissue, and palatal implants. [33][38][39]

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10
Q

two key epidemiological groups(risk factor) in which sarcoidosis is common?

A

gender, and race, of African descent and women ages 25–35 and 45–65 years

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11
Q

ankylosisng spondilitis PFT?

A

Normal compliance
low FVC1/FVC
Normal/increase ratio of Fvc1/FVC
Normal residual volume

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12
Q

confirmatory test for bronchiectasis?

A

A high-resolution CT scan of the chest is the

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13
Q

Findings?

A

include dilated bronchi with thickened walls and a possible signet ring appearance, tram track lines (i.e., parallel linear opacities caused by thickened walls of dilated bronchi), lower lobe cysts, and honeycombing.

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14
Q

Management of Myasthenia gravis?

A

Early endotracheal intubation
IVIg
Plasmapheresis

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15
Q

differentiation of MGC from cholinergic crisis?

A 
criteria.1st MGC/2nd CC
Pupil	
Normal
Miosis
Fasciculations	
None
Present
Heart rate	
Tachycardia
Bradycardia
Skin	
Cold and faint
Warm and flushed
Bronchial secretion	
Normal
Increased
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16
Q

complication?

A 
Infection: otitis media
Respiratory
Bordetella pertussis pneumonia
Hemoptysis, atelectasis, pneumothorax 
Neurologic: seizures, encephalopathy with possible permanent damage
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17
Q

MCC of pan cost tumor?

A

(usually a type of NSCLC such as bronchogenic adenocarcinoma)

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18
Q

treatment of choice for legionellosis?

A

Fluoroquinolones (e.g., levofloxacin) are the treatment of choice for legionellosis

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19
Q

apnea of prematurity cause?

A

Immature respiratory control

preterm and LBW is the risk

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20
Q

CM?

A

in first 2-3 day
episodes of breathing pauses (usually > 20 seconds) that are frequently accompanied by hypoxemia and/or bradycardia
is clinical diagnosis

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21
Q

management?

A 
Supportive care (e.g., supplemental oxygen, neutral thermal environment, maintaining a physiological neck position, avoidance of excessive nasal suctioning)
Nasal CPAP
Methylxanthine therapy (e.g., caffeine, theophylline)
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22
Q

diagnosis?

A

clinical

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23
Q

intermidiate risk solitary lung nodule?

A 
S;0.8-2 cm
A:40-60
scaloped border
UL lesion
current smoking
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24
Q

next step to do?

A

PET

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25
Q

Positron emission tomography (PET) function and indication?

A

Can determine if the nodule is metabolically active and should be Considered for the evaluation of low-risk or intermediate-risk nodules, which are ≥ 8 mm.
FDG-avid nodules should undergo biopsy for histopathological examination. FDG-nonavid nodules should be monitored with a follow-up CT scan.
Alternatively, patients with intermediate- or high-risk nodules can proceed directly to biopsy.

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26
Q

Direct surgical biopsy for ?

A

Is typically reserved for large lesions (> 30 mm) or smaller lesions with concerning features based on other modalities that assess risk.
Do tracheobronchial

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27
Q

the most appropriate diagnostic step for a case of recurrent pneumonia in the same anatomic region.

A

A CT scan of the chest

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28
Q

pneumonia and PE d/t?

A

Pneumonia–subacute

PE-acute

29
Q

aspirin-exacerbated respiratory disease (AERD) feature?

A

symptoms resembling those of a type 1 hypersensitivity reaction (e.g., wheezing, decreased breath sounds, cutaneous flushing) following the administration of aspirin or NSAIDs.

30
Q

the d/c b/n T1HRR?

A

But unlike a type 1 hypersensitivity reaction, which is an IgE-mediated process, AERD is a pseudoallergic reaction

31
Q

TB transmit ion prevension?

A

warranting airborne precautions in addition to standard precautions.
Airborne precautions include the use of an N95 respirator (or a higher-level respirator) when in contact with the patient. Patients with suspected or confirmed TB must be placed in airborne infection isolation rooms (AIIRs) because droplet nuclei can remain suspended in the air and travel long distances. The negative air pressure in AIIRs prevents contaminated air from escaping. Furthermore, patients with TB must wear surgical face masks in an ambulatory care setting or while being transported to another facility.

32
Q

other infection warranting airborne precautions?

A

measles
varicella
smallpox
severe acute respiratory syndrome (SARS) infections (e.g., COVID-19).

33
Q

What is the diagnosis for immunocompromised presented with acute-onset respiratory symptoms and a diffuse vesicular rash.

A

Disseminated varicella-zoster virus infection.

34
Q

patient with AAT deficiency with COPD have at which ca risk?

A

HCC

35
Q

Chlamydophila psittaci?

A

is the organism that causes psittacosis (“parrot fever”), a rare zoonotic disease that causes atypical pneumonia and is transmitted by infected birds via feces and dander.
Infected individuals typically have a history of close contact with birds and present with fever, chills, nonproductive cough, and headaches, as seen in this patient

36
Q

Coxiella burnetii ?

A

Is an obligate intracellular organism that causes Q fever, a zoonosis that presents with flu-like symptoms, high-grade fever, and other features of atypical pneumonia. It is also a common cause of culture-negative endocarditis.
However, it is transmitted by the inhalation of spores from contaminated feces, urine, milk, and birth products of sheep and cattle.

37
Q

Test and indication for lung cancer screening?

A

Low-dose CT scan of the chest
Age 50 to 80 years
A ≥ 20 pack-year smoking history
Have quit within the past 15 years.

38
Q

Management of COPD?

A

A short course of systemic corticosteroids (e.g., prednisone) for 4–7 days is used to reduce airway inflammation and improve airflow in patients with AECOPD. Corticosteroids, however, have a delayed onset of action (6–8 hours). Therefore, nebulization of a short-acting β2 agonist (e.g., albuterol) with or without a short-acting anticholinergic bronchodilator (e.g., ipratropium) is recommended in addition to corticosteroids as the initial therapy. In addition, a macrolide antibiotic given for 4–7 days can reduce the duration and severity of the exacerbation.

39
Q

Atelectasis PFT?

A

Hypoxia

Respiratory alkalosis

40
Q

Normal Po2?

A

80–100 mmHg.

41
Q

Congenital diaphragmatic hernia?

A

Prenatally diagnosed CDH: antenatal glucocorticoids
Postnatal therapy
Initial medical resuscitation
Correction of hypoxia
Intubation and mechanical ventilation: indicated in all infants with CDH
Extracorporeal life support (ECLS): A heart-lung bypass pump that circulates the infant’s blood through an artificial lung and then back into the bloodstream.
Indicated in infants who do not improve on mechanical ventilation/have persistent hypoxia or acidosis
Contraindicated in infants with large/expanding intracranial hemorrhages, as ECLS requires anticoagulation
Gastric decompression: insertion of a nasogastric tube and continuous suction
Inotropic support may be required to maintain blood pressure
Surfactant administration: in infants born < 34 weeks of gestation and x-ray findings suggesting neonatal respiratory distress syndrome
Surgical repair (thoracotomy or laparotomy)
Indicated in all cases of CDH
Timing: after the infant is stabilized, often after 24–48 hours
Procedure: reduction of the hernial contents and primary closure of the defect

42
Q

Blastomycosis dermatitidis?

A 
Typically manifests as pneumonia with extrapulmonary symptoms, which can involve the skin (e.g., verrucous skin lesions and granulomatous nodules Genitourinary system (e.g., prostatitis), Central nervous system (e.g., meningitis and brain abscesses)
Skeletal system (e.g., osteolytic lesions).
43
Q

Pulmonary nodules that are ≤ 4 mm in size and have a low risk for malignancy require?

A

No further evaluation or follow-up

44
Q

low risk factor?

A

aged < 40 years
not smoke
smooth borders
found in the middle lung field

45
Q

<=4 cm but have clinical risk factor(age >40,current smoking/asbestoses,P/F hx of malignancy or found in upper lobe?

A

require Pet/Follow Up

46
Q

Consistently low PCT levels (< 0.25 μg/L) after empiric pneumonia tx started?

A

stop Ab

indicate viral pneumonia, which is not treated with antibiotics.

47
Q

most appropriate next step after FBA suspected?

A

Bronchoscopy

48
Q

FBA CM?

A

acute onset cough
shortness of breath
unilateral wheezing and reduced air entry along with hyperlucency of the lung fields, which indicate a foreign body aspiration (FBA) with ball-valve foreign body obstruction.
Half of all FBA occur in children between the ages of 2 and 3
80% of cases involve the right main bronchus.

49
Q

effective method for both maintaining and improving lung function after surgery and decreasing the risk of atelectasis and pneumonia?

A

1- Incentive spirometry is a routine procedure in obese patients undergoing open surgery of the upper abdomen (adjacent to the diaphragm).
2-Smoking cessation >8 Week before surgery

50
Q

The patient is immunocompromised and presents with acute hypoxemic respiratory failure, elevated LDH and beta-d-glucan, with abnormal chest x-ray and has an elevated A-a gradient. The most likely diagnosis?

A

Pneumocystis jirovecii pneumonia (PCP)

51
Q

management?

A

Based on severity(mild and moderate only Ab, But sever AB+ Steroid)

52
Q

Mild to moderate( PCP: PaO2 ≥ 70 mm Hg and A-a gradient < 35 mm Hg on room air)

A 
1-Oral trimethoprim/sulfamethoxazole
2-If sulpha allergy/alternative
Oral dapsone PLUS oral trimethoprim
OR oral primaquine PLUS clindamycin
OR oral atovaquone
53
Q

Moderate to severe PCP: PaO2 < 70 mm Hg or A-a gradient ≥ 35 mm Hg on room air

A 
1-Oral trimethoprim/sulfamethoxazole
2-alternative
IV pentamidine 
OR oral primaquine PLUS oral clindamycin
3-Add Steroid
54
Q

next step in the management of patient, who is suspected of having a traumatic diaphragmatic rupture by X ray and Clinical sx after given ABC

A

A CT of the chest, abdomen, and pelvis is the most appropriate

55
Q

Hemodynamically stable patients (systolic blood pressure > 90 mm Hg) with a high probability for pulmonary embolism (Wells score > 6) and no contraindication for anticoagulation next step?

A

empiric anticoagulation even before the diagnosis is confirmed.

56
Q

The first step in the management of neonatal respiratory distress syndrome?

A

Nasal CPAP to provide positive end-expiratory pressure

57
Q

what to do after initiation of CPAP?

A

An ABG should be obtained to assess the effectiveness of this ventilatory method.
If FiO2 > 0.4 or pH < 7.25, then intubation and surfactant therapy is warranted.
The younger the gestational age, the increased risk for CPAP failure and worse outcomes.

58
Q

what to do if despite initial treatment, he has a decline in mental status, decreased wheezing (due to poor aeration), and decreased respiratory rate (due to fatigue from increased work of breathing)?

A

Which together are concerning for impending respiratory arrest.
So: Start intubation and MC

59
Q

What to do next after clinical diagnosis of tension pneumothorax without X-ray?

A

Successful placement of a needle thoracostomy allows the air to leave the thoracic cavity and results in immediate decompression of thoracic organs and resolution of hemodynamic compromise.

60
Q

A defective CD40 ligand sign?

A

The mechanism underlying type 1 hyper-IgM syndrome. A defect in the CD40 ligand renders T cells unable to switch IgM production in B cells to the production of other immunoglobulins (e.g., IgA, IgG, IgE), resulting in decreased IgA titers, as seen here, and decreased humoral immunity. The CD40 ligand defect also results in an inability of T cells to upregulate cells that express the CD40 molecule (e.g., B cells, macrophages, dendritic cells). Since these cells also happen to be cells that present antigens to T cells, the net effects are a decreased antigen-specific T-cell response and decreased cell-mediated immunity, which in turn increase the risk of infection by pathogens such as Pneumocystis. The onset of symptoms in type 1 hyper IgM syndrome can occur during early infancy and failure to thrive may occur as a result of recurrent infections.

61
Q

Post exposure prophylaxes after pertusis?

A

Macrolides (e.g., azithromycin, erythromycin, clarithromycin) are the treatment of choice for pertussis.
They are also given as postexposure prophylaxis to all close contacts of infected individuals, regardless of immunization status.
Macrolides, in general, are not used in infants < 1 month of age because of their adverse gastrointestinal effects; erythromycin, in particular, is associated with an increased risk of infantile hypertrophic pyloric stenosis.
However, the potential benefit of avoiding infantile pertussis with azithromycin therapy specifically outweighs the potential harm.
Regarding vaccination, adults < 65 years of age who have contact with infants should be vaccinated with Tdap to boost potentially waning immunity and prevent potential infection in the infant. Tdap administration is thus important in both the father (unknown immune status) and mother (last booster > 10 years ago). The mother in this case actually should have been vaccinated during the prenatal or postnatal period of her last pregnancy, but unfortunately was not.

62
Q

Coal miners are at increased risk of coal workers’ pneumoconiosis, also called black lung disease?

A

a more severe form of anthracosis caused by chronic occupational exposure to large amounts of carbon dust. Patients with coal workers’ pneumoconiosis present with symptoms of chronic bronchitis, which can progress to severe dyspnea indicating massive pulmonary fibrosis. Inhaled carbon particles accumulate in alveolar macrophages and induce inflammation and fibrosis of the lung parenchyma. Chest x-ray can reveal small, nodular, potentially coalescing opacities in the upper lung lobes. Finally, lung biopsy characteristically shows deposition of dark pigment in macrophages, interstitial tissue, and hilar lymph nodes.

Caplan syndrome is a rare complication of pneumoconiosis,

63
Q

If patient cough has persisted despite treatment with an antihistamine (diphenhydramine) and has no symptoms suggestive of GERD (e.g., retrosternal burning pain, regurgitation) next step to do?

A

Spirometry

64
Q

Tracheobronchial injuries such as a bronchial rupture feature?

A

occur after a high-speed trauma.
Hamman sign (as a result of a subcutaneous emphysema from air infiltration into the surrounding soft tissue) and respiratory acidosis (due to alveolar hypoventilation from airway obstruction and atelectasis).
The dullness on percussion in the right hemithorax suggests a fluid collection.

In the context of recent trauma, this finding likely represents an associated hemothorax.

65
Q

ABG in OSA in non apneic episode?

A

Borderline low pH, elevated pCO2, elevated serum bicarbonate concentration, and decreased serum chloride concentration are consistent with compensated respiratory acidosis.

66
Q

in patients with OSA during apneic events, normal bicarbonate is not a common finding.

A

While low pH, elevated pCO2, and reduced pO2 can be seen

67
Q

neonatal respiratory distress syndrome due to surfactant deficiency?

A 
premature infants 
respiratory distress (e.g., nasal flaring, expiratory grunting, costal retractions, decreased breath sounds) and bilateral lung opacity on x-ray with low lung volumes and air bronchograms.
68
Q

Transient tachypnea of the newborn feature?

A

Delayed reabsorption of lung fluid
Causes respiratory distress.
Chest x-ray will show hyperinflation, perihilar streaking, and fluid in the fissures. Additionally, this condition occurs most commonly in newborns > 35 weeks’ gestation who are delivered by cesarean section without labor.

step 2 ck pulmonology (4 decks)

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