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Respiratory Medicine > Final > Flashcards

Final Flashcards

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1
Q

What drug is linked to PH?

A

Fen-Phen

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2
Q

What are the CXR findings in PH?

A

peripheral hypervascularity, prominent central pulmonary artery, RV enlargement, prominent right descending pulmonary artery

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3
Q

Describe the PFT in patients with PH?

A

classicly: normal except reduction in DLCO, as well as findings of the primary cause(i.e., COPD)

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4
Q

What findings would be seen on the echo of a PH patient?

A

increased estimated PA preasures, RA & RV enlargement

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5
Q

What is the common treatment of PH?

A

treat the underlying cause

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6
Q

Is idiopathic PH common or uncommon?

A

uncommon

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7
Q

What is group 1 PH related to?

A

idiopathic and cumulative trauma disorder (CTD)

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8
Q

What is group 2 PH related to?

A

heart disease

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9
Q

What is group 3 PH related to?

A

lung disease

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10
Q

What is group 4 PH related to?

A

pulmonary emboli

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11
Q

What is group 5 PH related to?

A

all others besides 1-4

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12
Q

How are PH and IHD similar?

A

exertional dyspnea, elevated BNP, lack of asociated Sx

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13
Q

How are PH and IHD different?

A

PAH has increased P2, difference on CXR, echo and ECG

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14
Q

What tests can be done for PH?

A

6-minute walk test at the beginning and periodically after, serial echos and right heart caths as well

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15
Q

What history findings give clues for OSA?

A

Impaired daytime attention(MVAS, memory issues, sleepiness) snoring, witnessed apnea, mood changes

Must screen obese patients with depression

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16
Q

What clinical presentation is seen in OSA patients?

A

obesity, large neck circumference, nasal obstruction, enlarged tonsils, narrow oropharynx, large tongue, small jaw, short jaw

don’t rule out non-obese patients

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17
Q

What DDx should you include for OSA?

A

COPD, asthma, hypothyroidism, depression, narcolepsy, central sleep apnea, poor sleep hygiene, meds, pickwickian syndrome, laryngospasms(GERD)

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18
Q

What are the management goals for OSA?

A

improve daytime sleepiness and cognitive performance, prevent long-term sequelae

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19
Q

What tools can manage OSA?

A

Lifestyle modifications, CPAP

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20
Q

How does treating daytime sleepiness improve OSA?

A

decreased daytime somnolence, improved mood and depression, high QOL scores, lowered traffic accidents

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21
Q

Why should long term sequelae be treated?

A

OSA increases CA 2.5x, four times more likely to have CVA or die over non-OSA patients

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22
Q

What lifestyle changes are effective for OSA?

A

losing 10% or more of BW, avoid EtOH and sedatives 3-4 prior to bed, lateral decubitus sleeping position(protect airway), intranasal steroids for congestion

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23
Q

When should nocturnal CPAP be used and why?

A

if Sx persist after modifications, works to prop airway open with air and increases intraluminal pressure and FRC

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24
Q

What do you consider if nocturnal CPAP is not tolerated or working?

A

BiPAP has two pressures, one for inhalation and another for exhalation, improves comfort and adherence

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25
Q

What other tools can be used outside of PAP to treat OSA?

A

mandibular assist device, upper airway surgery: UPPP

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26
Q

How does mandibular assist work?

A

pulls lower jaw and tongue forward, can eliminate PAP machines

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27
Q

What are features of uvulopalatopharyngoplasty?

A

removes obstruction to airway, most common of upper airway surgeries, cut out the uvula and palate

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28
Q

Where is the spectrum of COPD?

A

between emphysema and chronic bronchitis

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29
Q

What is the Medical Research Council Dyspnea Scale?

A

describes breathlessness and grades the disease, part of BODE

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30
Q

What are MRCDS grades 0 & 1?

A

0: i only get breathless with exercise- 0 points
1: SOB hurrying on ground level or slight hill- 0 points

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31
Q

What are MRCDS grades 2 & 3?

A

2: slower then people own age or stopping to breath at normal pace- 1 point
3: stop for breath at 100yds or after a few minutes on level ground- 2 points

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32
Q

What makes up the BODE index for COPD survival and what does it predict?

A

FEV1 after bronchodilator, BMI, 6-minute walk distance, MRCDS dyspnea score

4 year survival rate

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33
Q

What is the scoring for BODE FEV1?

A 
>65% = 0
64-50 = 1
49-36 = 2
<36 = 3
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34
Q

What is the BODE 6-minute walk score?

A

> 350 meters = 0
349-250 = 1
249-150 = 2
<150 = 3

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35
Q

What is the BODE BMI score?

A 
>21 = 0
<21 = 1
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36
Q

What percentages correlate to MRCDS/BODE scores?

A

0-2 points= 80% 4 year survival
3-4 poionts= 67%
5-6 points= 57%
7-10 points= 18%

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37
Q

How does increased dead space cause dyspnea in COPD?

A

increases PaCO2

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38
Q

How does airway obstruction affect COPD?

A

causes dyspnea by limiting ability to meet increased demands

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39
Q

What is a byproduct of reduced mechanical advatnage of the diaphragm?

A

hoover sign, accessory respiratory muscle use, paradoxical respiratory motion

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40
Q

What is the outcome of altered V/Q ratio in COPD?

A

dyspnea and hypoxemia

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41
Q

What is description of the flow-volume loop in COPD?

A

obstructive, with a scooped out expiratory phase

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42
Q

What are similarities between asthma and COPD?

A

weather exacerbations, perennial Sx, cough/sputum, wheeze, prolonged expiratory phase

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43
Q

What are the differences in COPD and asthma?

A

complete reversibility, seasonal variants, associated ENT allergic Sx, younger onset in asthma

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44
Q

How is LVF similar to COPD?

A

progressive dyspnea, orthopnea, wheeze, cough, dyspnea

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45
Q

Name the differences between COPD and LVF.

A

Paroxysmal nocturnal dyspnea, heart disease Hx, crackles, edema, S3 gallop, JVD/HJR

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46
Q

What are the suffixes of medication classes?

A

SAMA/LAMA: -ium
SABA: -ol
LABA: -terol
ICS: -asone, -ide

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47
Q

What are the drug delivery methods?

A

metered dose inhaler(MDI) or dry powder inhaler(DPI)

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48
Q

Describe the MDIs.

A

non-breath activated- released by activation

breath activated- activated when you breath

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49
Q

Describe the DPIs.

A

single dose-uses a capsule

multiunit/multidose-dose built into device

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50
Q

What is respimat?

A

propellant free liquid inhaler that creates a cloud

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51
Q

What else can treat COPD outside of inhalers?

A

ABx, OCS-prednisone, prednisolone, Methyxanthines-theophylline, PDE-4 inhibitors- roflumilast, daliresp

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52
Q

What specific Tx is key for tounger patients?

A 
FEV1>50%, <65yo
doxycycline(macrolides are increasing)
TMP-SMX
Cephalosporins
advanced macrolides
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53
Q

What should older, sicker COPD patients be treated with?

A

amoxicillin-clavulunate

Fluoroquinolones(tendon rupture)

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54
Q

What steroids are most common to Tx COPD?

A

prednisone-common, cheap, range of dosing, usually 40-60mg/day
also, methylprednisolone

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55
Q

What parameters decide if O2 should be administered supplementally?

A

PaO2<56 or SpO2<89% twice per week over 3 wks

PaO2 56-60 with PH, CHF, erythrocytosis Hct>55%

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56
Q

What is GOLD I staging?

A

mild disease

Tx with SABA or SAMA, not usually together but can be as combivent

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57
Q

What makes up GOLD II staging?

A

moderate disease

Tx with LABA/LAMA

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58
Q

How does one treat GOLD III staging?

A

severe disease
ICS+LABA or ICS + LAMA
never use ICS alone in COPD

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59
Q

What is the treatment for GOLD stage IV and what is it?

A

very severe disease
ICS+LABA or LAMA or both
with or without roflumilast or theophylline

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60
Q

What tests should be used to monitor progression of COPD?

A

6-minute walk test, pulmonary rehab, PFT

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61
Q

What is involved in pulmonary rehabilitation?

A

exercise training-intensity and duration matter
education
psychosocial training- depression/anxiety
nutrional support
breathing training, inspiratory muscle training and CPT
vaccination-flu, PNA

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62
Q

What is are three typical identities of COPD patients?

A

A1AT, smokers, ex-smokers

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63
Q

When should you think A1AT?

A

young, unexplained dyspnea and cough

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64
Q

How is chronic bronchitis diagnosed?

A

chronic productive cough for 3 months a year in 2 consecutive years

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65
Q

How is emphysema diagnosed?

A

pathologically

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66
Q

Weird COPD/asthma treatment?

A

smoking lol

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67
Q

What will patients present with in ILD?

A

dyspnea, cough, crackles in bases, digital clubbing(not specific), exercise induced hypoxemia

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68
Q

Describe PFTs in ILD patients

A 
FRC-reduced
FVC- reduced
TLC- reduced
FEV1/FVC- normal
DLCO-reduced
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69
Q

What agents are linked to causing ILD?

A 
drug induced
inorganic dusts
lympangitic metastases
hypersensitivity pneumonitis
radiation
Idiopathic pulmonary fibrosis
smoking
connective tissue disorders
sarcoidosis
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70
Q

What are important topics to cover for H&P of ILD?

A

occupation, hobbies, environment, travel, Rx and non-Rx drug use

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71
Q

What are the inorganic dusts involved with ILD development?

A

silicosis, asbestosis, coal worker’s pneumoconiosis, berylliosis

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72
Q

What tests are indicated for ILD evaluation?

A

chest CT-specify Dx
PFTs
ANA/RF factor

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73
Q

What is seen in scleroderma and similar diseases?

A

pulmonary fibrosis
pulmonary HTN-due to fibrosis
aspiration-esophageal disease

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74
Q

What will rheumatoid arthritis present with?

A 
Interstitial pulmonary fibrosis
bronchiectasis
pulmonary rheumatoid nodules
pulmonary vasculitis
pleural disease ( very low pleural glucose)
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75
Q

What are the findings in Systemic Lupus Erythematous?

A

interstitial lung disease
extra-pulmonary restriction: shrinking lung disease
pulmonary HTN
pleural disease

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76
Q

What Autoantibodies are found in scleroderma?

A

anticentromere: 20-40%
SCL-70L 30-70%, more common in ILD
antinucleolar: 10-20%, with worse prognosis

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77
Q

What drugs can lead to lung disease?

A

chemotherapeutic agents- largest category
amiodarone-cardiac drug, dose related
nitrofurantoin- UTI ABx

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78
Q

What is the course of radiation induced lung disease?

A

early: 1-3 months after radiation
late: 6-12 months
newer radiation techniques have reduced occurence

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79
Q

What are the two courses of hypersensitivity pnuemonitis?

A

acute: abrupt dyspnea, cough, fever +/- myalgias
chronic: pulmonary fibrosis

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80
Q

What are the differences in CHF and ILD?

A

specific history differences in onset
CXR and CT findings
exam: clubbing, edema, S3 gallops in LVF

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81
Q

What are the similarities between ILD and CHF?

A

progressive dyspnea, exercise induced hypoxemia,
CXR infiltrate findings,
crackles in bases, pulmonary HTN

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82
Q

What is found in ILD compared to COPD and vice versa?

A

ILD- more rapid decline, non productive cough

COPD- slower decline with more frequent exacerbations, weather & NSAIDs make it worsen Sx, productive cough

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83
Q

What are the treaments in ILD?

A

treat or remove the cause
OCS are the mainstay of non-IPF causes
Tx of IPF only: pirfenidone and nintedanib
both of which reduce inflammation and fibrosis

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84
Q

What is characteristic of ILD presentation?

A

sudden, dyspnea, rapid respiratory failure.

difuse alveolar damage on histo

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85
Q

What is another name for acute interstitial pneumonia?

A

Hamman-Rich Syndrome

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86
Q

How does AIP present?

A 
all age groups, mostly adults
no specific etiology
diffuse, bilateral, symmetrical pattern
abrupt onset-flu-like
Dx with biopsy
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87
Q

How does IPF present?

A

exclusively adults
prior causative exposure
asymmetrical pattern favoring upper and lower lobes
gradual onset, afebrile
Dx based on PFT, history, imaging, biopsy not needed

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88
Q

What is the treatment of choice for sarcoidosis?

A

prednisone

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89
Q

What characteristics are found in sarcoidosis?

A

asymptomatic or mild
incidental finding
symmetrical CXR, no true with CT
leads to death and debilitation in some people

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90
Q

What are the similarities between PTX and effusion on exam?

A

diminished BS on auscultatio

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91
Q

What are the differences between PTX and effusion?

A

effusion is dull, PTX is hyperresonant

positional changes of BS, improve in effusion, not PTX

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92
Q

What are the potential causes of PTX?

A

spontaneous in young males
traumatic: post-procedural and direct trauma
disease related

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93
Q

Describe the lungs in open and tension PTX.

A

open: the trachea corrects slightly on expiration
tensions: the trachea deviates more on expiration to the normal side

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94
Q

How can exudate be confirmed in effusion?

A

pleural protein/serum protein of >0.5
pleural LDH/serum LDH > 0.6
Pleural fluid LDH >2/3 upper limit of serum LDH

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95
Q

What are the differentials for low pleural glucose?

A 
parapnuemonic effusion
malignant effusion
TB
hemothroax
RA
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96
Q

What is the normal cell count in pleural fluid?

A

75% macrophages, 25% lymphocytes

97
Q

When will you see increased eosinophils in the pleural fluid?

A 
>10%
air in the space
idiopathic
parapnuemonic
malignancy
98
Q

When are increased lymphocytes seen in pleural fluid?

A

> 50%

malignancy & TB

99
Q

What causes trasudative pleural fluid?

A

LVF or CHF
misplaced central line
massive cirrhosis
nephrosis

anything else is exudative

100
Q

How can a chronic effusion be managed?

A

PleurX cath allows for at home drainage

pleurodosis closes the potential space between pleura
via talc, tetracycline through thorascope or IR

101
Q

What major diseases can occur in the mediastinum?

A

masses, fluid or air and infection/inflammationWhat

102
Q

What are the 4 Ts of the anterior mediastinum?

A

thymoma, teratoma, thyroid mass, T cell lymphoma or B cell

103
Q

What are the middle mediastinal diseases?

A

VAC
vascular masses
adenopathy
cysts- pleuropericardial, bronchogenic

104
Q

What diseases are more typical of the posterior mediastinum?

A

nerves and guts
neurogenic tumors
meningoceles, meningomyeloceles
gastroenteric cysts and esophageal diverticula

105
Q

Which type of cancer is most common in the head and neck

A

Squamous cell carcinoma in the upper aerodigestive tract
death is more common in AA
typically males in 50-60s

106
Q

What is field cancerization?

A

entire upper aerodigestive tract is exposed to cancers due to its structure
investigate entire area when malignancy is identified

107
Q

What is the clinical presentation of head and neck cancer patients?

A

swallowing or intermittent choking, prompt work-up
trismus
ear pain-needs evaluation
weight loss

108
Q

What is trismus?

A

inability to op jaw due to CN V compression by mass or muscle invasion

109
Q

Should you assess nuritional and performance status in patients with head and neck cancer?

A

yes, to assess treatment efficacy, activity level and burden on family

110
Q

What are the available H/N cancer Tx’s?

A

radiotherapy, surgery: laryngectomy(removes vocal cords)

systemic therapy: chemo

111
Q

What are therapies available for those with laryngectomy to improve life?

A

electrolarynx: submandibular region, uses vibrations for speech

talking tracheostomy: provides synthetic vocal cords

112
Q

What is the#1 risk factor for lung cancer?

A

smoking- #1 cause, increase 10x for M, 5x for F

113
Q

What increases the risk of lung cancer in smokers?

A

number of years, PPD, length of cigarette, depth of inhalation, tar content

114
Q

What are the occupational risk factors for lung cancer?

A

uranium miners: radon gas, alpha particles damage DNA
Coal miners: CWP
Nickel, arsenic, mustard gas
petrochemical exposure
passive second hand smoking 3-10,000 lung CAs/year

115
Q

What is the origin of most lung CA?

A

epithelial

small and non-small cell carcinomas

116
Q

What are the Sx of pancoast syndrome and how?

A

superior sulcus tumor, lung apex

invade brachial plexus and cause shoulder pain or paresthesias along C7-T1 dermatomes

117
Q

What is the description and cause of Horner’s syndomre in CA?

A

compression of sympthatetic ganglion (stellate)

anhydrosis of face, ptosis of eye and pupillary constriction

118
Q

What category of conditions is hypertrophic pulmonary osteoarthropathy and what are the Sx?

A

paraneoplastic syndrome
HPO-> clubbing of digits and hypertrophy of joints
arthralgias, synovitis and periostitis
furrowing of brow, characteristic facies

119
Q

What causes HPO?

A

unknown, possibly humoral mediators, PDGF, TNF-a, TGF-B

hypoxia alone is not sufficient for development

120
Q

What is the category and what are the causes of superior vena cava syndrome?

A

extrinsin compression of SVC by mass

distension of superficial neck vv., face/neck edema

121
Q

What is the easiest diagnostic imaging used for lung CA suspicions?

A

CXR
identifies primary lesions and possibly lymph node metastases
serial XR are important, especially for nodular evaluation

122
Q

What are secondary imaging techniques for lung CA evaluation?

A

CT-most common for bronchogenic CA, evaluautes mediastinal tumors, nodes, vertebra and parynchema of lungs
MRI- expensive but no better than CT
PET scan- when fused with CT is better for malignancy vs. benign differentiation

123
Q

How is sputum cytology used in lung CA evaluation?

A

positive in 60-90% of lung CA and abnormal CXR

124
Q

What does bronchoscopy tell you in lung CA patients?

A

allows for airway visualization down to subsegmental bronchi
can use brushings and washings for DX
required if resection is considered

125
Q

How can mediastinoscopy be beneficial?

A

evaluates mediastinum for tumor expansion and can obtain lymph nodes
valuable for resection

126
Q

What are the uses of fine needle aspiration in CA patients?

A

plain film or CT guidance
used in peripheral lung lesions-90% accurate
risk of PTX is 20-25% but chest tubes in only 5%

127
Q

What is the staging system for small cell lung cancer?

A

based on VA staging

limited disease: tumor confined to one hemithorax and lymph nodes, single radiation field

extensive disease: disease outside of limited region

128
Q

What is the pediatric assessment triangle?

A

PAT, first general assessment

appearance, breathing circulation

129
Q

What is the appearance of a child in respiratory distress and what is the importance of the signs?

A

restless, anxious, combative: suggests hypoxia
SOMNOLENCE/LETHARGY: suggest severe hypoxia, hypercapnia or respiratory fatigue

vigorous movement: reassuring
poor tone, lethargy, listlessness: not reassuring

130
Q

What is an ominous sign in a child with respiratory Sx?

A

development of slower, irregular breathing pattern, in the setting of respiratory distress, arrest will develop without intervention

131
Q

What is Beck’s triad?

A

JVD, muffled cardiac sounds, hypotension–> cardiac tamponade

132
Q

What is the significance of a peritonsillar abscess?

A

EMERGENCY

hoarse voice with sore throat on swallowing, swelling and local pain

133
Q

What are the signs and symptoms of croup?

A

acture laryngotracheobronchitis
most common infectious airway obstruction in kids 6-36 months
usually viral, can be allergic
not only in children
trecheitis is a secondary bacterial infection
kid with stridor-> croup

134
Q

What are characteristics of asthma in children?

A

inflammation, edema, bronchospasms, mucous

triggers: infection, exercise, irritants, stress, GERD can rapidly worsen due to atelectasis or alveolar disease

135
Q

Describe anaphylaxis in children.

A 
commonly due to food or meds
life threatening pharyngeal edema, 
urticaria and facial edema
lower airway bronchospasm
ask what happens with reported allergies
136
Q

What is the immediate intervention in anaphylaxis?

A

assess: airway, breathing, circulation, consciousness

give epinephrine IM

137
Q

How do kids with tracheal/esophageal FB present?

A

trach: sudden dramatic coughing
stridor, drooling and choking

esophagus: drooling, dysphagia

40% of FB ingestions are not witnessed

138
Q

What is the presentation of a lower airway FB?

A

coughing, choking on ingestion

recurrent pneumonia, chronic cough

139
Q

What is Dr. Newman’s worst nightmare with FB?

A

button batteries

140
Q

What neurological Sx are associated with respiratory distress?

A

neuomuscular-secondary to hypoventilation
infection
trauma
medication effects

141
Q

What systemic diseases can lead to respiratory distress?

A

Cystic fibrosis, asthma, neuromusclar disease

sickle cell disease-> acute chest syndrome

142
Q

What is characteristic of acute chest syndrome?

A

SSD
sudden onset respiratory distress and CP
new infiltrate on CXR
fever

143
Q

What are the characteristics/histo aspects of asthma?

A

reversible airflow obstruction, spontaneously or with meds
limited airflow on PFT or methacholine challenge
thick inflammed walls and tight muscles

144
Q

What is a trigger for asthma?

A

allergens

145
Q

What are two histomorpholgical findings in prolonged status asthmaticus?

A

Curschmann spirals- in sputum of BAL, mucus plugs from glands or bonchioles

charcot-leyden crystals: in sputum of BAL specimen, coposed of galectin-10

146
Q

What is the major pathogenesis of asthma?

A

atopy(strongest predisposing factor)

allergen exposre: dust mites, cockroaches, seasonal

147
Q

What are key indications of asthma?

A

wheezing, cough, dyspnea

worse with exercise, weather changes, and at night

148
Q

What is the PFT loop for asthma?

A

obstructive pattern, scooped out

149
Q

What is the medication for quick asthma relief?

A

SABA

albuterol, levalbuterol

150
Q

How is asthma controlled long-term?

A

ICS, leukotriene modifiers

151
Q

What Sx are present when respiratory arrest is imminent?

A

breathlessness at rest, not talking, drowsy/confused
increased respirations, cannot recline, paradoxical movements of chest wall, no wheeze, low HR, low FEV1 and PaO2 with high PaCO2

152
Q

What are thes steps in treating an asthma attack at home?

A

inhaled SABA,
if good: repeat for 48 hours if needed
if incomplete response: add OCS, call doc
if poor response: add OCS, in nothing go to ED

153
Q

What is the classification of intermittent asthma?

A

<2 days/week of Sx and SABA use, minimal to no night time wakings, 0-1x per year with OCS

154
Q

How does well controlled asthma present?

A

0-4 years or >12 years: <2 days/week
5-11 years: same, not more than one/day
no activity interference,<2 days/week of SABA use

155
Q

What is a sign of good response to SABA?

A

decreased wheezes moving to increase, indicating more airflow

156
Q

Should Huter miss any CF questions?

A

Nah

157
Q

What is the etiology of CF?

A

AR, CFTR protein which functions as cAMP mediated Cl channel on mucosal surfaces, chromosome 7
exocrine gland dysfunction

158
Q

What ethnicities have the highest risk of being a CF carrier?

A

Ash Jews: 1/24
caucasian: 1/25
lower in others

159
Q

Why does CF not present the same way in all patients?

A

poor penetrance
commonly chronic, progressive ling disease
pancreatic insufficiency

160
Q

What other factors lead to CF presentation besides the mutation itself?

A

non-genetic factors: level of care, nutritional status, age of onset
modifier genes: mannose binding lectin-p. aeruginosa

161
Q

What are the main infections in CF patients?

A

S. aureus, H. influenzae

P. aeruginosa-older patients

162
Q

What is the major GI Sx in neonates with CF?

A

meconium ileus, abdominal distension, vomiting, no meconium passed

163
Q

What are the major GI Sx in all CF patients?

A

pancreatic insuffiency, malsborption, failure to thrive, low ADEK, jaundice or GI bleed as result of hepatobiliary disease, DM-insulin

164
Q

What is the cause of liver disease in CF patients?

A

epithelial lining biliary ducts get plugged by mucous and obstuctive cirrhosis occurs

165
Q

What is a common GU Sx in CF patients?

A

CBAVD, infertility

166
Q

What finding on nasal exam would put CF on the DDx?

A

nasal polyps

167
Q

What is the diagnostic criteria for CF?

A

a positive newborn screen AND elevated sweat chloride test on 2+ occasions

168
Q

What test is used in the neonatal screen for CF?

A

(immunoreactive trypsinogen)IRT levels are higher in babies with CF
if elevated repeat or do sweat test

169
Q

What is the importance of a CXR in a patient with breathing trouble?

A

rule out all causes, PNA, ILD, asthma or other

170
Q

What are characteristics of mycoplasma pneumoniae?

A

no cell wall, cold agglutinin positive, microcytic anemia

atypical, obligate IC, bullous myringitis, self-limiting, dry cough

171
Q

What treatment is not effective in M. pnuemoniae

A

cell wall synthesis inhibitors

172
Q

What is the empiric treatment for CAP in ambulatory patients?

A

macrolide or doxycycline

173
Q

What is CAP empiric treatment for drug resistant strains?

A

Fluoroquinolone or macrolide + beta-lactam

174
Q

Name with CAP empiric treatment in hospitalized patients.

A

fluoroquinolones

175
Q

What do you use for empirical treatment of ICU patients with CAP?

A

fluoroquinolone + antipneumococcal beta lactam

add piperacillin-tazobactam for P aeruginosa coverage

176
Q

What is the presentation of chlamydia pneumoniae?

A

atypical but with hoarse voice

177
Q

How dose legionella pneumoniae present?

A

more severe than other atypical pneumonias

178
Q

What is the atypical presentation of pneumonia?

A

younger adults, mild Sx, F/C, dry cough

follows URI like Sx-rhinitis, sinusitis etc

179
Q

What random lab finding can be elevated in penumonias?

A

procalcitonin-

high in proinflammatory stimuli, especially bacterial

180
Q

What is the CURB-65 score?

A

determines how to proceed in PNA cases

1 point for confusion, BUN>20, respirations>30
BP<60 or >90, age<65

total score 0-1 low risk
2 moderately severe
3-5 severe

181
Q

What are characteristics of P. aeruginosa?

A

gram - bacillus, capusle, pyocyanin and pyoverdine, grape smell, loves water, CF and bronchiectasis

182
Q

What are characteristics of H. influenzae

A

gram - diplococci, capsule(types), no capsule

(no type), chocolate agar(factors V and X), smokers, immmunocompromised

183
Q

What are the characteristics of Moraxella catarrhalis?

A

gram - coccobacillus, fastidious anaerobe, big time for smokers, COPD, asthmatics, malignancy
exacerbates pre-existing conditions then forms PNA

184
Q

What are characteristics of L. pneumophilia?

A

gram - bacillus, aerobic, flagellate, water lover, urinary antigen, does not ferment, yeast charcoal media, hyponatremia, bradycardia, multiple people

185
Q

What is MaConkey agar?

A

selectsfor G- bacteria, especially enteric, and fermentors due to lactose

186
Q

What are the characteristics for yersinia pestis?

A

G-, non fermenting, comes with pulmonary hemorrhage, severe presentation

187
Q

What is the presentation of Klebsiella pneumoniae?

A

capsule, G-. fermenter, mucoid colonies, bulging fissure, currant jelly sputum, immunocompromised and EtOH use

188
Q

What are the lactose fermenters and their speed?

A

Fast: oh, KEE
klebsiella, E. coli, enterobacter

slow: CS
citrobacter, serratia

189
Q

What are characteristics of strep pneumoniae?

A

gram + diplococci, capsule, alpha-hemolytic, optochin sensitive, urinary Ag, most common cause of CAP(& meningitis), lobar PNA, rust colored sputum, lancet shaped

190
Q

What are the characteristics of staph aureus?

A

G+, catalase and coagulase +, follows viral penumonia, necrotizing, hemorrhages, salmon colored sputum

191
Q

What vaccines exist for strep pneumoniae?

A

pneumovax-23 strains
Prevnar 13- 13 strains

for pts over 65, immunocompromised, asplenia, 2-64 with risk factors

can cause anaphylaxis

192
Q

What is characteristic of orthomyxovirus?

A

8 segments, -ssRNA, HN spikes, PCR test

193
Q

What is characeristic of adenovirus?

A

non-enveloped, dsDNA, icosahedral, common cold, conjunctivitis, overlapping Sx, direct assay or enzyme immunoassay

194
Q

What are the characteristics of MERS?

A

coronavirus, ssRNA, middle east respiratory syndrome, GI Sx, fecal-oral transmission, ARDS presentation

195
Q

What are characteristics of SARS?

A

severe acute respiratory syndrome, coronavirus, travel to east Asian countries, flu-like but progress to ARDS

196
Q

What is Reye syndome?

A

flu and ASA combined

197
Q

What are characteristics of H5N1?

A

similar to orthomyxovirus, exposure to dead or sick poultry, RT-PCR to detect, start oseltamavir

198
Q

What is the difference in antigenic shift and drift?

A

shift is pandemics

drift is epidemics

199
Q

What are characteristics of histoplasmosis?

A

micronidia in caves with bat/bird droppings, dimorphic yeast in body, fungi outside, mild PNA unless immunocompromised, ohio river valley, coin lesions

200
Q

What are characteristics of coccidioidomycosis?

A

valled fever, San Juaquin valley, SW USA, chronic PNA, erythema nodosum, self-limiting

201
Q

What are characteristics of blastomycosis?

A

chronic PNA, soil with decomposing matter, broad based budding yeast, skin, bone and CNS changes

202
Q

What are characterstics of burkholderia cepacia?

A

G- bacillus, catalase +, non- fermenter, BC agar, blue crystal, colonies pearly gray, CF or bronchiectasis, hard to Tx, multi-resistance

203
Q

What are characteristics of bunyavirus?

A

hantavirus, zoonotic, infected rodents and urine, feces, saliva, profromal phase mimics flu, rapidly progresses to hanta CP with resp distress, increased LDH

204
Q

What are characteristics of coxiella burnetti?

A

obligate IC, G- small, endospore, hepatitis, endocarditis, maculopapular rash, shepards, farmers, cattle birthers

205
Q

What are characteristics of enterobacter?

A

G- bacillus, fermenter, oxidase negative, anaerobe, oppurtunistic, mechanical ventilation, coliform, motile

206
Q

What are characteristics of leptospirosis?

A

spirochete, high fevers, HA, aseptic menigitis, hepatitis, reanl failure, subconjunctival hemorrhage, rodents, cattle, sheep, goats, aborted animals

207
Q

What are characteristics of francisella tularensis?

A

G- aerobe, abrupt nonspecific Sx, tick bite, pulmonary tularemia-infiltrates and effusion

208
Q

What are characteristics of chlamydia psittacosis?

A

obligate IC anaerobe, G-. no cell wall. resevoir-birds, pet shop owners, inhaled feather dust/feces, history is key

209
Q

What are CAP Sx?

A

fever cough w/ or w/o sputum, CXR with consolidation, urinary Ags, sputum Cx, blood Cx, elevaetd procalcitonin

210
Q

What bacteria are seen in neutropenia and CF?

A

P. aeruginosa

211
Q

What infections are seen in asplenia?

A

klebsiella, S. pneumonia, H. influenzae, nisseria spp

212
Q

What infections are seen in smokers/COPD?

A

moraxella, H. influenzae

213
Q

What infections are seen in EtOH?

A

klebsiella

214
Q

What infections are seen after the flu?

A

S. aureus

215
Q

What infection is seen in bird handlers?

A

C. psittaci

216
Q

What infections are seen in animal breeders?

A

coxiella burnetti- Q fever

217
Q

What infections are seen in hunters, lawn care and rabbit exposure?

A

francisella tularensis

218
Q

What are the bacteria and their sputum colors?

A 
currant jelly- klebsiella
rust- p. pnuemoniae
salmon- s. aureus
greeb tinge- p. aeruginosa
foul smelling- anaerobes
219
Q

What bacteria are encapusulated?

A

some killers have pretty nice capsules

220
Q

What is the definition of Hospital acquired PNA?

A

over 2 days in hospital

221
Q

What is the definition of health care assocaied PNA?

A

2 days in hospital in last 90 days
dialysis, nursing home, infusions in last 30 days
family member with multidrug resistanct organism

222
Q

What is the definition of ventilator associated PNA?

A

ET intubation with 2 of: F, leukocytosis, purulent sputum

new/progressive opacity on CXR

223
Q

How do you treat nosocomial PNA?

A

CBC, CMP, 2 anitpsuedomonal + MRSA coverage

224
Q

What is the description of mycobacterium tuberculosis?

A

weakly G+, non-motile, aerobe

225
Q

What is primary TB?

A

typically becomes latent, new TB in naive patient, air transmission, hilar lymphadenopathy, calcifications

226
Q

What is primary progressive TB?

A

if no fibrosis and calcification from primary TB, caseous-gohn complex expands
TB bronchopneumonia- spreads to entire lung, patchy foci
miliary TB- spread over entire organ, seed appearance, hematogenous spread

227
Q

What is secondary TB?

A

reactivation TB, insidious, most common TB presentation, apical posterior segments on CXR, F/C, weight loss, hemoptysis possible, cough

228
Q

What tests should you run with TB possibility?

A

CXR, morning sputum, PPD-mantoux test

229
Q

What does a positive PPD test indicate?

A

currently or previously infected with TB, false positive from BCG vaccine

230
Q

Know the induration levels for positive PPD.

A

> 5 immunocomprosised, positive CXR and close contact with TB, <10 everything except healthy people, >15 healthy people

231
Q

What type of hypersensitivity reaction is PPD?

A

type IV- delayed T cells

232
Q

What tests screen and confrim TB?

A

Ziehl-Neelsen(Kinyon) stain confirms, SPECIFIC

Auramine-Rhodamine- screens, SENSITIVE

233
Q

What does NAAT-R testing screen for?

A

detects resistance to Rifampin and INH, positive test confirms multi drug resistance

234
Q

Where do you admit TB patients?

A

negative pressure ventilation room, RIPE therapy

235
Q

What is the next step after positive PPD and negative CXR?

A

IFN-gamma release assay, if positive begin IH for 9 months

236
Q

What pleural fluid component is positive in TB?

A

adenosine deaminase

237
Q

What spinal disease can occur in TB?

A

Pott’s syndome, TB spondylitis

238
Q

What are extra-pulmonary manifestations of TB?

A 
lymphadenitis-scrofula-most common
pleural effusions w/ ADA and IFN-Gamma
meningitis
Pott's syndrome
intestinal TB w/ milk ingestion- M. bovis
239
Q

What is see with M. kansasii?

A

from the enviroment not people, midwest and southwest US, long course, older smokers apical cavitation
50% mortality if untreated,

Respiratory Medicine (1 decks)

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