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MTB STEP 3 (R) > MTB 3 - Pulmonary > Flashcards

MTB 3 - Pulmonary Flashcards

1
Q

How does asthma present?

A

Patient who is short of breath with expiratory wheezing. In severe cases, there is use of accessory muscles, and the patient is unable to speak in complete sentences.

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2
Q

What are the most important features of severe exacerbation?

A
  • Hyperventilation/increased respiratory rate
  • Decrease in peak flow
  • Hypoxia
  • Respiratory acidosis
  • Possible absence of wheezing
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3
Q

What is an ominous sign for asthma?

A

Absence of wheezing. To wheeze, one must have airflow

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4
Q

What test should be done if the diagnosis of asthma is unclear?

A

Pulmonary function testing before and after inhaled bronchodilators.

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5
Q

How much of a change should you see in FEV1 in order to confirm asthma/reactive airway disease?

A

Increase in FEV1 of > 12% and >200 mL increase

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6
Q

How can methacholine stimulation testing be useful in an asymptomatic asthmatic patient?

A

Looks for a decrease in FEV1 in response to synthetic acetylcholine. Methacholine will decrease FEV1 if the patient has asthma.

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7
Q

What are the best initial therapies that should be ordered for an asthmatic exacerbation?

A

Inhaled bronchodilators - There is no maximum dose of inhaled bronchodilators

Bolus of steroids (methyl prednisolone) - Steroids need 4-6 hours to be effective

Inhaled ipratropium

Oxygen

Magnesium - relaxes muscles

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8
Q

What should any patient that presents with shortness of breath receive?

A

Oxygen
Continuous oximeter
Chest x-ray
ABG

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9
Q

Where should any patient with asthma and respiratory acidosis with CO2 retention be placed?

A

In the ICU. Persistent respiratory acidosis is an indication for intubation and mechanical ventilation

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10
Q

When is terbutaline the right answer choice for a patient with asthma?

A

Terbutaline is less efficacious than inhaled albuterol. Terbutaline is always the wrong answer choice

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11
Q

What benefit does epinephrine have for patients with asthma?

A

Subcutaneously administered epinephrine has no benefit in addition to inhaled bronchodilators

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12
Q

What is the best initial therapy for nonacute asthma?

A

Inhaled bronchodilators (albuterol)

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13
Q

If an asthmatic patient is not controlled with albuterol then what is the next medication that should be used?

A

Chronic controller medication such as an inhaled steroid

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14
Q

If inhaled albuterol and inhaled steroids do not control asthma symptoms, what should be added next?

A

Long-acting inhaled beta agonist, such as salmeterol or formeterol

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15
Q

What is the last resort medication for asthma?

A

Oral steroids

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16
Q

What is the alternate long-term controller medication besides inhaled steroids for:

1) Extrinsic allergies, such as hay fever
2) Atopic disease
3) Chronic COPD
4) High IgE levels, no control with cromolyn

A

1) Cromolyn or nedocromil
2) Montelukast
3) Tiotropium, iptratropium
4) Omalizumab (anti-IgE antibody)

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17
Q

What is the treatment for exercise-induced asthma?

A

Inhaled bronchodilator (albuterol) prior to exercise

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18
Q

What are the three mechanisms by which antimuscarinic medications affect the lungs?

A

Antimuscarinic activity 1) dries the secretions of goblet cells, 2) decreases bronchoconstriction, and 3) inhibits excess fluid production in bronchi

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19
Q

T/F Antimuscarinic medications are more effective in COPD than asthma?

A

True

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20
Q

What conditions presents ina long-term smoker with increasing shortness of breath and decreased exercise tolerance?

A

COPD

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21
Q

What is the only way to assess CO2 retention in COPD patients?

A

In cases of COPD, order ABG because it is critical in acute shortness of breath from COPD. No other way to assess for CO2 retention.

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22
Q

How do you handle acute episodes of SOB in COPD?

A 
Oxygen and ABG
Chest x-ray
Albuterol
Ipratropium
Bolus of steroids
Chest, heart, extremity, and neurological exam
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23
Q

If fever, sputum, and/or a new infiltrate is present on chest x-ray for a patient with COPD exacerbation, then what abx should you add and what are you treating?

A

Ceftriaxone and azithromycin for community-acquired pneumonia

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24
Q

On CCS, move the clock forward 15-30 minutes and reassess the patient. O2 administration in COPD may worsen the shortness of breath by eliminating hypoxic drive

A

On CCS, move the clock forward 15-30 minutes and reassess the patient. O2 administration in COPD may worsen the shortness of breath by eliminating hypoxic drive

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25
Q

Should you intubate patients with COPD for CO2 retention alone?

A

No. These patients often have chronic CO2 retention. Only intubate if there is a worsening drop in pH indicative of a worse respiratory acidosis.

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26
Q

When can you use CPAP or BiPAP for COPD exacerbation?

A

For mild respiratory acidosis. Answer CPAP or BiPAP and move the clock forward 30-60 minutes. If the CO2 retention and hypoxia are improved the patient is spared from intubation.

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27
Q

What are physical findings suggestive of COPD?

A
  • Barrel-shaped chest
  • Clubbing of fingers
  • increased anterior-posterior diameter of the chest
  • Loud P2 heart sound (sign of pulmonary HTN)
  • Edema as a sign of decreased right ventricular output (blood is backing up due to pulmonary hypertension)
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28
Q

What findings will be seen on EKG in a COPD patient?

A

Right axis deviation, right ventricular hypertrophy, right atrial hypertrophy

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29
Q

What findings will be seen on a chest x-ray for a COPD patient?

A

Flattening of the diaphragm (due to hyperinflation of the lungs), elongated heart, and substernal air trapping

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30
Q

What findings will be seen on a CBC of a COPD patient?

A

Increased hematocrit is a sign of chronic hypoxia. Reactive erythrocytosis from chronic hypoxia is often microcytic. An EPO level is not necessary

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31
Q

What is the 50/50 club for COPDers?

A

In moderate to severe cases of COPD, patients may become members of the 50/50 club - the pCO2 is 50 mm Hg and the pO2 is also 50 mm Hg

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32
Q

What findings will be seen on chemistry of a COPD patient?

A

Increased serum bicarbonate is metabolic compensation for respiratory acidosis

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33
Q

What findings will be seen on ABG of a COPD patient?

A

Done to assess CO2 retention and the need for chronic home oxygen based on pO2 (you expect the pCO2 to rise and pO2 to fall).

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34
Q

What is the mechanism of right heart enlargement in COPD?

A

Hypoxia in the lungs causes capillary constriction, in which precapillary sphincters in the lungs constrict to shung blood away from hypoxic areas of the lung. Since the hypoxia of COPD is global throughout the lung, this diffuse vasoconstriction increases pressure in the right ventricle and right atrium. Over time, the result is hypertrophy of both chambers, leading to cor pulmonale, or right heart failure.

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35
Q

What findings will be seen on PFT for a COPD patient?

A
  • Decrease in FEV1
  • Decrease in FVC from loss of elastic recoil of the lung
  • Decrease in FEV1/FVC ration
  • Increase in total lung capacity from air trapping
  • Increase in residual volume
  • Decrease in diffusion capacity lung carbon monoxide (DLCO) caused by destruction of lung interstitium
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36
Q

What is the chronic medical therapy of COPD?

A
  • Tiotropium or ipratropium inhaler
  • Albuterol inhaler
  • Pneumococcal vaccine: Heptavalent vaccine, Pneumovax
  • Smoking cessation
  • Long-term home O2 if the pO2
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37
Q

What lowers mortality in COPD?

A

Smoking cessation

Home O2 therapy (continuous)

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38
Q

What is the mechanism of bicarbonate increase in COPD?

A

Chronic respiratory acidosis increases new bicarbonate generation at the distal tubule of the kidney

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39
Q

Genetic disorder that presents with combination of cirrhosis and COPD?

COPD at an early age (

A

Alpha-1 antitrypsin deficiency

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40
Q

What do you see on chest x-ray and on blood tests in patients with Alpha-1 antitrypsin deficiency?

A

Chest x-ray: Findings of COPD (bullae, barrel chest, flat diaphragm)

Blood tests: Low albumin level and elevated PT time (caused by cirrhosis)

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41
Q

How do you definitively diagnose alpha-1 antitrypsin deficiency?

A

Alpha-1 antitrypsin level is low

Genetic testing

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42
Q

Caused by an anatomic defect of the lungs, usually from an infection in childhood. Results in profund dilation of bronchi. Presents as chronic resolving and recurring episodes of lung infection that give a very high volume of sputum. Hemoptysis and fever occur as well.

A

Bronchiectasis

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43
Q

What is the most accurate diagnostic testn for bronchiectasis?

A

High-resolution CT scan of the chest

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44
Q

What does chest x-ray show in bronchiectasis?

A

Dilated bronchi with tram tracking, which are parallel line consistent with dilated bronchi.

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45
Q

What is the curative therapy for bronchiectasis?

A

There is none. Treat infectious episodes as they occur.

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46
Q

What is the treatment for bronchiectasis?

A

Chest physiotherapy with cupping and clapping will help dislodge secretions

Rotating antibiotics are tried to avoid the development of resistance.

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47
Q

What are some drugs that can cause interstitial lung disease?

A

Nitrofurantoin and bactrim

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48
Q

What are potential causes of interstitial lung disease?

A

Secondary to occupational or environmental exposure or medications.

If no cause is found, the diagnosis is idiopathic pulmonary fibrosis

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49
Q

Causes/diseases of ILD

1) Asbestos
2) Glass workers, mining, sandblasting, brickyards
3) Coal worker
4) Cotton
5) Electronics, ceramics, fluorescent light bulbs
6) Mercury

A

1) Asbestosis
2) Silicosis
3) Coal worker’s pneumoconiosis
4) Byssinosis
5) Berylliosis
6) Pulmonary fibrosis

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50
Q

Shortness of breath with a dry, nonproductive cough, and chronic hypoxia. Punctuated by episodes of bronchitis and pneumonia

A

ILD

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51
Q

What are the physical findings for ILD?

A
  • Dry, velcro rales
  • Loud P2 heart sound
  • Clubbing
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52
Q

What EKG findings will you see on ILD?

A

EKG will show pulmonary hypertension with right atrial and right ventricular hypertrophy

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53
Q

How does pulmonary hypoxia cause pulmonary hypertension?

A

Pulmonary hypoxia causes vasoconstriction of the lungs. Chronic vasoconstriction causes increased pressure in the pulmonary artery. Pulmonary hypertension kills patients.

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54
Q

What diagnostic testing should be done for ILD?

A

Chest x-ray - interstitial fibrosis
High-resolution CT scan - shows more detail on interstitial fibrosis
Lung biopsy
Pulmonary function testing (PFT) - shows decreased FEV1 and decreased FVC with a normal ratio, decreased total lung capacity, and decreased DLCO. All measures are decreased, but they are decreased proportionately.

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55
Q

What is the most common type of cancer in asbestosis?

A

Lung cancer, not mesothelioma

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56
Q

What treatment is there for ILD?

A

There is no specific therapy to reverse any of the forms of ILD.

If the biopsy shows an inflammatory infiltrate, a trial of steroids is used.

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57
Q

What is the only form of ILD that definitely responds to steroids?

A

Berylliosis because it is a granulomatous disease

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58
Q

What systemic findings are found in ILD?

A

None. Fever, malaise, and myalgias that may be found in BOOP/COP are absent in ILD.

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59
Q

Rare bronchiolitis or inflammation of small airways with a chronic alveolitis of unknown origin, presents with cough, rales, shortness of breath, fever, malaise, and myalgias

A

BOOP/COP

60
Q

How does BOOP/COP differ from ILD?

A

1) Presentation is more acute over weeks to months
2) Systemic findings such as fever, malaise, and myalgias
3) No occupational exposure in history

61
Q

What diagnostic testing can be done for BOOP/COP

A

Chest x-ray - shows bilateral patchy infiltrates

Chest CT - shows interstitial disease and alveolitis

Open lung biopsy - only definitive way to make diagnosis

62
Q

What is the most accurate diagnostic test for BOOP/COP?

A

Open lung biopsy is the only definitive way to make the diagnosis of BOOP/COP.

63
Q

How do you treat BOOP/COP?

A

Treat with steroids. No response to abx

64
Q

What extrapulmonary findings are there with sarcoidosis?

A
  • Eye - Uveitis that can be sight threatening
  • Neural - Seventh cranial nerve involvement
  • Skin - Lupus pernio (purplish lesion of the skin and face), erythema nodosum
  • Cardiac - Restrictive cardiomyopathy, cardiac conduction defects
  • Renal and hepatic - occurs without symptoms
  • Hypercalcemia - Occurs in a small number of patients secondary to vitamin D production by the granulomas of sarcoidosis
65
Q

What is the best intial test for sarcoidosis?

A

Chest x-ray, which always shows enlarged lymph nodes. There may be ILD in addition to nodal involvement

66
Q

What is the most accurate diagnostic test for sarcoidosis?

A

Lung or lymph node biopsy showing non-caseating granulomas

67
Q

Can calcium and ACE levels help diagnose sarcoidosis?

A

No. They may be elevated, but these are not specific enough to lead to a specific diagnosis

68
Q

What do you find on BAL of sarcoidosis?

A

Increased numbers of helper cells.

69
Q

What is the best therapy of sarcoidosis?

A

Steroids are the undisputed best therapy

70
Q

Idiopathic cause of shortness of breath, more often in young women, from overgrowth and obliteration of pulmonary vasculature leading to decreased flow out of the right ventricle

A

Pulmonary hypertension

71
Q

What are some secondary causes of pulmonary hypertension?

A 
Mitral stenosis
COPD
Polycythemia vera
Chronic pulmonary emboli
Interstitial lung disease
72
Q

What are some physical findings with pulmonary hypertension?

A

Loud P2
Triscuspid regurgitation
Right ventricular heave
Raynaud’s phenomenon

73
Q

What are some diagnostic tests that can be done for pulmonary hypertension?

A

Transthoracic echo (TTE): shows right ventricular hypertrophy and enlarged right atrium

EKG: shows the same findings as well as right axis deviation

Right heart catherization

74
Q

What is the most accurate test for pulmonary hypertension?

A

Right heart catheterization (Swan-Ganz catheterization) with increased pulmonary artery pressure

75
Q

What is the treatment for Pulmonary Hypertension?

A

Bosentan - endothelin inhibitor that prevents growth of the vasculature of the pulmonary system

Epoprostenol and treprostinil - prostacyclin analogs that act as pulmonary vasodilators

Calcium channel blockers (weak efficacy)

Sildenafil

76
Q

Condition that presents with sudden onset of shortness of breath and clear lungs

A

Pulmonary embolism

77
Q

What are the risk factors for DVT?

A
  • Immobility
  • Malignancy
  • Trauma
  • Surgery, especially joint replacement
  • Thrombophilia, such as factor V mutation, lupus anticoagulant, or protein C and S deficiency
78
Q

What are the physical findings for PE?

A

No specific physical findings for PE

79
Q

What are the diagnostic tests for PE?

A

Chest x-ray: The most common result is normal. The most common abnormality is atelectasis. Wedge-shaped infarction and pleural based humps are rare

EKG: The most common finding is sinus tachycardia. The most common abnormality is nonspecific ST-T wave changes. Right axis deviation and right bundle branch block are uncommon

ABG: This shows hypoxia with an increased A-a gradient and mild respiratory alkalosis

80
Q

Right heart strain + Hypotension requires

A

Thrombolytics

81
Q

If a case clearly suggests a PE, then what is the next step after a chest x-ray and a blood gas?

A

Start heparin

82
Q

What is the standard to confirm the presence of a PE?

A

CT angiogram. The test of choice if an x-ray is abnormal

83
Q

Is the CT angiogram sensitive and specific?

A

Only specific. The sensitivity of CT angiogram is not ideal, and the test can miss some emboli if they are small and in the periphery.

84
Q

What is the utility of V/Q scan in PE?

A

For a V/Q scan to be accurate, the chest x-ray must be normal. The less normal the x-ray, the less accurate the V/Q scan. This is still a good test for PE, but only a truly normal scan excludes a PE.

Of patients with low-probability scans, 15% still have a PE, and 15% of those with high-probability scans don’t have a PE.

85
Q

What is the usefulness of Lower extremity dopplers?

A

These are excellent tests if they are positive, if positive, no further diagnostic testing is necessary. However, 30% of PEs originate in pelvic veins, and the Doppler scan is normal even in the presence of PE.

86
Q

What is the sensitivity of lower extremity dopplers?

A

70%

87
Q

Does D-dimer testing have a high specificity?

A

No. This is a very sensitive test with poor specificity. If the D-dimer is negative, PE is extremely unlikely. The best use of D-dimer testing is in a patient with a low probability of PE in whom you want a single test to exclude PE.

88
Q

What is D-dimer?

A

Metabolic breakdown product of fibrin. Plasmin chops up fibrin into D-dimers, but it is only effective with fresh, new clots that have formed over the last day. Older clots have been stabilized with factor XIII or clot stabilizing factor, which make them impervious to dissolution by plasmin.

D-dimers = Plasmin chopped up fresh clot

89
Q

What is the single most accurate test for PE?

A

Angiography. Unfortunately angiography is invasive with a significant risk of death about 0.5%

90
Q

When a patient has a PE and there is a contraindication to anticoagulation, what should be done?

A

A vena cava interruption filter should be placed.

91
Q

What is the standard of care for PE?

A

Heparin and O2

92
Q

What are other modes of treatment in PE?

A

Warfarin: should be used for at least 6 months after the use of heparin

Venous interruption filter: This should be placed in all patients who have contraindication to anticoagulation

Thrombolytics: Used in patients who are hemodynamically unstable. Hemodynamic instability can be defined as hypotension. Essentially replace embolectomy, which is rarely performed because of the high operative mortality.

93
Q

What is the mechanism of thrombolytics?

When can they be used?

A

Activate plasminogen to plasmin. Plasmin dissolves only fresh cloths, not cloths stabilized by factor XIII.

Only useful 12 hours post-MI. In PE, clots are older than the coronary clots of MI, but when they have formed is unclear, This is why there is no precise time frame for using thrombolytics in PE.

94
Q

What is the best initial test for pleural effusion?

A

Chest x-ray. Decubitus films with the patient lying on one side should be done next to see if the fluid is freely flowing.

Chest CT may add a little more detail to a chest x-ray.

95
Q

What is the most accurate test for pleural effusion?

A

Thoracentesis

96
Q

What are some characteristics of exudative pleural effusions?

A

Cancer and infection

Protein level high (>50% of serum level)

LDH level high (>60% of serum level)

97
Q

What are some characteristics of transudative pleural effusions?

A

Congestive heart failure

Protein level low (

98
Q

What tests should be done on pleural fluid?

A 
Gram stain and culture
Acid-fast stain
Total protein (also order serum protein)
LDH (also order serum LDH)
Glucose
Cell county w/ differential
Triglycerides
pH
99
Q

Do small pleural effusions need therapy?

A

No. Diuretics can be used especially for those caused by CHF

100
Q

What do you do with large pleural effusions?

A

For larger effusions, especially those caused by infection (empyema), a chest tube for drainage is placed

101
Q

If pleural effusions are recurrent and large?

A

If they are from a cause that cannot be corrected, pleurodesis is performed

102
Q

What is pleurodesis?

A

Pleurodesis is the infusion of an irritative agent, such as bleomycin or talcum powder, into the pleural space. This inflames the pleura, causing fibrosis so the lung will stick to the chest wall. When the pleural space is eliminated, the effusion cannot reaccumulate.

103
Q

What if pleurodesis fails?

A

Decortication is performed if pleurodesis fails. Decortication is the stripping off of the pleura from the lung so it will stick to the interior chest wall. This is an operative procedure

104
Q

Condition most commonly seen with obese patients complaining of daytime somnolence. The patient’s sleep partner will report severe snoring. There can also be HTN, headaches, erectile dysfunction, and a fat neck.

A

Sleep apnea

Majority (95%) of cases are obstructive sleep apnea from fatty tissues of the neck blocking breathing. A small number of patients will have central sleep apnea, which is decreased respiratory drive from the central nervous system.

105
Q

How do you diagnose sleep apnea?

A

Sleep study, polysomnography. Patient is observed for periods of apnea lasting >10 seconds each. The patient’s oxygen saturation is also monitored. Mild sleep apnea is defined as 5-20 apneic periods an hour. Severe sleep apnea is defined as >30 periods an hour.

106
Q

What is the treatment of obstructive sleep apnea?

A

Weight loss and CPAP or BiPAP.

If this is not effective, surgical resection of the uvula, palate, and pharynx can be performed

107
Q

What is the treatment of central sleep apnea?

A

Avoiding alcohol and sedatives

May respond to acetazolamide, which causes a metabolic acidosis. This may help drive respiration

Medroxyprogesterone, which is also a central respiratory stimulant

108
Q

What is the mechanism of acetazolamide?

A

Acetazolamide is an inhibitor of carbonic anhydrase. This enzyme is needed for reabsorption of bicarbonate that has been filtered at the glomerulus. In the absence of carbonic anhydrase, the bicarbonate is urinated off and the body becomes acidotic. Acidosis acts as a stimulant to the medulla to drive respiration.

109
Q

Presents as an asthmatic patient with worsening asthma symptoms who is coughing up brownish mucous plugs with recurrent infiltrates.

A

Allergic bronchopulmonary aspergillosis

110
Q

What would you find on labs and imaging with Allergic bronchopulmonary aspergillosis?

A

Peripheral eosinophilia. Serum IgE is elevated

Central bronchiectasis

111
Q

What is the diagnostic testing for allergic bronchopulmonary aspergillosis?

A
  • Aspergillus skin testing
  • IgE levels elevated
  • Circulating precipitins
  • A. fumigatus-specific antibodies present
112
Q

What is the treatment for ABPA?

A

Corticosteorids and in patients with refractory disease, itraconazole.

113
Q

Suddent, severe respiratory failure syndrome resulting from diffuse lung injury secondary to a number of overwhelming systemic injuries

A

Acute respiratory distress syndrome

114
Q

What are some causes of ARDS?

A 
Sepsis
Aspiration of gastric contents
Shock
Infection: pulmonary or systemic
Lung contusion
Trauma
Toxic inhalation
Near drowning
Pancreatitis
Burns
115
Q

What is the diagnostic testing for ARDS?

A

Chest x-ray
Normal wedge pressure
pO2/FIO2 ratio

116
Q

What will you see on x-ray for ARDS?

A

Diffuse patchy infiltrates that become confluent. May suggest congestive failure

117
Q

Are steroids effective in treatment of ARDS?

A

No

118
Q

What is the treatment for ARDS?

A
  • Vent support with low tidal volume (6 ml/kg of ideal body weight)
  • PEEP to keep the alveoli open
  • Prone positioning of the patient’s body
  • Possible use of diuretics and positive inotropes, such as dobutamine
  • Transfer the patient to the ICU
119
Q

What is the mechanism of PEEP?

A

Positive-end expiratory pressure (PEEP) keeps the alveoli open. When the alveoli are thus expanded, more surface area is available for gas exchange. Without PEEP, there is more atelectasis and less surface area for gas exchange

120
Q

What are the Swan-Ganz (pulmonary artery) catheterization findings for hypovolemia, cardiogenic shock, and septic shock?

A

Hypovolema
- Low CO, low wedge pressure, high SVR

Cardiogenic shock
- Low CO, high wedge pressure, and high SVR

Septic shock
- High CO, low wedge pressure, and low SVR

121
Q

Fever, cough, and often sputum. Severe illness also presents with SOB

A

Pneumonia

122
Q

What are the most likely organisms for CAP and HAP?

A

CAP: Pneumococcus
HAP: Gram-negative bacilli

123
Q

What are conditions that lead to poor progrnosis in pneumonia?

A 
Age >65
Chronic diseases of the lungs, liver, or kidney
Diabetes
HIV
Steroid use
Lack of spleen
124
Q

What is the best initial diagnostic test for pnuemonia?

A

Chest x-ray

125
Q

What ist he most accurate test for pneumonia?

A

Putum gram stain and culture

126
Q

What other tests should be done for pneumonia?

A

All cases of respiratory disease should have a chest x-ray and oximeter

SOB –> oxygen

SOB and/or hypoxia –> order an ABG

127
Q

What is the treatment for outpatient pnuemonia?

A

Macrolide (azithromycin, doxycycline, or clarithromycin)

0r

Respiratory fluoroquinolone

128
Q

What do you treat inpatient pneumonia with?

A

Ceftriaxone and azithryomycin

or

Fluoroquinolone as a single agent

129
Q

How do you treat ventilator-associated pneumonia?

A

Imipenem or meropenem, piperacillin/tazobactam or cefepime

Gentamicin and Vancomycin or linezolid

130
Q

Pneumonia presentation (give causeative agent):

1) Recent viral syndrome
2) Alcoholics
3) GI symptoms, confusion
4) Young, healthy patients
5) Persons present at the birth of an animal
6) Arizona construction workers
7) HIV with

A

1) Staphylococcus
2) Klebsiella
3) Legionella
4) Mycoplasma
5) Coxiella burnetii
6) Coccidioidmycosis
7) Pneumocystis (PCP)

131
Q

How does VAP present?

A

Fever, hypoxia, new infiltrate, increasing secretions

132
Q

What is the best treatment for PCP?

A

Bactrim

133
Q

Occurs in specific risk groups, such as immigrants, HIV-positive patients, homeless patients, prisoners, and alcoholics. Presnts as fever, cough, sputum, weight loss, and night sweats

A

Tuberculosis

134
Q

What are the diagnostic tests for TB?

A

Best initial test: chest x-ray

Sputum acid-fast stain and culture should be done to confirm the presence of TB

135
Q

What is the treatment for active TB?

A

Once the acid-fast stain is positive, treatment with 4 antituberculosis medications should be started. 6 months of therapy is the standard of care

  1. Isoniazid (INH): 6 months
  2. Rifampin: 6 months
  3. Pyrazinamide: Stop after 2 months
  4. Ethambutol: Stop after 2 months
136
Q

What are the adverse effects of the anti-TB drugs (RIPE)?

A

All can lead to liver toxicity

Isoniazid: Peripheral neuropathy
Rifampin: Red/orange-colored bodily secretions
Pyrazinamide: Hyperuricemia
Ethambutol: Optic neuritis

137
Q

If patient has liver toxicity s/s RIPE agents, then when should TB meds be stopped?

A

Stop if the transaminases reach 5 times the upper limit of normal

138
Q

What conditions require TB treatment for more than 6 months?

A 
Osteomyelitis
Meningitis
Miliary TB
Cavitary TB
Pregnancy
139
Q

What is a positive PPD test?

A

5 mm: Close contacts, steroid users, HIV-positive

10 mm: Homeless, immigrants, alcoholics, health care workers, and prisoners

15mm: Those without an increased risk

140
Q

When should 2-stage PPD testing be done?

A

If the patient has never been tested or it has been several years since the last test. If first test is negative, a second test should be done 1-2 weeks later to make sure the first test was truly negative

141
Q

What effect does Bacille-Calmette Guerin (BCG) administration have on recommendations for treatment of latent TB?

A

None

142
Q

What is the treatment for latent TB?

A

Isoniazid for 9 months. This reduces the percent lifetime risk of developing TB to 1 percent.

143
Q

SHould you repeat a PPD if it has been positive in the past?

A

No. Never repeat

144
Q

How does the interferon gamma release assay (IGRA, quantiferon) differ from PPD?

A

Both used for detection of latent TB

Main difference is that IGRA is more specific than a PPD.

There are no false positive on an IGRA with previous BCG infection

IGRAs have 90% sensitivity for previous TB exposure

145
Q

What is the lifetime risk of TB with a positive PPD or positive IGRA (quantiferon)?

A

10% lifetime risk of TB

146
Q

If PPD is positive what do you do next?

A

1) Chest x-ray to make sure occult active disease has not been detected
2) If the chest x-ray is abnormal, sputum staining for TB should be performed
3) If this is positive, then full-dose, 4-drug therapy is used

MTB STEP 3 (R) (9 decks)

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