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Pulmonology > Final > Flashcards

Final Flashcards

1
Q

cystic fibrosis

A
  • autosomal recessive disorder

- most common fatal of this type among Caucasians

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2
Q

cystic fibrosis pathophysiology

A
  • mutation of cystic fibrosis transmembrane receptor (CFTR)
  • prevents chloride transport in exocrine tissues
  • results in thick mucus and increased salt content in sweat
  • can effect pancreas, GI tract, liver, reproductive
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3
Q

cystic fibrosis diagnosis

A
  • elevated sweat chloride > 60 mmol/L

- two tests of this level = confirmation

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4
Q

cystic fibrosis treatment goals

A
  • clear secretions
  • reverse bronchoconstriction
  • treat respiratory infection
  • replace pancreatic enzymes
  • nutritional support
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5
Q

community acquired pneumonia

A
  • streptococcus pneumonia most common cause
  • right middle lobe most common site
  • x-ray gold standard for diagnosis
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6
Q

atypical pneumonia

A
  • mycoplasma pneumoniae most common (walking pneumonia) with CXR bilateral patchy infiltrate
  • pneumocystis jiroveci in HIV positive
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7
Q

tools to admit pneumonia patient

A
  • PORT score to assess outpatient CAP Tx

- CURB score for admission decision

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8
Q

hospital acquired pneumonia

A

develops 48 hours after admission

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9
Q

ventilator associated pneumonia

A

develops 48 hours after intubation

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10
Q

viral pneumonia

A
  • flu like
  • patchy infiltrates on CXR
  • most common in kids
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11
Q

strep pneumonia

A
  • red-brown rusty sputum
  • lobar
  • gram + diplococci
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12
Q

H influenzae pneumonia

A
  • COPD patients

- small gram - rods

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13
Q

klebsiella pneumonia

A
  • alcoholics, aspiration
  • currant jelly sputum
  • encapsulated gram - rod
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14
Q

staph pneumonia

A
  • pink salmon colored sputum
  • often nosocomial
  • gram + cocci in cluster
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15
Q

mycoplasma pneumonia

A
  • young adults

- CXR looks worse than patient

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16
Q

pseudomonas pneumonia

A

ICU
immunocompromised
CF patients

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17
Q

legionella pneumonia

A
  • air conditioners

- GI and CNS symptoms that start later

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18
Q

pneumocystitis jiroveci

A
  • HIV patients
  • white out CXR
  • Tx with bactrim
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19
Q

TB pneumonia

A

fever, night sweats, weight loss, bloody sputum

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20
Q

occupational disease

A

need to identify source so that it can be avoided to prevent worsening disease from more exposure

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21
Q

pertussis

A
  • respiratory tract infection caused by bordetella pertussis
  • consider for cough lasting more than 3 weeks
  • 50% in <2 years old
  • no lasting immunity from vaccine or active infection
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22
Q

pertussis catarrhal stage

A
  • 7-10 days
  • insidious onset
  • mild fever
  • hacking cough at night
  • coryza
  • conjunctivitis
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23
Q

pertussis paroxysmal stage

A

7-28 days

  • spasmodic rapid coughing
  • followed by inspiratory stridor
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24
Q

pertussis convalescent stage

A
  • several months

- decreasing severity and frequency of symptoms

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25
Q

pertussis diagnosis

A

nasopharyngeal culture swab = gold standard

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26
Q

pertussis treatment

A

-macrolides for all suspected cases
(end in -thromycin)
-prophylaxis for those exposed within 3 weeks

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27
Q

RSV

A
  • form of paramyxovirus
  • leading cause of hospitalization of children
  • highly contagious
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28
Q

RSV presentation

A 
fever
rapid breathing
cough
possible accessory muscle
runny nose
nasal flaring
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29
Q

RSV treatment

A
  • O2
  • hydration
  • treat the fever
  • ribavirin in extreme cases
  • clear nasal passages
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30
Q

bronchiolitis

A
  • generic term for inflammatory processes that affect the bronchioles
  • usually caused by RSV
  • most common in under 2
  • clinical diagnosis
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31
Q

bronchiolitis treatment

A
  • majority can be discharged

- deep nasal suctioning

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32
Q

croup causes

A
  • parainfluenza most common
  • also RSV and flu
  • bacterial pneumonia may be secondary

children 3-36 months

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33
Q

croup clinical findings

A
  • gradual onset of symptoms
  • barking cough
  • hoarse voice
  • inspiratory stridor
  • mild fever
  • often at night
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34
Q

croup severity

A

westley croup score

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35
Q

croup treatment

A
  • mild: humidified air, antipyretics, fluid
  • moderate: single dose dexamethasone, nebulized Epi
  • severe: repeated nebulized epi with admission if no improvement
  • impending respiratory failure: O2, ICU, scheduled epi, IV steroids
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36
Q

epiglottitis

A
  • inflammation of epiglottis and adjacent supraglottic structures
  • in children primarily caused by H. influenza type B, strep, and staph
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37
Q

epiglottitis clinical findings

A
  • febrile toxic appearing children with rapid onset
  • dysphagia
  • drooling
  • tripoding
  • hot potato voice
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38
Q

epiglottitis treatment

A
  • defer pharyngeal exam
  • stabilize airway
  • draw labs before ABX
  • empiric ABX cefotaxime or ceftriaxone plus clindamycin or vancomycin
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39
Q

mild westley score

A

0-2

  • at home care
  • humidified air
  • antipyretics
  • fluid
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40
Q

moderate westley score

A

3-7

  • single dose PO steroid
  • racemic epi nebulized
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41
Q

severe westley score

A

8-11

  • repeated doses racemic epi
  • admission unless marked improvement
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42
Q

impending respiratory failure westley score

A

12+

  • supplemental O2
  • scheduled racemic epi
  • IM/IV steroid
  • ICU admission
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43
Q

Virchow’s Triad

A
  • hypercoagulability
  • vessel injury
  • venous stasis
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44
Q

sensitive findings for PE

A
  • dyspnea
  • pain on inspiration
  • tachypnea
  • tachycardia
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45
Q

types of emboli with PE

A
  • most common is thrombus

- PE develop with 50-60% patients with proximal DVT

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46
Q

Wells score for DVT

A

stratifies risk for DVT
0 = low
1-2 = moderate probability
3 or more = high probability

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47
Q

Wells score for PE

A

stratifies risk of PE
0-1.5 = low probability
2-6 = moderate probability
> 6 = high probability

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48
Q

testing for PE/DVT

A

pulmonary angiography = gold standard

  • V/Q scan no radiation = good for pregnant
  • CT scan
  • CXR
  • EKG
  • ultrasound
  • ABG/VBG
  • D dimer
  • CBC
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49
Q

D-dimer

A
  • degradation product of cross linked fibrin that are elevated in presence of a thrombus
  • have a high negative predictive value
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50
Q

PERC criteria

A
  • if all are negative can rule out PE for the patient
  • can only be used for low risk Wells score patients

positive PERC = perform D dimer

  • negative: rule out PE
  • positive: CT scan
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51
Q

doppler ultrasound

A
  • test of choice for DVT detection*

- indicated for patients with high pretest probability of DVT and positive D dimer

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52
Q

ABG and PE

A
  • acute respiratory alkalosis from hyperventilation

- profound hypoxia

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53
Q

CXR and PE

A
  • rule out other lung diseases
  • Westermark’s sign
  • Hampton’s hump
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54
Q

DVT prophylaxis

A
  • low risk: mechanical or Rx

- high risk: mechanical and Rx

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55
Q

PE treatment with anticoagulation

A

-not definitive therapy but form of secondary prevention that allows endogenous fibrinolytics to clear the existing clot

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56
Q

PE treatment duration with anticoagulation

A
  • first episode w/ reversible cause: 3 months
  • first episode w/ idiopathic cause: at least 3 month
  • all others long term
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57
Q

nodule versus mass size

A
  • nodule < 3cm

- mass > 3cm

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58
Q

benign nodule characteristics

A
  • size: <1-2 cm
  • shape: spherical
  • margins: well defined
59
Q

malignant nodule characteristics

A
  • size: > 1-2 cm
  • shape: lobulated
  • margins: spiculated
60
Q

Intermittent asthma

A
  • symptoms: less than or equal to 2 days/week
  • night awakenings: less than or equal to 2/month
  • use of SABA: less than or equal to 2 days/week
  • ADL interference: none
  • FEV1: >80% predicted
  • FEV1/FVC: normal
  • treatment: step 1
61
Q

mild persistent asthma

A
  • symptoms: >2 days/week but not daily
  • night awakenings: 3-4/month
  • SABA use: >2/week but not daily and no more than 1/day
  • ADL interference: minor
  • FEV1: >80% predicted
  • FEV1/FVC: normal
  • treatment: step 2
62
Q

moderate persistent asthma

A
  • symptoms: daily
  • night awakenings: >1/week, but not nightly
  • SABA use: daily
  • ADL interference: some limitation
  • FEV1: >60% but <80% predicted
  • FEV1/FVC: reduced 5%
  • treatment: step 3
63
Q

severe persistent asthma

A
  • symptoms: throughout the day
  • night awakenings: often 7/week
  • SABA use: several times per day
  • ADL interference: extreme limitation
  • FEV1: <60% predicted
  • FEV1/FVC: reduced >5%
  • treatment: step 4 or 5
64
Q

obstructive PFT

A
  • FEV1: reduced
  • TLC: normal or increased
  • FEV1/FVC: reduced
65
Q

restrictive PFT

A

FEV1: normal or reduced
TLC: reduced
FEV1/FVC: normal or increased

66
Q

PFT reversible obstruction definition

A

increase of 12% or more and 200mL increase in FEV1 or FVC

67
Q

5 components of asthma management

A
  1. assess control and severity
  2. severe versus uncontrolled
  3. appropriate pharmacology
  4. address modifiable risk factors and environmental concerns
  5. self management and education
68
Q

LABA

A
  • indicated for bronchodilation maintenance

- helps with nocturnal symptoms

69
Q

short acting anticholinergic

A
  • reduces vagal tone of the airway

- useful for severe exacerbation when combined with SABA

70
Q

long acting muscarinic agent

A
  • reduces vagal tone of the airway
  • works well in COPD
  • slow onset of action 60-90 minutes
71
Q

inhaled corticosteroids

A
  • suppress acute and chronic airway inflammation
  • inhibit inflammatory cell migration
  • block late phase reaction
  • first line maintenance therapy for persistent asthma
72
Q

leukotriene receptor antagonist

A
  • decreases airway smooth muscle activity
  • decreases mucus production
  • used in long term control but with variable effect
  • alternative to ICS in mild persistent
73
Q

mast cell stabilizers

A
  • prevent bronchoconstriction
  • for prevention and maintenance
  • trial of 6-8 weeks needed before effectiveness known
74
Q

methylxanthines

A
  • causes bronchodilation
  • suppresses response of airway to stimuli
  • 2nd/3rd line treatment for moderate to severe
  • can cause toxicity and drug interactions
75
Q

step 1 treatment

A

SABA

76
Q

step 2 treatment

A
  • low dose ICS

- SABA

77
Q

step 3 treatment

A

-low dose ICS and LABA combo

78
Q

step 4 treatment

A

-medium dose ICS and LABA

79
Q

step 5 treatment

A

medium to high dose ICS/LABA and LAMA

80
Q

emphysema

A
  • permanent enlargement of airspace due to alveolar destruction
  • increased CO2 retention
  • pursed lip breathing
  • thin with barrel chest
  • accessory muscle use
81
Q

chronic bronchitis

A
  • extensive bronchial mucus
  • daily productive cough for 3 consecutive months
  • cyanotic/dusky
  • hypoxic
  • digital clubbing
  • exertional dyspnea
  • accessory muscle use
82
Q

COPD causes

A
  • smoking #1
  • occupational dust/chemicals
  • air pollution
  • genetic factors
  • Hx allergies and recurrent bronchitis
  • alpha1 antitrypsin deficiency
83
Q

COPD GOLD 1

A
  • mild

- FEV1 greater than or equal to 80% predicted

84
Q

COPD GOLD 2

A

-moderate

FEV1: 50-80% predicted

85
Q

COPD GOLD 3

A

-severe

FEV1 30-50% predicted

86
Q

COPD GOLD 4

A

-very severe

FEV1: <30% predicted

87
Q

COPD group A treatment

A
  • 0-1 moderate exacerbation but no admission
  • mMRC 0-1
  • CAT <10

bronchodilator

88
Q

COPD group B treatment

A
  • 0-1 moderate exacerbation but no admission
  • mMRC 2 or more
  • CAT 10 or more

LABA or LAMA

89
Q

COPD group C treatment

A
  • 2 or more moderate exacerbation or 1 or more exacerbation with admission
  • mMRC 0-1
  • CAT <10

LAMA

90
Q

COPD group D treatment

A
  • 2 or more moderate exacerbation or 1 or more exacerbation with admission
  • mMRC 2 or more
  • CAT 10 or more

LAMA
LAMA + LABA (highly symptomatic CAT>20)
ICS + LABA (eos >300)

91
Q

COPD treatment steroids

A
  • inhaled reduce exacerbation frequency in combination with LABA
  • not responsive to oral steroids but a subset of steroid responsive may warrant a trial
92
Q

COPD treatment when hospitalized

A
  • oxygen
  • broad spectrum antibiotics (levofloxacin, ceftriaxone, piperacillin tazobactam)
  • usually nebulizers/IV steroids
93
Q

pH normal

A

7.35 - 7.45

94
Q

PaCO2 normal

A

35 - 45

95
Q

HCO3 normal

A

22 - 26

96
Q

PaO2 normal

A

> 80

97
Q

SaO2 normal

A

> 95

98
Q

respiratory acidosis

A

decreased pH

increased pCO2

99
Q

respiratory acidosis with compensation

A

decreased pH

increased HCO3

100
Q

respiratory alkalosis

A

increased pH

decreased pCO2

101
Q

respiratory alkalosis with compensation

A

increased pH

decreased HCO3

102
Q

alpha 1 antitrypsin deficiency

A

genetic cause of COPD

103
Q

influenza diagnosis

A
  • rapid antigen test

- often clinical diagnosis

104
Q

influenza Rx treatment

A
  • neuraminidase inhibitors
  • give within 48 hours of symptom onset
  • for high risk patients and prophylactically for high risk patients that were close contact to diagnosed
105
Q

wegner’s granulomatosis

“granulomatosis with polyangiitis”

A

-idiopathic

clinical triad

  • glomerulonephritis
  • necrotizing & inflammatory vasculitis of upper respiratory tract
  • necrotizing & inflammatory vasculitis of lower respiratory tract
106
Q

wegner’s granulomatosis labs

“granulomatosis with polyangiitis”

A
  • normochromic normocytic anemia

- elevated C-ANCA in 90% of patients

107
Q

wegner’s granulomatosis treatment

“granulomatosis with polyangiitis”

A
  • corticosteroids

- immunosuppressant

108
Q

churg-strauss syndrome

“eosinophilic granulomatosis with polyangiitis”

A

-idiopathic

three phases

  • prodromal: allergic rhinitis, asthma
  • eosinophilic: eosinophilic infiltration of lungs and GI
  • vasculitic: life threatening systemic vasculitis
109
Q

churg-strauss labs

“eosinophilic granulomatosis with polyangiitis”

A
  • elevated IgE

- elevated P-ANCA

110
Q

churg-strauss treatment

“eosinophilic granulomatosis with polyangiitis”

A
  • corticosteroids

- immunosuppressant

111
Q

high risk individuals for TB

A
  • close contacts
  • foreign born where TB common
  • visits TB prevalent country
  • high risk congregate settings
  • health care workers
  • medically underserved
  • low income who abuse drugs or alcohol
112
Q

multidrug resistant TB

A

-resistant to isoniazid and rifampin

113
Q

extensively drug resistant TB

A

-resistant to isoniazid and rifampin
plus
-fluoroquinolones and at least 1 of the 3 injectable 2nd line drugs

114
Q

≥ 5mm induration TST positive patients

A
  • HIV infected
  • recent infectious TB contact
  • fibrotic changes on CXR consistent with prior TB
  • immunosuppressed
115
Q

≥ 10mm induration TST positive patients

A
  • recent arrival from TB prevalent country
  • injection drug user
  • resident/employee high-risk congregate area
  • mycobacteriology lab personnel
  • have condition that increase risk for progressing to TB
  • children under 5
  • children and youth exposed to high risk adults
116
Q

≥ 15 mm induration TST positive patient

A

has no known risk factors

117
Q

TB diagnosis

A

culture is gold standard for confirming TB diagnosis

  • all specimens get cultured even if acid fast smear and NAA are negative
  • patient is negative with 2 consecutive negative cultures
118
Q

latent TB treatment

A
  • isoniazid for 9 months

- before treatment check LFT and screen for HIV

119
Q

isoniazid adverse reaction

A
  • peripheral neuropathy can be treated with vitamin B6

- fatal hepatitis (pregnant/postpartum = higher risk)

120
Q

TB treatment

A 
"RIPE"
Rifampin
Isoniazid
Pyrazinamide
Ethambutol

gets directly observed therapy

121
Q

pulmonary hypertension

A

pathologic elevation of pulmonary arterial pressure
mean > 20 mmHg
or
systolic > 30 mmHg

122
Q

pulmonary hypertension and HIV

A

treatment of pulmonary HTN can interfere with HIV treatment

-always get HIV test

123
Q

pulmonary hypertension scoring

A

NYHA classes I-IV

124
Q

group 1 pulmonary hypertension

A

primary pulmonary hypertension

125
Q

group 2 pulmonary hypertension

A

due to left heart disease

126
Q

group 3 pulmonary hypertension

A

due to lung disease or hypoxia

127
Q

group 4 pulmonary hypertension

A

due to chronic PE

128
Q

group 5 pulmonary hypertension

A

multifactorial

129
Q

right sided heart failure signs

A
  • JVD
  • pedal edema
  • possible systolic ejection murmur
  • loud or split S2
130
Q

transudate pleural effusion

A
  • increased hydrostatic pressure or low plasma oncotic pressure
  • low protein and LDH
  • CHF, cirrhosis, nephrotic syndrome, PE, hypoalbuminemia
131
Q

exudate pleural effusion

A
  • due to inflammation and increased capillary permeability
  • high protein and LDH
  • pneumonia, cancer, TB, viral infection, PE, autoimmune
132
Q

lights criteria

A
  • determine if fluid is exudative

- looks at serum protein and serum LDH

133
Q

lofgren’s syndrome

A

associated with sarcoidosis

  • erythema nordosum
  • bilateral hilar adenopathy
  • polyarthralgia and fever
134
Q

sarcoidosis labs

A
  • increased ACE

- restrictive PFT

135
Q

sarcoidosis imaging staging

A

stage 1: bilateral hilar adenopathy
stage 2: bilateral hilar adenopathy and infiltrates
stage 3: infiltrate only
stage 4: honeycomb

136
Q

spontaneous pneumonthorax

A
  • primary: no lung disease

- secondary: lung disease

137
Q

traumatic pneumothorax

A

simple: blunt trauma
tension: penetrating trauma

138
Q

iatrogenic pneumothorax

A

provider caused (central line placement)

139
Q

ARF criteria

A

dysfunction of oxygenation and ventilation
PO2 < 60
PCO2 > 50
Sa O2 < 88

140
Q

ARF presentation

A
  • dyspnea
  • headache
  • cyanosis
141
Q

ARF respiratory support

A

supplemental O2 to keep PO2 >60 or SaO2 >90

142
Q

assist control ventilation

A

-inspiratory attempt triggers mechanical breath

143
Q

synchronized intermittent mechanical ventilation

A

-patient can breath spontaneously between synchronized mechanical breath

144
Q

ARDS

A
  • acute onset hypoxemic respiratory distress after clinical insult
  • new bilateral pulmonary infiltrate
  • impaired oxygenation of arterial blood not caused by HF

Pulmonology (2 decks)

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