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Clinical Medicine > Pulm2 > Flashcards

Pulm2 Flashcards

1
Q

classications of pneumothorax

A

classified (primary, secondary)

traumatic (iatrogenic, tension)

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2
Q

primary spontaneous pneumothorax

A

pneumo without an underlying lung disease

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3
Q

—Secondary Spontaneous Pneumothorax

A

pneumo resulting from a complication of a preexisting disease

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4
Q

things that can result in iatrogenic pneumothorax

A

thoracentesis,

pleural biopsy,

subclavian or internal jugular vein catheter placement,

percutaneous lung biopsy,

bronchoscopy with transbronchial biopsy

positive-pressure mechanical ventilation

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5
Q

what is the most serious type of pneumothorax

what is the typical cause

A

tension pneumo

penetrating trauma, lung infection, CPR, positive pressure ventilation

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6
Q

what causes tension pneumothorax

A

air pressure in the pleural space exceed the pressure in the lungs allow air to enter the pleural space and not escaping on expriation

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7
Q

life threatening complications of tension pneumo

A

compromised ventilation

compression on the heart due to positive pressure, resultiing in decreased venous return

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8
Q

risk factors for primary pneumo

A

—Tall, thin boys and men between 10 and 30 years old

—Family history

—Cigarette smoking

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9
Q

risk factors for secondary pneumo

A

—COPD

—Aerosolized pentamidine and prior history of Pneumocystis pneumonia

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10
Q

etiology of primary pneumo

A

rupture of subpleural apical blebs in response to high negative intrapleural pressures

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11
Q

etiology of secondary pneumo

A

—Most commonly as complication from COPD

—Can also occur as complication of asthma, cystic fibrosis, TB, Pneumocystis pneumonia, menstruation (catamenial pneumothorax), and wide variety of interstitial lung diseases

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12
Q

catamenial pneumo defined

etiology

A

a typically right side pneumo thorax cause by endometriosis or diaphragm perforation that needs surgical repair 1/3 of the time

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13
Q

typical presentation of pneumothorax

A

chest pain, dyspnea

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14
Q

T/F chest pain and dyspnea realted to pneumothorax often starts during exertion and doesn’t resolve

A

false, it usually occurs during rest and resolves in 24 hrs

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15
Q

despite the fact that chest pain and dyspenia usually resolves, when can pneumothorax cause a respiratory failure

A

when there is underlying COPD or asthma

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16
Q

signs and symptoms of pneumothorax

A

chest pain

dyspnea

occassionally mild tachycardia

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17
Q

what additional signs of pneumothorax will be present if its large

A

diminished breath sounds

decreased fremitus

decreased movement of the chest

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18
Q

signs and symptoms of tension pneumothorax

A

—Marked Tachycardia

—Hypotension

—Mediastinal or Tracheal Shift to contralateral side

—Enlarged hemithorax without breath sounds

—Hyperresonance to percussion

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19
Q

lab studies for pneumothorax

A

ABG - often not needed but will show hypoxia and respiratory alkalosis

ECG - a left sided pneumo may produce changes misinterpreted as an acute MI

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20
Q

how will a right pneumothorax present on ECG

left

A

right will look like right bundle branch block

left will have axis deviation and low amplitude QRS

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21
Q

imaging for pneumothorax

A

CXR

pleural line

may need expiratory film

poss air fluid level from secondary pleural effusion

deep sulcus sign

tension: blacked out lung and contralateral mediastinal shift

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22
Q

DDx in pneumothoerax

A

—Emphysematous bleb

—Myocardial Infarction

—Pulmonary embolization

—Pneumonia

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23
Q

complications with spontaneous pneumo

A

pneumomediastinum

subcutaneous emphysema

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24
Q

if pneumomediastinum is found in conjunction with pneumothorax, what should be be considered

how can this be confirmed

A

esophageal or bronchial rupture

swallow study

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25
Q

treatment of a small stable spontaneous pneumo

A

oxygen to induce absorption

observation

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26
Q

treatment for a large or progressive spontaneous pneumo

A

—Aspiration drainage of pleural air with a small-bore catheter (16 gauge angiocatheter or larger)

—Small bore catheter or chest tube attached to a one-way Heimlich valve

—Follow with serial chest radiographs every 24 hours

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27
Q

pneumothorax indication for chest tube placement

A

Secondary Pneumothorax, Large Pneumothorax, Tension Pneumothorax or severe symptoms or those who have a pneumothorax on mechanical ventilation should undergo

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28
Q

describe the process of a chest tube placement (tube thoracostomy)

A

The chest tube is placed under water-seal drainage

suction is applied until the lung expands and maintains.

the tube is water-seal trialed to ensure resolution of leak.

Removed after the leak subsides

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29
Q

emergency management of tension pneumo

does this confirm pneumo

how long does the needle stay in

A

insertion of a large bore needle into the second anterior intercostal pleural space

if there is gas escaping it is confirmation of pneumothorax

the needle stays in place until a chest tube is put in

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30
Q

what would indicate thorascopy or open thoracotomy treatment for pneumothorax

A

—Recurrence of spontaneous pneumothorax

—Bilateral pneumothorax

—Failure of tube thoracostomy for the first episode (failure of lung to reexpand or persistent air leak)

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31
Q

what does surgical treatment of pneumothorax entail

A

resection of blebs responsible for the pneumothorax

pleurodesis by mechanical abrasion and application of talc or povidone-iodine

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32
Q

risk factors for pneumothorax

A

smoking increases risk by 50%

exposure to high altitudes, flying without cabin pressure, or scuba diving can cause recurrence

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33
Q

what percent of patients with spontaneous pneumowill have recurrence

what if there is a surgical repair

are there any sequela after treatment

A

30%

recurrance is less frequent after surgery

no long term sequela

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34
Q

A tall, thin 24yo male presents to the clinic with sudden onset of left-sided chest pain and dyspnea.

Examination shows:

Vitals: T 99.2, R 24, P 112, BP 146/76

Neck: supple

Pulmonary: appears dyspneic, decreased breath sounds to the left chest on auscultation

Cardiac: tachy, but regular rhythm

what labs or studies are needed

what is the treatment

A

CXR, supplemental oxygen

needle decompression

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35
Q

pleural effusion

A

abnormal accumulation of fluid in the pleural space

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36
Q

etiolgy of pneumothorax

A

normal fluid secretion into the pleural space outpaces normal fluid absorption

can come from too much fluid or too little absorption

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37
Q

five pathological processes that account for most of pleural effusion

A

—Transudates

—Exudates (increased fluid)

—Exudates (decreased removal of fluid)

—Empyema

—Hemothorax

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38
Q

transudate causes of pleural effusion

A

Increased production of fluid in the setting of normal capillaries due to increased hydrostatic or decreased oncotic pressures

—Increased hydrostatic pressure

—CHF (accounts for greater than 90% of transudates)

—Decreased oncotic pressures

—Hypoalbuminemia, cirrhosis

—Greater negative pleural pressure

—Acute atelectasis

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39
Q

causes of transudate pleural effusion

A

CHF

cirrhosis with ascities

nephrotic syndrome

peritoneal dialysis

myxedema

acute atelectasis

constrictive pericarditis

pulmonary empbolism

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40
Q

what causes exudative pleural effusion

A

Local factors that influence the formation and absorption of pleural fluid are altered

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41
Q

what would differentiate effusion form heart failure and that from pneumonia

A

bilateral pneumonia is pretty rare, so if effusion is bilateral its probably not pneumonia

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42
Q

causes of exudative pleural effusion

A

pneumonia

cancer

pulmonary embolism

tuberculosis

CTD

infection

uremia

chylothorax

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43
Q

general considerations for empyema

A

infection in the pleural space confirmed with cultures

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44
Q

why is history important to idenify when working up pleural effusion

A

if left alone the fluid will start wall itself off and make pockets which can make thoracentesis more difficult

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45
Q

general presention of pleural effusion

A

Dyspnea

Cough

Respirophasic Chest Pain

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46
Q

T/F small pleural effusions generally have no physical findings

A

true

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47
Q

signs and symptoms associated with large pleural effusion

A

Dullness to percussion

Diminished or absent breath sounds over the effusion

Compressive atelectasis may cause bronchial breath sounds and egophony over the effusion

Contralateral shift of the trachea and bulging of intercostal spaces (massive effusion with increased intrapleural pressure)

Pleural friction rub (infarction or pleuritis)

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48
Q

imaging studies for pleural effusion

A

upright CXR

lateral decubitus

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49
Q

how much fluid need sto be present on lateral upright chest xray to be a visible sign of pleural effsion

AP

A

75-100 mL

175-200m<

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50
Q

howmuch fluid on lateral decubitus is needed to attempt blind thorocentesis

A

1 cm of fluid

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51
Q

what is the advantage of CT imaging in pleural effusion

A

it can decet small amounts of fluid (10mL) and help with thoracentesis

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52
Q

what is the advantage in ultrasound imaging for pleural effusion

A

can help guide thoracentesis of small effusions

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53
Q

Dx pleural effusion

A

fluid on x ray

thoracentesis

serum protein, LDH, glucose levesl

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54
Q

when is a diagnostic thoracentesis reccomended for pleural effusion

A

—New pleural effusion and no clinically apparent cause

—Atypical presentation

—Failure of an effusion to resolve as expected

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55
Q

what information can be gathered from a diagnostic thoracentesis of pleural effusion

A

—Visualization of the fluid

—Micobiologic and chemical analysis to identify pathophysiology

—Presumptive diagnosis based on DDx

—Definitive diagnosis with positive cytology and culture of infectioous agent

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56
Q

what should be pleural fluid be tested for

A

—pH

—Description of fluid

—Protein

—Glucose

—LDH

—Amylase

—Total WBC count

—Differential WBC count

—RBC count

—Gram stain

—Culture

—Cytology

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57
Q

gross appearance of pleural fluid

A

—Normal= clear to straw-yellow

—Grossly Purulent= empyema

—Greenish= bilopleural effusion

—Yellow-green= rheumatoid effusion

—Milky White= chylous effusion

—Bloody

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58
Q

when pleural effusion is bloody what should be obtained from the fluid

A

hematocrit

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59
Q

diffentiating between exudative and transudative pleural effusion based on lab tests of pleural effusion labs

A

if your protein ratio is is >.5, its exudative

if the LD ratio is >0.6, its exudative

if the pleural fluid LDH is in the upper 2/3 of the limits, its exudative

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60
Q

T/F only one part of light’s criteria needs to be positive for exudate to assume exudative pleural effusion

A

true

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61
Q

distinguishing lab findings for transudative pleural effusion

A

glucose in the fluid equal to serum glucose

pH between 7.4 and 7.55

fewer than 1000 WBC/mcL with mostly mononuclear cells

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62
Q

labratory findings that would indicate a more agressive draiing proceudre than thoracenesis

A

loculated pleural fluid

pleural fluid pH<7.3

positive gram stain or culture

presence of gross pus in the pleural space

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63
Q

decreased pH of pleural fluid indicates what

A

empyema

malignancy

esohpageal rupture

TB

rheum onditions

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64
Q

elevated amylase in pleural fluid would indicate what

A

pancreatic pleural effusion (pancreatitis or pseudocyst)

malignancy (lung or pancreas)

esophageal ruture

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65
Q

glucose <60 in pleural fluild would indicate what

A

malignancy

infection

TB

esophageal rutpure if <60 is less than serum

rheumatoid pleuritis

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66
Q

what would be indicative of TB pleural effusion

A

thoracentesis with pleural biopsy shows exudate with small lymphocytes and high levels of TB markers in the fluid

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67
Q

general characteristics of treating transudative pleural effusion

A

treat the underlying condition

theraputc thoracentesis offers only transient relief

pleurodesis and tube thoracostomy are rarely indicated

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68
Q

wha percent of terminal cancer patients have malignany pleural effusion

A

15%

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69
Q

90% of malignant pleural effusions are exudative

A

treu

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70
Q

treatment of malignant pleural effusion

A

—Systemic or local (thoracentesis or chest tube)

—Pleurodesis after chest tube

—Indwelling pleural catheter

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71
Q

Parapneumonic Pleural Effusion definded

three categories

A

Exudates that accompany ~40% of bacterial pneumonias

simple, complicated, empyema

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72
Q

define simple —Parapneumonic Pleural Effusion

A

—Free-flowing sterile exudates of modest size that resolve quickly with antibiotic therapy

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73
Q

treatment for complicated —Parapneumonic Pleural Effusion

A

—Tube thoracostomy if pleural fluid glucose is <60mg/dL or the pH is <7.2

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74
Q

treatment for empyema

A

Gross infection in the pleural space via positive gram stain or cultureà drain by tube thoracostomy

often will need intrapleural lytic therapy or surgical decortication

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75
Q

how are small volume hemothorax managed

A

if stable or improving on chest x-ray may be managed with close observation

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76
Q

treatment large volume or hemodyanmically unstable hemothorax

A

—Large-bore thoracostomy tube, Drain existing blood and clot, Quantify amount of bleeding

—Permit apposition of the pleural surfaces in an attempt to reduce hemorrhage

—Thoracotomy may be needed to control hemorrhage, remove clot and treat complications

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77
Q

DX and treatment of mesothelioma

A

—Diagnosis- thoracoscopy or open pleural biopsy

—Treatment- chest pain- opiates; oxygen for SOB

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78
Q

T/F people with viral infections causing pleural effusion rarely get better on their own

A

false, they often recover with no sequela

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79
Q

dx of pulmonary embolism

A

—Diagnosis with CT or pulmonary arteriography

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80
Q

general chacteristics of community acquired pneumonia

A

Acquired in the home or nonhospital environment

In most cases of CAP, the causative agent is not identified. However, in those cases where an agent is identified, bacteria are more commonly found.

Common causative agents include Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis,

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81
Q

typical presentation of community acquire pneumonia

A

1- to 10-day history of increasing cough, purulent sputum, shortness of breath, tachycardia, pleuritic chest pain, fever or hypothermia, sweats, and rigors.

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82
Q

PE findings indicative of community acquired pneumonia

A

altered breath sounds and crackles,

dullness to percussion if an effusion is present,

bronchial breath sounds over an area of consolidation.

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83
Q

diagnostic studes for community acquired pneumonia

A

Organisms may be detected with conventional sputum Gram stain or sputum culture

Chest radiography (CXR) shows lobar or segmental infiltrates, air bronchograms, and pleural effusions.

Procalcitonin levels rise in response to a proinflammatory stimulus, especially bacterial infection.

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84
Q

age/gender/race bias for sleep apnea

A

most common in men, age 50-70, more prevalent in african americans

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85
Q

T/F sleep apnea increses with increased weight and age

A

true

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86
Q

T/F asian populations have a lower risk of sleep apnea because of their cranofacial make up

A

false, their risk is higher even without obstity

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87
Q

spectrum of sleep apnea diease

A

normal

primary snoring

upper airway resistance syndrome

obstructive hypoventilation

obstructive sleep apnea syndrome

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88
Q

causes of respiratory effort related arousals

A

➢Crescendo snoring

➢Thoraco-abdominal paradoxing

➢Increased intercostal EMG

➢Terminated by arousal or jerk

➢Oxygenation does not have to be affected

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89
Q

cumuluative RERAs lead to what

A

upper air way resistance syndrome

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90
Q

hypopnea

A

shallow breath that least to SaO2 decrease in 3% over 10 seconds

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91
Q

pathophysiology of apnea

A

soft palate and tounge slide back to close off the airway

leads to hypoxia

increased ventillatory effort

arousal from sleep

pharyngeal muscle tone is restored

airway opens

hyperventilation to correct hypoxia

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92
Q

criteria of apnea on a sleep study

A

complete blockage of the airway despite attempts to breath, requires a 3% desat and have >10second duration

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93
Q

risk factors for sleep apnea

A

➢Obesity (BMI>30)

➢Habitual snoring

➢Excessive daytime sleepiness

➢Age

➢Gender (male:female = 2-3:1)

Race (African-Americans, Hispanics

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94
Q

pediatric risk factors for sleep apnea

A
  • Adenotonsillar hypertrophy
  • Neurologic/Genetic Conditions (CP, Low Birth Weight)
95
Q

clinical presentation of sleep apnea

A
  • Decreased memory
  • Morning headache
  • Fatigue
  • Decreased motor coordination
  • Nocturnal gasping/choking
  • Loss of libido/secondary impotence
  • Irritability/depressed mood
  • Frequent Napping/Falling asleep while sedentary
96
Q

co-morbid conditions with sleep apnea

A

oPulmonary HTN

oCVA/TIA

oDiabetes

oFibromyalgia

oCardiovascular Disease

97
Q

what is the link between sleep apnea and depression

A
  • 18% of individuals with a major depressive disorder diagnosis also have a breathing-related sleep disorders diagnosis
  • 18% of subjects with a breathing-related sleep disorders diagnosis have a major depressive disorder diagnosis
98
Q

mimicers of the nocturnal symptoms of apnea

A
  • Nocturnal heartburn
  • Chest pain, palpitations
  • Coughing and choking
  • Asthma attacks
  • Night sweats
99
Q

differential for obstructive sleep apnea syndrome

A

❖PLMD/RLS

❖Shift Work Syndrome/Circadian Rhythm Disorder

❖Narcolepsy

❖Chronic Fatigue Syndrome

❖Primary Snoring

❖Nocturnal GERD

100
Q

STOPBANG questionairre for sleep apnea

A
  • Snoring
  • Tired
  • Observed Apnea
  • Pressure
  • BMI >35
  • Age >50
  • Neck Circumference
  • Gender
101
Q

PE findings indicative of sleep apnea

A

✴Neck circumference (>17 inches in males,>16 inches in females)

✴craniofacial anatomy

✴posterior oropharynx

○BMI>30 with 8-12 fold increase in risk

102
Q

retrognathia

A

back set jaw

103
Q

mallampati score

A

a scoring system that indicates a class I mallampati has a naturally open airway, while a class IV has no airway

104
Q

lab studies for management of apnea

A
  • Nurse observation record - Hospital/Home Health - not diagnostic
  • Overnight oximetry (Profox) - Screen Only
  • Home sleep test (HST)
  • Portable - Inpatient stay
  • In lab polysomnogram (PSG) - Gold Standard
105
Q

how is the severity of sleep apnea measured

A

polysomnograph or home sleep test

106
Q

apnea hypopnea index scores indicative of astham

A

No evidence of apnea

•AHI of 0-5

▪Mild Sleep Apnea

•AHI of 5-15

▪Moderate Sleep Apnea

•AHI of 15-30

▪Severe Sleep Apnea

•AHI >=30

▪Extremely Severe Sleep Apnea

•AHI >100

107
Q

clinical criteria for sleep apnea that requires treatment

A

AHI of >15 without comorbidity

AHI between 5-15 with at least one comorbid factor (DM, HTN, CAD, BMI)

108
Q

mortality conditions associated with sleep apnea

A
  • Ischemic heart disease
  • Congestive heart failure
  • Cerebrovascular disease
  • Pulmonary hypertension
  • Atrial Fibrillation
109
Q

what comorbity puts a patient at the highest risk for apnea

A

drug resistant HTN

110
Q

T/F a higher AHI score will lead to a greater increase in in HTN

A

treu

111
Q

apnea puts patient at risk for what types of CHD

A

fatal and non fatal CV events

arrhytmias

112
Q

Men with AHI >19 are 2.86 times likely to have a ischemic stroke

A

true

113
Q

why can obstructive sleep apnea be more prone to weight gain

A
  • OSA patients are more desensitized leptin
  • Ghrelin hormone secreted by the intestinal tract when empty. Tells us we are hungry. OSA patients have more
  • Neuropeptide Y - Released by sympathetic nervous system. It is a strong vasoconstrictor and also increases adipose cell production. It also acts to increase food intake and store energy as fat.
114
Q

•Patients with untreated severe OSA have a 2-3 fold increase in all cause mortality

A

true

115
Q

descrive the link beween MVA and sleep apnea

A

▪MVA’s are 2-3 times more likely in individuals with OSAS

▪Can be due to excessive daytime sleepiness, impaired cognition, inattention, etc due to fatigue of untreated sleep apnea.

116
Q

treatments for sleep apnea

A
  • Behavioral (lose weight, stop smoking)
  • PAP Therapy (sleep on your back)
  • Mandibular Advancement Devices
  • Provent
  • Surgical Interventions
117
Q

how does a continuous positive airway pressure (CPAP) work

A

it forces air dow you nasopharynx and keeps your airway open with positive airway pressure

118
Q

patient issues with CPAP

A
  • Mask Discomfort
  • Pressure intolerance
  • Patient Acceptance
  • Claustrophobia
  • Aerophagia
  • Chest Discomfort
  • Nasal congestion
119
Q

T/F treating apnea will decrease nighttime and daytime blood pressure

A

treu

120
Q

describe the link between CPAP and CHF

A

CPAP will reduce LV afterload, increase stroke volume, reduce cardiac sympathetic tone, reduce atrial naturetic peptide, and increase LVEF

121
Q

what is a mandibular advancement device used for

A

to pull the jaw forward during sleep so it won’t close off the airway

122
Q

non CPAP treatment of apnea

A

mandibular advancement devices

tongue retainer device

provent nasal system

123
Q

surgical options for treatment of apnea

A

genioglossus stimulatir

snoreoplasty

Uvulopalatopharygoplasty
(UPPP)

Mandibular Osteotomy with
Genioglossus Advancement (GAHM)

Maxillomandibular Advancement Osteotomy

124
Q

two conditions that can cause apnea and be treated by •Maxillomandibular Advancement Osteotomy

A

crouzons syndrome

mandibular hypoplasia and retrognathia

125
Q

when would trachestomy be indicated for apnea treatment

A

❖Morbid obesity

❖Severe facial deformity

❖Significant cardiac arrhythmias

❖CPAP/BiPAP intolerance

❖Definitive Treatment for OSAS

126
Q

describe asthma as an inflammatory disease

A
  • Asthma is a chronic inflammatory process
  • Results of inflammation (leads to Airway obstruction, Airway hyper-responsiveness, Limitation of airflow)
127
Q

what happens due to remodeling found in asthma patients due to chronic inflammation

A
  • Sub-basement fibrosis
  • Mucous hypersecretion
  • Injury to epithelial cells
  • Smooth muscle hypertrophy
  • Angiogenesis
128
Q

three predictors of asthma development

A

genetics and environmental factors

atopy (genetic predispositon to getting allergies)

viral infection can trigger onset and exacerbation of asthma

129
Q

signs and symptoms of asthmaq

A
  • Wheezing
  • Coughing
  • Shortness of Breath
  • Chest Tightness
  • Difficulty with Exercise
  • Nighttime Cough
  • Throat Clearing
  • Recurrent “bronchitis” or “pneumonia”
130
Q

what is the gold standard for diagnosting asthma

A

spirometry with and without albuterol

improvement in FEV1 of 12% or 200L with albuterol is consistent with asthma

131
Q

Asthma is an obstructive pattern, not restrictive

therefore, what will the values for FVC and FEV1 look like

A

FVC is usually normal

FEV1 is decpreased

132
Q

FEV1/FVC ratio indicative of asthma

  • <20 years
  • 20-39 years
  • 40-59 years
  • 60-80 years
A
  • <20 years =>85%
  • 20-39 years =>80%
  • 40-59 years =>75%
  • 60-80 years =>70%
133
Q

Which viral infection is most commonly associated with the development of asthma?

A.Metapneumovirus

B.RSV

C.Rhinovirus

D.Parainfluenza

A

C rhinovrius

134
Q

why is it important to know FEV1 and FVC in diagnosing ashtma

A

people who have less than 100% of predicted FVC can have normal results

FEV1/FVC gives a true representation to obstructooon

135
Q

if a pediatric patient has a history of multiple pneumonia and risk factors for asthma what might you suspect

A

inflammation from asthma can cause mucous that makes a good breeding ground for bacteria or could just mimick pneumonia

136
Q

what lab tests might be ordered if asthma is suspected but spirometry is normal

(bronchoprovocation testing)

A

methacholine challenge

eucapnic voluntary hyperventiliation

exercise challenge

137
Q

pediatric diagnostic factors for ashtma

A
  • Symptom patterns
  • Response to medications
  • Ruling out other common causes
  • Risk factors
  • Modified Asthma Predictive Index
138
Q

what is the Modified Asthma Predictive Index used for

A

Used to predict asthma in patients <3 years with at least 4 episodes of wheezing in the past year

139
Q

how many major predictive factors on the Modified Asthma Predictive Index indicate a positive result

what are they

A

one

  • Parent with asthma
  • Child with eczema
  • Child with environmental allergies (skin test/Immunocap)
140
Q

how many minor predictive factors on the Modified Asthma Predictive Index indicate a positive result

what are they

A

2 or more

  • Food allergies
  • Eosinophilia >4%
  • Wheezing outside of colds
141
Q

what percent of children who are postiive on the Modified Asthma Predictive Index will be asthmatic in 5 years

A

75%

142
Q

DDx when faced with asthma symptoms

A
  1. Vocal cord dysfunction
  2. Airway lesions or congenital malformations
  3. Foreign body aspiration
  4. Chronic aspiration
  5. CHF
  6. COPD/emphysema
  7. Reflux
  8. Allergies/chronic sinusitis
  9. Cystic fibrosis
143
Q

EPR-3 Asthma Guidelines

Four Components of Asthma Care

A
  • Assessing Severity, Monitoring Control
  • Education
  • Control of Triggers
  • Medications
144
Q

what is the severity of asthma based on

what are the grades

A

impairment and risk

  • Mild intermittent
  • Mild persistent
  • Moderate persistent
  • Severe persistent
145
Q

T/F methacholine challenge is useful for ruling out asthma but not for ruling in

A

treu

146
Q

general rules of asthma treatment

A

step up when you need to, step down when you can

  • Maintain the patient on the lowest dose of medication that effectively controls symptoms
  • Treatment plan should be individualized based on the patient’s triggers and patterns
147
Q

environmenta triggesr of asthma

A
  • Viral infections
  • Allergens
  • Irritants, especially cigarette smoke!!!
  • Exercise
  • Emotions
  • Cold air
148
Q

what is the role of medication in asthma treatment

A
  • Controller medications vs rescue medications
  • Safety of inhaled steroids vs oral steroids
  • Safety of LABA medications
149
Q

LABA

A

long acting broncodilators

150
Q

T/F taking a long acting bronchodilator with an inhaled steroid is fatal

A

false, LABA only therapy will increase risk of death

151
Q

T/F everyone should use a spacer for meter dosed inhalers

A

treu

152
Q

inhaler technique for infants, toddlers, or impaired people

A
  1. Shake the inhaler several times (unless QVar)
  2. Remove the plastic cap from the inhaler
  3. Insert the inhaler into the rubber ring in the back of the chamber
  4. Check the mask to make sure there is nothing in it
  5. Place the mask over the nose and mouth with enough pressure to get a good seal
  6. Spray one puff of medication into the chamber
  7. Observe the child taking 5-6 breaths (may count also)
  8. Remove the mask, allow the child to rest for at least a minute
  9. Repeat steps 5 through 9 if a second puff is prescribed
153
Q

Inhaler Technique—School Age & Up

A
  1. Shake the inhaler several times (unless QVar)
  2. Remove the plastic cap from the inhaler
  3. Insert the inhaler into the rubber ring in the back of the chamber
  4. Check the mouthpiece of the chamber to make sure there is nothing in it
  5. Exhale fully
  6. Place the mouthpiece of the chamber in your mouth
  7. Spray one puff of medication into the chamber
  8. Take a SLOW DEEP breath in, taking XX seconds to fill your lungs completely (determined by formula below from FEV1)
  9. Hold your breath for 10 seconds
  10. Exhale and relax for at least a minute
  11. Repeat steps 5 through 10 if a second puff is prescribed
154
Q

co-morbidities that can worsen asthma if left untreated

A

allergic rhinitis

chronic sinusitis

GERD
obestiy

155
Q

simple methods to help manage allergic rhinitis

A

saline rinses

dust mite covers

proper technique for nasal steroids

avoid triggers

156
Q

clinical pearls for the managment of chronic sinusitis

A

saline nasal rinses

treat empirically with broad spectrum ABx for 14-21 days

157
Q

clinical pearls for management of reflux associated with asthma

A
  • H2 blocker therapy to start with in a THERAPEUTIC DOSE
  • Consider adding Atrovent for asthma symptom flares
  • Non-pharmacologic interventions

üElevate head of bed

üNo food or drink 2 hours prior to bed

üSmall frequent meals, avoid overeating

üAvoid trigger foods

158
Q

vocal cord dysfunction is a condition where vocal folds are “twitchy” or adduct during breathing that causes acute shortness of breath, especially with exercise that can be called asthma

what sets it apart

A

asthma medications is not effective

attacks with no trigger

not waking up at night

159
Q

treatment for vocal cord dysfunction

A
  • Treated with breathing exercises
  • Sometimes complicated by reflux
  • Referral to speech therapy may be indicated
160
Q

Sources of clots that lead to PE

A

venous circulation (most from DVT)

right side of the heat

invasive tumors

air embolis

fat embolus

amniotic fluid

161
Q

risk factors for a pulmonary embolism

A

virchow’s triad

surgical procedures

cancer

oral contraceptive

pregnancy

IV drug use

162
Q

Signs of PE

A

sudden pleuritic chest pain

dyspnea

apprehension

cough

hemoptysis

diaphoresis

163
Q

What is the 3rd most common cause of death in hospitalized patients

why?

A

PE

because they are frequently misdiagnosed

164
Q

Timing classification of PE

A

Acute

subacute

chronic

165
Q

hemodynamic classification of PE

A

–Massive

–Hypotension (SBP <90 mmHg or drop in SBP ≥40 mmHg from baseline for >15 min)

–Frequently results in acute RV failure and death (often within 1-2 hours)

–Usually large clot, but could be due to small clots if underlying CV disease

166
Q

location classification of PE

A

–Lobar

–Segmental

–Subsegmental

–Saddle

167
Q

Symptomoligy classification of PE

T/F all patients be symtomatic

A

–Symptomatic

–Asymptomatic

No, but almost all will have SOME sign

168
Q

Virchows triad

A

hypercoagulable state

venous stasis

vascular intimal inflammation of injurty

169
Q

•Virchow’s Triad

–Hypercoaguable States

  • Meds: ____________________
  • Disease: _________________
  • Inherited genetic disorders: _______________________
A

HRT, Oral contraceptives

170
Q

•Virchow’s Triad

–Hypercoaguable States

  • Meds: ____________________
  • Disease: _________________
  • Inherited genetic disorders: _______________________
A

malignancy, surgery

171
Q

•Virchow’s Triad

–Hypercoaguable States

  • Meds: ____________________
  • Disease: _________________
  • Inherited genetic disorders: _______________________
A

Factor V Leiden

Protein S & C def

antithrombin III

prothrombin gene mutation,

antiphospholipid ab syndrome

172
Q

Virchows triad: Venous stasis

A

immobility (post op, stroke)

hyperviscosity (PCV)

increased central venous pressure (low cardia output)

173
Q

Virchows triad: vascular intimal infammation

A

prior thrombus

surgery

trauma

174
Q

What is the pathophysiology of dysfunction related to PE

A

increased peripheral vasuclar resistance, vasoconstiction

175
Q

what causes increased periperal vasuclar resistannce in a PE

increased PVR does what

A
  • Physical obstruction of the vascular bed with thrombus and hypoxic vasoconstriction leads to increased PVR.
  • Increased PVR impedes RV outflow and reduces LV preload
176
Q

what might precipitate a more rapid deterioration in cardiac output during a PE

A

preexisting cardiopulmonary disease

177
Q

what will increase the risk of respiratory failure with a PE

A

coexisting coronary artery disease

178
Q

what is the value of D dimer in PE Dx

A

a positive D dimer cannot rule in PE, but a negative D-Dimer will rule out a PE

179
Q

describe the process that impairs gas exchange related to PE

A
  • Mechanical obstruction of the vascular bed alters the ventilation to perfusion ratio
  • Release of inflammatory mediators causes surfactant dysfunction and atelectasis, resulting in intrapulmonary shunting
  • Hypoxia
  • Increased respiratory drive resulting in hypercapnia and respiratory alkalosis
180
Q

what makes Dx of PE difficult

A
  • Clinical findings depend on size of embolus and patient’s preexisting cardiopulmonary status
  • Common symptoms and signs of PE are not specific to the disorder
181
Q

symptomaic presentation of PE

A

•Dyspnea/ Breathlessness

•Pleuritic CP/ Painful inspiration

•Cough

  • Orthopnea (>2 pillow or more)
  • Calf or thigh pain or swelling
  • Wheezing
  • Hemoptysis
  • Diaphoresis
182
Q

clinical signs of PE

A

•Tachypnea (> half of patients diagnosed)

•Tachycardia

•Erythema, edema, tenderness, or palpable cord in calf or thigh

  • Rales
  • Diminished breath sounds
  • Accentuation of the pulmonary component of the 2nd heart sound
  • Elevated JVD
  • Hypoxia
  • Low grade fever
183
Q

Signs of circulatory collapse related to PE

A
  • Dyspnea
  • Tachypnea
  • Acute right heart failure (JVP, cyanosis, right sided S3)
184
Q

signs of probable RV strain and impending shock in a PE

A

Transition from tachy to brady, or from a narrow complex to a broad complex tachycardia

185
Q

hypotension with elevated CVP is _____ unless proven otherwise

A

PE

186
Q

labratory studies for PE: routine labs

A

–Leukocytosis

–Elevated ESR

–Elevated serum LDH or AST with normal bili

187
Q

lab studies for PE: ABGs

A

–Respiratory alkalosis secondary to hyperventilation

–Hypoxemia

–Hypocapnia

188
Q

Labs used for PE Dx

A

non-specific labs

ABGs

D-Dimer

Troponin

BNP

189
Q

EKG findings related to PE

A
  • non specific ST-T wave changes and tachycardia
  • Severe right ventricular dysfunction: T-wave inversion in the precordial leads
190
Q

EKG findings related to massive acute PE or cor pulmonale (uncommon)

A

–Classic S1Q3T3 Pattern

–Right ventricular strain

–New incomplete RBBB

191
Q

EKG signs of a PE that indicate a poor prognosis

A
  • Atrial arrythmias
  • RBBB (new)
  • Inferior Q waves (II, III, Avf)
  • T-wave inversion and ST-segment changes (anterior leads)
  • Bradycardia
192
Q

CXR signs of PE

A
  • Atelectasis
  • Pleural effusion
  • Cardiomegaly
193
Q

Imaging studies for PE

A

Pulmonary angiography

CT Pulmonary angiography

VQ Scan

Venous ultrasound

194
Q

what is the intial test of choice for PE

why is it prefered over the gold standard

A

CT pulomnary angiography

its faster and can provide alternate explanation for symptoms

195
Q

If a patient is postive for DVT and you suspect PE, but CTA is negative, what should you do

A

treat and do further testing

196
Q

what is the primary utility of pulmonary angiography in treating a PE

A

it gives a definitive dx

if the patient can’t take anticoags and you want to put in an IVC filter

197
Q

when is echocardiogram useful in Dx of PE

what is the limitation

A

can be useful to Dx a massive PE if you ned to confirm a presumptive Dx

•Only 30-40% will have echocardiographic abnormalities suggestive of PE

198
Q

echocardiogram signs of PE

A
  • Increased RV size
  • Decreased RV function
  • Tricuspid regurgitation
  • RV thrombus
  • Regional wall motion abnormalities that spare the right ventricular apex “(McConnell’s sign”)
199
Q

what is the best diagnostic approach to confirm a Dx of PE

A

•Combine clinical assessment/ suspicion with D-dimer testing and imaging (CT-PA)

200
Q

wells criteria

what would indicate PE

A

a diagnostic test that indicates probability of a PE

<4, PE unlikely

>4, PE likley

201
Q

immediate treatment of PE

A

STABILIZE

O2, IV access, consider empiric anticoagulation

202
Q

Resuscitation of a critical patient with PE

A

Respiratory support

Hemodyanmic support

empiric coagulation if not contraindicated

203
Q

Resuscitation of a critical patient with PE: respiratory spport

A

–Supplemental oxygen

–Mechanical ventilation

204
Q

Resuscitation of a critical patient with PE: hemodyanmic support

A

–IVFs (500-1,000 mL NS during initial period)

–IV vasopressors: norepinephrine, dobutamine

205
Q

Resuscitation of a critical patient with PE: empiric anticoagulation

when would you used this?

A

–If no excess risk for bleeding

–High clinical suspicion (Wells score >6)

–Moderate clinical suspicion and diagnostic w/u >4 hours

–Low clinical suspicion and diagnostic w/u >24 hours

206
Q

if empiric coagulation is contraindicated, what should you do

A

expedite diagnosis so alternate therapies can be initiated if PE is confirmed

207
Q

adjunctive therapy for PE

A

General (O2, analgesics, IVFs)

  • Encourage early ambulation/ mobility
  • Compression garments
  • SMI
208
Q

when should anticoagulation be initiated for treatment of PE

when should it stop

A

once PE is confirmed

empirically if needed and low risk for bleeding

if the PE is excluded

209
Q

parenteral anticoag therapy to treat PE

A

low molecular weight heparin

fondaparinux

IV UFH

SC UFH

210
Q

caution with LMWH should be used if what condition is present

A

renal insufficiency CrCl<30

211
Q

risk factors for uncontrolled bleeding related to anticoagulation

A

age >65 yrs,

previous bleed,

thrombocytopenia,

antiplatelet therapy,

poor anticoagulant control,

recent surgery,

frequent falls,

reduced functional capacity,

previous stroke,

DM,

anemia,

cancer,

renal failure,

liver failure,

alcohol use

212
Q

how many risk factors for anticoagulation therapy are considered moderate risk

high risk

A

one

two or more

213
Q

when is fonaperinux contraindicatied

when should caution be used

A

CrCl <30

CrCL 30-50

214
Q

when would IV or SC unfractionated heparin be used in treatment of PE

A

–Persistant hypotension due to massive PE

–Increased risk of bleeding

–Consideration for thrombolysis

–Concern for subcutaneous absorption (obesity)

215
Q

when would warfarin treatment be used in treating PE

what testing must be used with this therapy

lag time?

what is the goal of therapy

A

the same day or after parentaeral therapy

requires daily INR

you need at least 5 days for the drug to become effective

INR of 2.5

216
Q

what is the advantage of new novel agents for anticoagulation treatment of PE

A

–Fixed dose, oral agents

–No routine laboratory monitoring

–No antidotes

–Renal insufficiency parameters

217
Q

two exampes of new, novel agents for PE treatment

A

•Factor Xa Inhibitors

–Rivaroxaban

–Apixaban

–Endoxaban

•Direct Thrombin Inhibitors

–Dabigatran

218
Q

what determine the duration of anticoagulation therapy following PE

A

the clinical situation that precipitated the event

219
Q

Duration of Anticoagulation Therapy: reversible risk factor

A

–3 months

220
Q

Duration of Anticoagulation Therapy: unprovoked

A

–3 months and reassess

221
Q

Duration of Anticoagulation Therapy: recurrent

A

–3 months and reassess

–Consider lifetime

222
Q

Duration of Anticoagulation Therapy: special considerations

A

–Cancer

–Pregnancy

223
Q

thrombolytic treatment agents used for PE

A

•tPA, Streptokinase, Urokinase

224
Q

when is thrombolysis used in treating PE

A

•Patients with confirmed PE and persistent hemodynamic comprise (“Massive PE”) and no risk of bleeding

225
Q

what is the action of thrombolytic treatment for PE

risks?

can it be used with anticoagulation

A
  • Accelerates clot lysis and has short term hemodynamic benefits
  • Increases risk of major bleeding
  • Still follow with anticoagulation therapy
226
Q

when is embolectomy warranted in treatment of PE

A

•Presentation severe enough to warrant thrombolysis, but thrombolysis fails or contraindicated.

227
Q

when are IVC filters indicated for treating PE

A
  • Contraindications to anticoagulation
  • Failed anticoagulation
  • Developed complication due to anticoagulation
  • Hemodynamic or respiratory compromise severe enough that recurrent PE would be lethal
228
Q

T/F May be prophylactic in selected populations if high risk DVT and contraindication to mechanical or pharmacological prophylaxis

A

true

229
Q

indications that outpatient treatment is viable for a PE

A

•Low risk of death

•No supplemental oxygen

•No need for narcotic pain control

•Normal pulse and BP

•No recent h/o bleeding

  • No serious comorbid conditions (ischemic heart disease, chronic lung disease, liver or renal failure, thrombocytopenia, or cancer)
  • Normal mental status with good understanding of risks and benefits
  • Good home support
  • No concomitant DVT
230
Q

T/F PE has a good prognosis

A

True, if Dx and Tx quickly and there is not an unerlying condition

231
Q

what is the most cause of morbidity associated with PE

A

shock or recurrent PE

232
Q

factors that will increase mortality risk associated with PE

A
  • RV dysfunction
  • Accompanying DVT
  • RV thrombus
  • BNP
  • Troponin
  • Hyponatremia
  • Lactate levels
233
Q

key prevention considerations for patients at high risk for PE

A
  • Early ambulation
  • Intermittent pneumatic compression stockings
  • Low-dose heparin/ Low-dose LMW heparin
  • Combination of mechanical and pharmacological measures
  • Compression stockings
  • STOP SMOKING!
234
Q
A

Clinical Medicine (11 decks)

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