Pulmonolgy Flashcards
(179 cards)
1
Q
asthma
A
chronic pulmonary disorder characterized by episodic reversible airflow obstruction
2
Q
what causes airflow obstruction in asthma
A
smooth muscle contraction, vascular congestion, edema, thick sputum
brought on by airway inflammation
3
Q
evidence for airway inflammation as the primary underlying cause of asthma
A
increased inflammatory cells (eosinophils, basophils, etc) on bronchial washings and lung biopsy even when assymptomatc
4
Q
two main types of asthma
which is more prevalent
A
allergic and idosyncratic
allergic
5
Q
differentiate allergic asthma from idiosyncratic
A
allgeric asthma often has a personal of FHx of allergic disease and commonly present at an early age
idiosyncratic has no Hx, negative skin tests, normal serum IgE
6
Q
two long term complications of asthma
A
airway remodeling in response to chronic inflammation leading to gradual decline in pulmonary function
7
Q
treatment strategies for asthma
A
reduce inflammation
increase airway diameter
improve airway secretions
8
Q
asthma treatment principles
A
preventing inflammation is key
use Beta-2 agoninsts for acute episodes
prevent recurrence with anti-inflammatories and long actings Beta-2
9
Q
types of goals of two asthma intervention
A
acute: relieave acute bronchspasm
chronic: reduce frquency of acute episodes
10
Q
outpatient devices for inhalation treatment of asthma
A
metered dose inhalers
dry powder inhaler
11
Q
deliniate where particles of varying sizes can be used in aerosol therapy fo asthma
>10 microns
1-5 microns
<.5 microns
A
>10microns: mouth and oropharynx
1-5: smaller airways
<0.5: minimal deposition (in and out)
12
Q
ingeneral how much of an aersol asthma medication is inhaled vs swallowed
A
2-10%
13
Q
what is the goal of corticosteroid treatment for asthma
A
to reduce underlying inflammation related to chronic asthma
14
Q
typical methods of adminstration for corticosteroids
A
inhaled aerosol (most common)
oral or parenteral (emergency situation)
15
Q
what is needed to use the dry powder inhalers
A
a good inspiratory effort, because inspiration is what breaks up the powder
16
Q
three inhaled glucocorticoids
A
¨Flunisolide (Aerobid)
¨Budesonide (Plumicort)
¨Fluticasone (Flovent)
17
Q
typical dosage of inhaled glucocortocoids for asthma treatment
A
200-400 mcg/day
18
Q
adverse drug reactions related to corticosteroid treatment of asthma
A
pituitary-adrenal suppression >1600 micrograms/day
bone loss
hyperglycemia significant >1000mcg/day
19
Q
thrush prevention in corticosteroid treatment of asthma
treatment
A
use a spacer to catch larger particles that would deposit in the mouth
rinse mouth with water after dose
nystatin
20
Q
T/F most patients will benefit from some level of corticosteroid therapy for asthma
A
true
21
Q
two good glucocortcoid inhalers that have high compliance
A
¤Fluticasone (Flovent) or budesonide (Plumicort)
22
Q
why does long term corticosteroid therapy cause adrenal suppression
A
because the pituitary-adrenal axis takes time to adjust when corticosteroid therapy is disonctinued
23
Q
when are oral corticosteroids used in asthma treatment
dose?
goal?
taper?
A
in severe attacks
40-60 mg prednisone/day 5-10days or 1mg/kg/day
prevent hospitalization
not if the course lasts less than 14 days
24
Q
non-steroid anti-inflammatory choices
A
leukotriene inhibitors
cromolyn
anti-IgE monoclonal antibodies
25
what is the function of leukotriene inhibitors
decrease action to prevent bronchoconstriction
26
two leukotriene receptor agonists
5-lipooxygenase inhibitor
¤Zafirucast (Accolate)
¤Montelukast (Singulair)
¤Zileuton (Zyflo)
27
what is the function of 5-lipooxygenase
it converts arachadonic acid to leukotrienes
28
what leukotriene is 1000x more potent than histamine
LLTD4
29
uses of leukotriene inhibitors in asthma treatment
lowered glucorticoid dose
30
adverse effects of leukotriene inhibitos
liver toxicity (esp zilueton) that requires peroidic liver enzyme testing
31
what is the function of cromolyn
stabilizes mast cells to prevent antigen induced broncospasm but has no bronchdilating properties
32
when is cromolyn the first line treatment of asthma
mild to moderate cases
33
Anti-IgE Monoclonal Antibody treatment for asthma
why is it saved for difficult cases
¨Omalizumab (Xolair)
it is costly
34
methods for reducing bronchospasm assocaited with asthma
relax bronchial smooth muscle by stimulating Beta2 sympathetic receptors
block parasympathetic muscarinic receptors
35
effect of beta-2 agonists
adverse drug reactions
bronchdilation
hyperglycema, tachycardia, poss HTN
36
examples of short acting beta 2 agonists
¨Albuterol (Proventil, Ventolin)
¨Metaproterenol (Alupent)
¨Terbutaline (Brethine, Bricanyl)
37
which method of treating bronchospams is associated with asthma is more effective
beta2 agonists
38
beta-1 agonist effects from Beta-2 crossover
HTN, tachycardia
39
short acting beta2 onset
duration
benefits
1-5 minutes
2-6 hours
bronchodilation with minimal anti-inflammatory effects
40
what is a patient controlled adverse effect of short acting Beta2 treatment of asthma
patient mange deteriorating asthma due to progressive inflammation with more frequent doeses
41
long acting beta2s
¨Salmeterol (Servent)
¨
¨Formoterol (Foradil)
42
duration and utility of long acting beta2's
duration: 12 hours
utility: preventing recurrent acute attacks
43
cautionary statements of long acting beta2's
not effective for acute attacks
15% of patients will not respond as predicted
increased mortality if used as the sole treatment
44
examples of long acting Beta2's with glucocortcoids
¨Fluticasone + salmeterol (Advair)
¨Mometasone + formoterol (Dulera)
¨Budesonide + formoterol (Symbicort)
45
two examples of muscarinic receptor blockers used in asthma treatment
action
ipratropium, tiotrpoium
helps relieve bronchospasm, reduces airway secretion
46
what is the action of theophylline
inhibits phosphodiesterase to decrease muscarinic receptor function
some anti-inflammatory effect
47
how are theophyllines used in treatment of ashtma in kids
adults
kids: in place of inhaled glucocortcoids
adults: time release for nocturnal asthma
48
strategy to block secretions in asthmatic patients
¨Decrease bronchial secretions with anticholinergic/ anti-muscarinic agents
49
derivatives of atropine used as anticholinergic/muscarinic drugs in management of secretions in asthma
side effects
¨Ipratropium (Atrovent), ¨Tioptropium (Spiriva)
urinary retention, constipation, glaucoma
50
¨Ipratropium (Atrovent) and Tioptropium (Spiriva) are synergistic with what other asthma treatments
beta 2 inhalers (ipratropium + albuterol)
51
types of emergency asthma therapy
1st line: beta2 inhlaers
subQ epi is useful
corticosteroid IV or oral
52
cautionary statements of using beta2 agonists in asthma treatment
frequen use may reduce effectiveness due to down regulation
bronchospasm may worse in some patients with long acting beta2
53
treatments safe for asthma and pregnancy
¤Beta 2 agonists
¤Glucocorticoids
¤Cromolyn
¤Ipratropium, tiotropium
54
typical causes of hay fever (allergic rhinitis)
¤Pollens, animal dander, dust, molds, etc.
¤Hyperemia, enhanced secretions
¤IgE involved in inflammatory cascade
¤Histamine & other mediators
55
rhinitis treatment strategies
avoid allegerns
desensitize the immune system
prevent mast cell degranulation
block histamine
reduce nasopharyngeal hyperemia
block/reduce inflammtion
56
drugs used to prevent IgE activation in the treatment of allerigc rhinitis
cromolyn nose spray before allergen exposure
omalizumab as an anti-IgE monoclonal antibody
57
1st generation antihistamines
drawbacks
Chlortrimeton, Benadryl
effective but cause drowsiness
58
2nd generation antihisamines
are 1sts or 2nd gen better
Loratadine (Claritin), cetirizine (Zirtek), Fexofenadine (Allegra)
2nd gens
59
why do 1st generation anti-histamines cause drowsiness
they can cross the blood brain barrier
60
what is the action of alpha adrenergic agonists in treatment of allergic rhinitis
vasoconstriction to reduce hyperemia
61
long and short acting alpha agonists used in the treatment of allergic rhinitis
¨Phenylephrine (Neosynephrine) - Short acting drops/spray
¨Oxymetazoline (Afrin) - Longer action (12 hours)
62
reactive hyperemia
after 2 or three days of alpha adrenergic use your nose will swell up due to compensatory mechcanisms activated in response to ischemia
63
what are nasal glucoortcoids used for in treating allergic rhinitis
how often are they dosed
how long will it take to get effective
what is their most effecitve use
block or reduce inflammation
1-2x daily
1-2 wks
most effective for seasonal allergic rhinitis
64
three types of nasal corticosteroids
¨Beclomethasone (Beconase, Vancenase)
¨Fluticasone (Flonase)
¨Flunisolide (Nasalide)
65
useful combination in the treatment of allergic rhinitis
¨Inhaled glucocorticoids as main preventative
¨Cromolyn/nedocromil added if needed to keep steroid dose low
¨Inhaled antihistamine
66
types of inhaled antihistamines
benefit of use
¨Azelastine nasal spray (Astelin)
¨With fluticasone: Dymista
¨Risks of sedation seem very low
67
treatment of allergic conjunctivitis
systemic antihistamines work
topical is better
68
pathophysiological hallmarts of COPD
¤Airflow obstruction
¤Alveolar dilation and destruction
¤Airway infection (chronic and acute)
69
possible etiology of COPD
¤Cigarette smoking (99%)
¤Other toxins (such as coal dust, silica)
¤Genetic (Cystic fibrosis, A-1antiproteinase (anti-trypsinase) deficiency)
70
differentiate between chronic bronchitis and emphysema
chronic bronchitis is caused by airway obstruction that destroys alveoli
emphysema is cause by alveolary loss that least to air way obstruction
71
two main symptoms of chronic bronchitis
¤Chronic productive cough
¤Mucopurulent sputum
72
two main symptoms of emphysema
¤Shortness of breath (dyspnea) with exertion
¤Shortness of breath at rest
73
how is COPD related to asthma
smoke damaged epithelium, leading to frequent infection, chronic inflammtion, and asthma like reactive airways
74
COPD treatment strategies are preventing new damange and improve airways
how to prevent new damage
reducing exposure to irritants
ABx to control infetion
75
COPD treatment strategies are preventing new damange and improve airways
how to improve airways
¤Bronchodilators
¤Glucocorticoids
¤Other anti-inflammatory drugs (leukotriene inhibitors)
¤Improve or reduce airway mucus (Respiratory therapy, Drugs such as ipratropium (Atrovent))
76
T/F nearly all asthma treatments can be used with COPD and are very effective
false, asthma treatment for COPD is less effective depending on how extensive the damage is
77
what is the value of ABx use in COPD treatment
they are valuble to prevent acute flare of bronchitis but have dubious value in long term treatment
78
two benefits of supplmental oxygen treatment of COPD
improves activty tolerance and improves survivability
79
where is capilary blood flow in the lungs greatest
in the bases due to gravity
80
T/F pulmonary arteries have a very low resistance to blood flow
true
81
glucorticoids deal with what
mineralocortoids deal with what
inflammation
fluid retention
82
where must gas diffusion happen for O2 and CO2 exchange
alveolar gas
alveolar and capillary walls
plasma
membrane and cytoplasm of RBC
83
oxygen in blood is found in what two places
either bound to Hgb or dissolved in plasma
84
%O2 is determined by whay
arterial Po2
Hbg level
85
tissue oxygenation depens on what
oxygen content in the arterial blood
cardiac output
86
pulmonary infection types
Pneumonias (Community acquired, (CAP)Hospital acquired, (HAP)Fungal)
Tuberculosis
Acute Bronchitis
Influenza
Pertussis
Acute Bronchiolitis
Acute epiglottitis
Croup
87
three pulmonary diseases commonly found in kids
Acute Bronchiolitis
Acute epiglottitis
Croup
88
how is diffusion measured
DLCO (diffusion capacity of the lung to carbon monoxide)
89
three types of pulmonary neoplasms
solitary nodules
mesothelioma
lung cancer
90
what is the common cause of mesothelioma
asbestosis
91
two types of lung cancer
small cell (oat cell)
non-small cell
92
three types of non-small cell lung cancer
squamous cells carcinoma
adenocarcinoma
large cell carcinoma
93
four types of obstructive pulmonary disease
bronchiectatsis (tumors, foreign bodies)
* Asthma
* Chronic obstructive pulmonary disease (COPD)
* Cystic Fibrosis
94
three pleural disorders
* Pleuritis (“pleurisy”)
* Pleural effusion
* Pneumothorax
95
three disorders of pulmonary circulation
* Pulmonary thromboembolism
* Pulmonary hypertension
* Pulmonary vasculitis
96
three types of restricive lung disease
* Idiopathic fibrosing interstitial pneumonia
* Pneumoconioses ()Asbestosis, Coal dust, Silicosis)
* Sarcoidosis
97
three miscellaneous pulmonary disease
* Acute Respiratory Distress Syndrome (ARDS)
* Foreign Body Aspiration
* Hyaline Membrane Disease (pre-term infants)
98
two cardinal symptoms of pulmonary disase that can be identified in a history
Dyspnea
Cough
99
notable features associated with dyspnea that can be picked up on history
cough
Acute or progressive, Triggers
Duration, Productive of sputum, Acute or chronic
100
PE findings correlated with pulmonary disease
low O2 sat
tachypnea, bradypnea
adventitious breath sounds
cyanosis or clubbing
suspected or visible foreign bodies
101
pneumoconioses are pulmonary disease acquired from what
work place exposure to things like silica and coal dust
102
adventitious breath sounds associated with pulmonary disease
stridor
wheeze from airway obstruction
Rhonchi (obstruction of medium bronchi)
crackles and rales
no breath sounds
103
rhonchi are associated with what pulmonary disease
bronchitis, COPD, bronchiectasis
104
cor pulmonale
right sided heart failure which may or may not be precipitated by left sided heart failure
105
crackles and rales are signs of what
alevolar disease
pneumonia
pulmonary edema
106
egophony can be used to differentiate between what
cracklse of pneumonia and interstitial pulmonary ffibrosis
107
T/F stridor is often present in the lower airway
false, stridor is usually found in the neck and upper respiratory tract
108
conditions that may result in absent or decreased breath sounds
emphysema (quiet or diffuse)
pneumothorax
pleural effusion
109
increase tactile fremitus is indicative of what
lung consolidation
110
decreased tactile fremitus and/or dullness on percussion is indicative of what
pleural effusion
111
hyperresonance on percussion is indicative of what
pneumothorax
112
signs of pulmonary disease in other systems
* Pedal edema
* JVD
* Joint examination
* Skin examination
* Clubbing
113
what is the goal of PFTs
objective assessment of a pesron with known or suspected pulmonary disorder
determine if teh lung disease is sufficient to explain the patients symptoms
is the functional pattern of the disease obstrictive or restrictive
114
indications for PFTs
* Pre-operative evaluation of pulmonary risk
* Assess the severity of pulmonary disease
* Evaluation of dyspnea or other pulmonary complaints
* Evaluate abnormal findings on other studies
* To measure and evaluate response to treatment
* To quantitate the improvement or deterioration in a patient’s condition
* To measure the effects of environmental exposures
* To evaluate disability
115
three main categories of information in PFTs
the size of the lungs (lung volumes)
measurement of maximum flow rates in the air way
how readily gas exchanges between alveoli and capillaries (diffusion)
116
spirometry
a meassure of pulmonary function based on assessing air flow obstruction
117
what is the criteria for diagnosis of an obstuctive condition based on spirometry
Decreased forced expiratory volume in 1 second (FEV1)/ forced vital capacity (FVC) defined as \<70% of predicted is diagnostic of obstruction
118
what should be done when spirometry is normal or with symmetric decreases in FEV 1 and FVC get
lung volumes, total lung volume less than 80% indicates restictive
DLCO, restruction plus decreased DLCO indicates parenchymal disease
119
what spirometry values are indicative of obstructive diseas
restrictive
decrease in FEV1, increase in residual volume
decrease in TLC, FEV1/FVC remains normal
120
lab tests of pulmonary disease
* Arterial Blood Gas
* Complete Blood Count
* Chemistry profile
* Sputum gram stain, culture, sensitivity
* Pleural Fluid Analysis
* Cytologies
121
indications for arterial blood gas measurement
* Assessing and managing a patient’s respiratory (ventilation) and metabolic (renal) acid-base and electrolyte homeostasis
* Assess adequacy of oxygen
122
normal ABG values
pH
PaO2
PaCO2
HCO3
pH 7.35 - 7.45
PaO2 70-100mmHg
PaCO2 35-45mmHg
HCO3 22-30 nm or 22-26 mEq/L
123
increased pH indicates what
decreased pH indicates what
respiratory and metabolic **alkalosis**
respiratory and metabolic **acidosis**
124
decreased PaO2 indicates what
oxgenation issues (pneumonia)
125
HCO3 changes are indicative of what
as HCO3 increases what happens to pH
acid-base equilibrium
HCO3 increases lead to pH increases
126
distrubances in acid base balance
* Metabolic acidosis
* Respiratory acidosis
* Metabolic alkalosis
* Respiratory alkalosis
127
metabolic causes of acidosis
Metabolic
* Renal failure
* Ketoacidosis
* Ingestion of acidic compounds (i.e. aspirin overdose)
128
respiratory causes of acidosis
Respiratory failure (high PaCO2, causing acidosis)
COPD (Increased PaCO2 and HCO3-) (Ions increased to compensate for chronic hypoventilation)
129
metabolic causes of alkalosis
Metabolic
* Prolong vomiting
* Ingestion of large amounts of bicarbonate
130
respiratory causes of alkalosis
Respiratory
* Hyperventilation (low PaCO2)
* Hypoxemic states (cystic fibrosis, PE, acute severe pulmonary disease)
* Breathing increased and CO2 is blown off
131
how does pulmonary compensation take place in falling pH (acidosis)
ventilation rate increases
causes a fall in PaCo2 that increases HCO3
132
pulmonary compenstion in response to rising pH levesl
ventilation falls to increase PaCO2, increase pH
133
what is the goal of pleural fluid analysis
helps determine between transudative or exudative effusion based appearance, protein, glucose content
134
two causes of transudative effusions
heart failure, cirrhosis with ascities
135
two causes of exudative effusions
infection and cancer
136
diagnostic imaging for pulmonary conditison
* Chest radiography
* Chest computerized tomography (CT)
* Magnetic resonant imaging (MRI)
* Ventilation and Perfusion Scan
* PET Scan
137
structures and patterns that can be assessed on CXR
Structures
* Mediastinum (lymph nodes, vessels, tumor)
* Pleura (effusions, air space)
* Lung parenchyma (infiltrates, lesions)
Patterns
* Interstitial (lacy, reticular, reticulonodular)
* Airspace (lobar, segmental, air bronchograms)
138
what is the key advantage of chest CT over xray
excellent resolution
Cross-sectional images allow distinction between densities super-imposed on plain films
Can characterize tissue density= accurate size of lesions
139
chest CT allows for better delination of what
uParenchymal processes
uPleural disease
uHilar and mediastinal masses
uMasses or nodules
uLarge airways
uAny unclear lesion or problem on routine chest radiograph
140
why is MRI less used than chest CT
breathing causes motion artifact, less detail between parenchymal structure
141
what is chest MRI used for
discriminating between enlarged mediastinal vessels and lymphadenopathy
142
what is a Ventilation perfusion scan used for
Used in the detection of PE and evaluation of lung function in patients considering lung resection
143
what is thoracentesis used for
Diagnostic sampling of pleural fluid by blind needle aspiration or US guided
Allows for collection and evaluation of fluid- micro and cytology
144
what is bronchoscopy used for
Direct visualization of the tracheobronchial tree
Done with flexible fiberoptic instrument
Done to retrieve foreign bodies and obtain endobronchial pathology for cytology, stains, cultures, etc.
145
different types of mycobacterium that people can be exposed to and hwere they cause issues
tubercolsis (lungs)
Bovis (gut)
leprae (skin leprosy)
abscessus and fortinuitum (skin)
avium (bone marrow)
146
T/F late stages of tuberclosis can affect all organs in the body
true
147
what percentange of the world's population has active or inactive TB
20-43%
148
what US citizens are most at risk based on ethnicity
asian (25x)
hispanic (7.3x)
non hispanic black (6.6x)
149
what is the primary method of transmission for TB
breathing, except for non-pulmonary TB
150
what is required for transmission of TB
how effiecient is it
fairly close, prolonged contact
23%
151
how many peole will an untreated person with active TB infect per yar
15-20
152
what is the key pathphyisologic finding in TB
caseating granuloma with necrotic center caused by the body's attempt to wall of the infection
153
what determines the chance of a person exposed to TB will be come infected
the innate and active immune responses
154
conditions that can alter immune response and make people susceptible to TB
Calcified / fibrotic lung lesions
Silicosis
Chronic RF
DM
IV Drug use
Immunosuppresive Rx HIV infection & Others
155
risk factors for TB exposure and infections
HIV positive? 7.7%
Are you homeless? 5.6%
Do you drink excessive alcohol? 12.1%
Have you been in prison? 4.2%
156
symptoms of latent TB
are people with latent TB infectious
usually none with a positive skin test
not infectious
157
symptoms of active TB
high fever with night sweats
weight loss
cough/hemoptysis
fatigue
malaise
158
how is the diagnosis of TB made
HP
chest xray
PPD/TB gold/T-SPOT
159
how can you confirm your diagnosis of TB without skin or blood tests if you have high suspicion
sputum evaluation
blood evaluation
160
two types of sputum evaluation for Dx of TB
drawbacks of each
acid fast smear (only a screen, any mycobacterium will be +)
culture (takes 2-6 weeks)
161
two types of blood evaluation for Dx of TB
if these tests are positive, can you assume TB infection
Nucleic Acid Amplification test detection (NAAT-TB)
Nucleic Acid Amplification test resistance marker (NAAT-R)
yes, assume they have TB and start treatment
162
should bronchoscopy be used in Dx of TB
for the most part, no
163
are CT and MRI used to Dx TB
Ct may be useful for distinguishing undertermined masses
MRI not typical but can be used
164
how does the PPD test work
it injects a protein derivative from the TB cell wall into the skin and looks for an inflammatory reaction
165
a PPD test produces a lesion \>=5mm
when might that indicate TB infection
HIV, exposure, immunosuppresion, fibrotic changes from old TB
166
a PPD test produces a lesion \>=10mm
when might that indicate TB infection
people coming from overseas
IVDA
residents or employees of prison, hospitals, homeless shelters
167
a PPD test produces a lesion \>=15mm
when might that indicate TB infection
anyone
168
what might cause false negatives on a PPD test
patients with disseminated TB
immunocompromised patients
reading the test too soon
169
what would produce a false positve
people who received the BCG vaccine
170
BCG (Baccile Calmette-Guerin)
a vaccine derived from a weak strain of TB commonly used in the UK with variable efficaacy
171
what is the benefit of Interferon Gamma Release Assays (IGRAs such as TB fold or Tspot)
24-48 hours to interpret
less susceptible to false recordings
172
what patients are most at risk for widespread miliary TB
Infants
The elderly
Immuno-compromised adults
173
booster phenomenon
repeat PPD tests can be false negatve due to decreased reactivity of the immune system, may need a second exposure in close proximity to trigger a true result
174
four different approaches for latent TB treatment
INH (+B6) daily or twice weekly for 9 months
Or INH (+B6) daily or twice weekly for 6 months
Or INH and Rifapentine – once weekly for 3 months
Or Rifampin – daily for 4 months
175
treatment regimines for active TB
Daily for 8 weeks (EMB may be d/c is drug susceptible TB)
INH / Rifampin (RIF) / Ethambutol (EMB)/ Pyrazinamide (PZA)
Daily or two-times weekly for 18 more weeks
INH and RIF
176
what determines what treatment regimine to use for active TB
population demographic
risk factors
how long it take to convert to latent TB
177
after treatment for latent TB, when should CXR be done
only if the patient develops signs or symptoms suggestive of TB
178
factors that can cause the conversion of latent TB to active
HIV infection
iatrogenic immune depression form chemo, steroids, DMARDs
starvation
179
