Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Shelf Exams/USMLE Step 2 CK ❄️ > UWorld - Med/Pulm-CC > Flashcards

UWorld - Med/Pulm-CC Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

What are the features of acute bronchitis and initial steps to care?

A

Cough productive of yellow purulent sputum following URI, rhonchi that clear with cough, possible to have small amounts of blood

Tx = Supportive care initially

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the indication for emergent bronchoscopy?

A

major, life threatening, hemoptysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the first step that should be taken if a patient presents with clinical features highly suggestive of PE?

A
  1. Start IV heparin infusion if no contraindication to anticoagulation (then do CT and stop heparin if no PE)
  2. Diagnostic test to evaluate for PE if anticoag is contraindicated (consider IVC filter if PE +)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the flow volume loop features of fixed upper airway obstruction? Possible causes of this?

A

Lung volume ranging from 1.7 - 6.3, with proportional decreases in inspiration and expiration flow rates (basically same as normal but stunted)

-Food stuck in throat, laryngeal edema from anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What characteristics are consistent with Flail chest?

A

Blunt thoracic trauma, respiratory distress despite bilateral chest tubes, multiple rib fractures on CXR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the proper management protocol for someone with acute exacerbation of COPD (AECOPD)?

A
  1. inhaled short acting bronchodilators, glucocorticoids and Abx
  2. Noninvasive positive pressure ventilation (NPPV)
  3. Mechanical ventilation only if Hypercapnic pt. + poor mental status, hemodynamic instability, or profound acidemia (pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are some key signs of pneumothorax in someone with COPD, and what is the cause of this?

A

Acute onset chest pain and SOB, w/ markedly reduced breath sounds, chest hyperresonant to percussion

Cause = dilated apical alveoli (blebs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Differences between Transudative vs. Exudative effusions?

A

Trans = imbalance of hydrostatic/oncotic pressures -> fluid similar to serum (high glucose, low cells etc.)

Exud = pleural/lung inflammation (pneumonia, malignancy) -> increased capillary/pleural membrane permeability (high LDH, high protein, low glucose, WBCs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do beta-agonists affect potassium ion levels and what can result from excess beta-agonist effects?

A

Reduce K+ by driving ions into cells –> Significant hypokalemia -> muscle weakness, arrhythmia, and EKG changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What pathophysiological abnormality occurs in Pulmonary embolism?

A

V/Q mismatch leading to A-a gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can lead to elevated A-a gradient?

A

Any process that results in impaired gas exchange: interstitial disease, V/Q mismatching (PE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are chest radiographical findings that may be seen w/ PE?

A

Atelectasis, infiltrates, pleural effusions, Westemark’s sign (peripheral hyperlucency due to oligemia), Hampton’s Hump (peripheral wedge of lung opacity from infarction), Fleischer sign (enlarged pulm artery), or NORMAL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does low diffusion of CO (DLCO) indicate?

A

Impaired diffusion across alveolar/epithelial membrane

DLCO Decreases w/ interstitial diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can you distinguish asthma from obstructive lung diseases?

A

Dyspnea, wheezing, cough, and a positive bronchodilator response (>12% increase in FEV1) confirm asthma

Only asthma shows complete reversibility of the obstruction w/ bronchodilators (partial reverse in COPD early stage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What pulmonary complications can occur in patients w/ diffuse systemic sclerosis (SSc)?

A

Pulmonary fibrosis (interstitial fibrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is light’s criteria used for and how does it work?

A

Distinguishes transudative vs. exudative pleural effusion. Exudate characters:

  1. Pleural fluid protein/serum protein ration > 0/5
  2. Pleural fluid LDH/serum LDH > 0.6
  3. Pleural fluid LDH >2/3 upper limit of normal serum LDH
17
Q

What acid base abnormality can result from opioid use?

A

Hypoventilation –> subsequent resp acidosis (compensatory rise in bicarb)

18
Q

What is the clinical presentation for a Pancoast tumor?

A

1 - Shoulder pain

  • Horner’s syndrome (Ipsilateral ptosis, miosis, enopthalmos, anhidrosis), C8-T2 neuro involvement (weak/atrophy of hand muscles, pain/paresthesia of 4/5 digits/medial arm/forearm)
  • Supraclavicular lymph node enlargement, weight loss
19
Q

What are the methylxanthine drugs and their clinical use? Cromolyn?

A
  1. aminophylline - phosphodiesterase inhibitors that cause bronchodilation (not useful for acute COPD)
  2. Cromolyn - Mast cell stabilizer (prevents histamine and LKT release) used to treat asthma
20
Q

How do you differentiate chronic bronchitis vs. bronchiectasis?

A

CB- Chronic productive cough for 3 months in 2 successive years, cigarette smoking is leading cause

Bronch - More assoc. w/ hx of recurrent respiratory tract infxns and chronic cough w/ daily production of copious mucopurulent sputum, crackles, ronchi, and wheezing more common

21
Q

How can you differentiate chronic bronchitis and panacinar emphysema w/ COPD?

A

-Both have obstructive pattern (FEV1/FVC

22
Q

What are the features of non-allergic rhinitis and how do you treat this?

A
  • Nasal congestion, rhinorrhea, sneezing, postnasal drainage, erythematous nasal mucosa
  • Onset at >20 y/o w/ no obvious allergic triggers, but may worsen w/ season change

Tx: Topical aka intranasal anti-histamines (Azelastine, Olopatadine) or intranasal glucocorticoids

23
Q

How can one assess increased sound transmission over a consolidated lung lobe?

A

Ask patient to say letter E, if it sounds like A w/ nasal/bleating quality via stethoscope this is egophony and suggests consolidation
-Crackles often heard

24
Q

A patient presents with candida esophagitis presents w/ hypoxia, what is the most likely cause and what pulmonary function would be impeded?

A

Most likely HIV/AIDS -> Pneumocystis jiroveci pneumonia (PCP) –> alveolar interstitial inflammation –> areas of V/Q mismatch –> increased A-a gradient

25
Q

What are the ideal ventilator settings for a patient w/ ARDS and why? What is the best way to increase oxygenation?

A
  1. Low tidal volumes, helps prevent lung damage and decrease mortality
  2. PEEP, prevents alveolar collapse at the end of expiration -> Increases FRC and decreases work of breathing
    - -> you can increase oxygenation by increasing PEEP
26
Q

What is the pathophysiology of ARDS?

A

Inflammatory mediators released, secondary to local or distant injury, go on to damage the alveoli. This leads to increased capillary permeability -> pulmonary edema
-Injury can be from sepsis, severe bleeding, severe infection, toxic ingestion, or burns

27
Q

What is the goal for PaO2 for patients on ventilators w/ ARDS? How can you achieve this and prevent over treatment?

A
  • Maintain paO2 >60

- Keep FiO2 low early on if possible to prevent O2 toxicity of lungs (i.e. below 50-60% range)

28
Q

Why does oxygen saturation change with position changes when a lung lobe is consolidated?

A

-Physiological shunting of blood flow to poorly consolidated regions increases if patient lies on the side of body w/ consolidated lobe (more blood to less Oxygenated regions results in less oxygenation overall)

29
Q

What is the most important intervention to increase oxygenation in patients w/ ARDS?

A

Increase PEEP

30
Q

How does respiratory rate affect resp alkalosis?

A

increasing RR would worsen alkalosis, because it would generate more bicarb

31
Q

What are the main pulm values and vent settings that should be maintained in patients w/ ARDS?

A

-Keep FiO2 below

32
Q

What is sudden dyspnea in the setting of underlying malignancy, chest pain, tachycardia and hypoxia highly suggestive of? What would result from this condition?

A
  • Prothrombotic state of malignancy puts this patient at high risk for a massive pulmonary embolism
  • This would increase pulm vasc resistance –> RV dilation -> compress on LV decreasing preload and CO
33
Q

What are causes of exudative effusion?

A

Infection (PNA, TB), malignancy, pulmonary embolism, connective tissue disease, iatrogenic

34
Q

What is the presentation of aspiration PNA?

A

Fever, leukocytosis, parenchymal infiltrates

35
Q

What can be an indication of worsening prognosis in someone with asthma and why?

A

Normal/increased PCO2 b/c signifies CO2 retention which could be from air trapping and/or resp muscle fatigue

36
Q

What paraneoplastic syndromes are associated w/ small cell lung CA? squamous cell?

A

Small Cell- ACTH and SIADH

Squamous - PTHrP

37
Q

What is the most common acid/base disturbance in PE?

A

Resp alkalosis from hyperventilation as patient tries to overcome hypoxia and V/Q mismatch

38
Q

What is the reason for decreased vital capacity in COPD?

A

Air-trapping during expiration

Shelf Exams/USMLE Step 2 CK ❄️ (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions