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resp 2 exam 1 > resp exam 1 > Flashcards

resp exam 1 Flashcards

1
Q

which are the 3 values you can’t directly measure and why

A

Residual volume, functional residual capacity and TLC (because residual volume cant be directly measured and these all include residual volume

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2
Q

which value is decreasd in a patient with obesity

A

ERV: the maximum volume of air that can be exhaled from the end expiratory tidal position

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3
Q

anything below ___ is a normal PFT value

A

LLN

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4
Q

FVC is

A

forced vital capacity: the total volume that can be forcefully expired from a maximum inspiratory effort

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5
Q

in obesity which value is decreased and which is increased

A

ERV and FRC are decreased and IC is increased

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6
Q

what does FEV1 reflect and what is a normal value

A

upper airway patency: should be 80% of FVC

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7
Q

what does it mean when a flow volume loop is flattened

A

vocal cord dysfunction

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8
Q

what does a low FVC mean and how do you confirm

A

possible restriction, confirm by looking at lung volumes

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9
Q

which value can be used to determine the presence of reversibility

A

FEV1: (asthma or COPD) a 10% or more increase post bronchodilator is considered significant

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10
Q

will COPD or asthma patients demonstrate full reversibility

A

patients with asthma demonstrate full reversibility which is not seen in patients with COPD

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11
Q

what test is the gold standard for TLC

A

plethysmography (measures residual volume, confirms presence of restriction)

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12
Q

total lung capacity = ___+___

A

residual volume + FVC

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13
Q

which test is reserved for patients that cannot perform plethymosgraphy

A

nitrogen wash, not as accurate

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14
Q

what are the 2 restriction categories

A

parenchymal like pulmonary fibrosis, and extraparenchymal like obesity, chest wall deformity(kyphosis)

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15
Q

in which type of restriction is diffusion capacity decreased

A

parenchymal, it is normal with extraparenchymal

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16
Q

when does hyperinflation occur

A

when the total lung capacity is above 120%

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17
Q

what is used to measure DLCO

A

carbon monoxide bc of high hemoglobin affinity so its able to measure diffusion across membranes

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18
Q

what could decrease DLCO

A

thickened alveolar-capillary barrier (fibrosis), decreased blood flow (embolus), decreased Hgb(anemia), decrease in surface area (most commonly emphysema)

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19
Q

what are two instances where DLCO can rise above 140%

A

CHF and polycythemia due to diffuse alveolar hemorrhage (RBCs in alveoli lead to increased abs of CO)

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20
Q

which test is used to assess the need for supplemental O2 with exertion and endurance

A

six minute walk (pulse oximetry and HR monitored during the test)

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21
Q

when is supplemental oxygen prescribed

A

when the sat is less than or equal to 88% or 89% if the patient also has polycythemia, right heart failure, cor pulmonale during six minute walk

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22
Q

what is the GOLD criteria used for

A

to help grade COPD and determine therapy

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23
Q

what must the FEV1/FVC ratio be to determine COPD

A

below 70%

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24
Q

COPD grade 1 FEV1?

A

greater than 80%

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25
Q

^grade 2?

A

between 50% and 80%

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26
Q

^grade 3?

A

between 30% and 50%

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27
Q

^grade 4?

A

below 30% or 50% + chronic resp failure

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28
Q

what are the other chronic diffuse restrictive disorders

A

pneumoconioses, idiopathic interstitial fibrosis and infiltrative disorders such as sarcoidosis, and hypersensitivity pneumonitis

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29
Q

which type of emphysema is the most common

A

centriacinar

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30
Q

centriacinar emphysema first affects respiratory ___

A

bronchioles

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31
Q

what does “pan” mean in panacinar emphysema

A

the entire acinus not the entire lung

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32
Q

what is paraseptal emphysema most likely assoc with

A

spontaneous pneumothorax in young adults due to rupture of bullae from vaping

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33
Q

where is the most common space to see bullous emphysema

A

apical is most common

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34
Q

what are the inflammatory mediators that damage lung structures

A

LTB4, IL-8 and TNF

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35
Q

when are the majority of people diagnosed with emphysema

A

below age 40

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36
Q

what is the role of smoke particles in emphysema

A

it paralyses the cila and causes influx of neutrophils and macrophages

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37
Q

what is the first symptom of emphysema

A

dyspnea

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38
Q

what type of bronchitis is productive cough but no physiologic evidence of airflow obstruction

A

simple chronic bronchitis

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39
Q

hyperreactive airways with intermittent bronchospasm and wheezing?

A

chronic asthmatic bronchitis

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40
Q

what bronchitis is airflow obstruction + assoc emphysema

A

obstructive chronic bronchitis

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41
Q

in older pt with chronic bronchitis you may see ____ of the bronchiolar wall

A

fibrosis

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42
Q

what is the reid index in chronic bronchitis

A

increased >0.5

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43
Q

how could you diagnose atopic asthma

A

high total serum IgE or RAST for antibodies, also wheal and flare rxn skin test

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44
Q

what is a mucous plug/inspissated mucus a result of

A

its coughed up during an asthmatic attack (status asthmaticus), it is a cast of the bronchial tree formed by inspissated mucus

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45
Q

what two things are needed to cause bronchiectasis

A

obstruction and iinfection

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46
Q

why would a male pt with bornchioectasis have sterility

A

he probs has primary ciliary diskinesis (inmorile cilia syndrome), causing sperm dysmotility

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47
Q

what lung lobe does CF most commonly affect in bronchioectasis

A

upper and central lobe

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48
Q

what lung lobe does immunodeficiency most commonly affect in bronchioectasis

A

lower lobe

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49
Q

CF is a disorder of ____ transport affecting___

A

epithelial ion transport affecting fluid secretion

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50
Q

what are the mucus secretions like in CF and what do they lead to

A

abnormally viscin, lead to airway and pacreatic duct blockages → eventually leading to pancreatic insufficiency

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51
Q

what is the classic biomechanical abnormality in CF and what gene is defective

A

high sodium chloride level in sweat, CFTR gene

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52
Q

what are the most common causes of death in CF

A

cardiopulmonary: lung infections w pseudomonas and bronchioectasis–> right heart failure

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53
Q

what does CF affecting the pancreas cause

A

exocrine gland atrophy and fibrosis

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54
Q

what are the most common bacteria in pulmonary cystic fibrosis

A

pseudomonas aeruginosa and burkholderia cepacia

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55
Q

what can CF cause if it affects the reproductive system

A

infertility in mails due to absence of vas deferens

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56
Q

what is pulmonary htn defined as

A

25 mmHg or more at rest

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57
Q

what is the clinical presentation of pulmonary htn

A

dyspnea and fatigue progressing to cyanosis, resp distress, RVH and decompensated cor pulmonale and death

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58
Q

what is the most common cause of pulmonary htn

A

idiopathic

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59
Q

what are the other 4 causes

A

arterial htn, left sided heart disease, lung disease, hypoxia or chronic thromboembolic htn

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60
Q

what protein signaling pathway is involced in idiopathic pulmonary htn

A

defects in BMPR2 signaling → lead to dysfunction of endothelium and proliferation of vascular smooth muscle

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61
Q

pulmonary htn causes ____ hypertrophy of the pulmonary muscular and elastic arteries and ____ ventricular hypertrophy

A

medial, right

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62
Q

Bronchiolitis is defined as

A

nonspecific inflammatory injury affecting small airways without cartilage

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63
Q

in a patient with cough and chronic SOB w/o asthma or COPD you should suspect

A

bronchiolitis obliterans

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64
Q

airway obstruction in bronchiolitis obliterans is (reversible or irreversible)

A

irreversible

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65
Q

which cells cause cellular bronchiolitis?

A

inflammatory cells like lymphocytes, neutrophils and eosinophils

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66
Q

which type of bronchiolitis is not assoc w respiratory symptoms and presents with tan macrophages (smokers macrophages) on histo?

A

Respiratory bronchiolitis-assoc interstitial lung disease (RB-ILLD)

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67
Q

How can you differentiate RB-ILLD and interstitial pneumonia

A

RB-ILLD lacks fibroblastic foci (pneumonia has fibrosis)

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68
Q

how do you differ blebs and bullae?

A

blebs are <1-2 cm in diameter and are subpleural, bullae are >2 cm and occupies pleural cavity

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69
Q

how much do you generally have to smoke to get COPD

A

20 pack years

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70
Q

what is the major contributor to worldwide prevalence of COPD and what are two less common causes

A

biomass fuels w indoor cooking and heating, IV drug use and HIV infections are less common causes

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71
Q

what syndrome is more prone to COPD and pneumothorax, and what is the deficiency

A

Marfans, type 1 collagen deficiency

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72
Q

what is a difference between asthma and COPD in the persistence of symptoms

A

COPD has daily progressive symptoms (asthma has good days and bad days)

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73
Q

COPD has ___ to percussion

A

hyperressonance, bc of the emphysema

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74
Q

what could you see in advanced COPD on PE

A

cyanosis, JVP elevation and peripheral edema

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75
Q

are patients with AAT1 deficiency likely to develop COPD

A

not likely if they do not smoke

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76
Q

significant reversibility is defined by

A

an increase in FEV1 or FVC of 10% or more

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77
Q

the GOLD criteria is used for? what test do you need?

A

stage patients with COPD< use post-bronchodilator FEV1/FVC and FEV1

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78
Q

what is mandatory FEC/FVC post bronchodilator to meet criteria for COPD

A

less than 0.7

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79
Q

what is the difference between stage E and stage A and B criteria in GOLD staging

A

Group E two+ moderate exacerbations or 1 with hospitalization, Group A and B are 0-1 moderate exacerbations NOT leading to hospitalizations

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80
Q

what oxygen test can be performed to determine the presence of hypercapnia

A

ABGS

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81
Q

when should you presvribe long term oxygen therapy

A

if oxygen saturation is less than or equal to 88% or PaO2 is less than 55mm Hg

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82
Q

what is a spacer used for and when do you five it

A

always provide, it doubles the amt of medicine reaching the lung in COPD

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83
Q

what is the first line therapy for COPD and waht does it target

A

LABA targets symptoms and exacerbations

84
Q

if using a single agent should you use LABA or LAMA

A

LAMA is preferred bc they have a greater effect on exacerbation reduction

85
Q

when do you give a SABA

A

consider for all patients, prescribe to all symptomatic patients

86
Q

when should you give LAMA/LABA

A

in patients w advanced disease (B and E) or persistent sx

87
Q

when should you consider ICS in the context of triple therapy

A

pt w hx of exacerbation because it reduces exacerbations even more than LAMA/LABA

88
Q

what patient would benefit from a PDE4 inhibitor

A

pt w very severe COPD (3 or 4 GOLD) and history of exacerbations

89
Q

can you give steroids for exacerbations?

A

yes, some pt are even stroid dependent. generally not used for long txt tho

90
Q

what are the 3 signs you should give antibiotics in exacerbations

A

change in amt, color of sputum and increased dyspnea(only need 2/3)

91
Q

asthma characterized by ____

A

chronic airway inflammation

92
Q

most common asthma phenotype? when does it start

A

allergic asthma, starts in childhood

93
Q

triggers for allergic asthma? respond well to

A

pollen, cat dander, foot etc. respond well to ICS

94
Q

the triggers exercise, viral infection, mold weather and cigarette smoke belong in what asthma phenotype

A

non allergic asthma

95
Q

how could you treat aspirin induced asthma

A

LTRA and biologics

96
Q

when does exercise induced bronchoconstriction occur?

A

minutes after exercise

97
Q

TRAIN in asthma stands for

A

triggers, reversibility, age of onset, intermittent symptoms, nocturnal symptoms

98
Q

if a spirometry test and x rays are normal, can you rule out asthma?

A

no, spirometry may be normal in between exacerbations or when asthma is controlled. xrays are used to rule out other diseases

99
Q

what are the rescue inhaler use, daytime symtpms and nocturnal symptoms in mild persistent asthma

A

rescule inhaler and symtpms: more than 2x week but not daily, nocturnal symptoms: 3-4x p month

100
Q

which asthma pt are considered controlled

A

intermittent

101
Q

what do u prescribe in intermittent asthma

A

prn ICS/SABA

102
Q

mild persistent asthma prescription

A

daily inhaled corticosteroid or LTRA if u cant use ICS

103
Q

Moderate?

A

combination: ICS/LABA

104
Q

severe?

A

multiple agents like ICS+ LABA/LAMA and steroids

105
Q

what could give a false diagnosis of asthma

A

vocal cord dysfunction: pt are anxious and dont respont to asthma treatment

106
Q

name the 5 pulmonary htn groups in order

A

arterial htn, l heart disease, lung disease/hypoxia, Pulm a. obstruction, unclear or multifactorial

107
Q

how do u diagnose and confirm pulm htn

A

echo diagnose, r heart catherization confirms

108
Q

most common initial sx of pulm htn

A

dyspnea and fatigue

109
Q

which symptom is common and specific to pulm htn

A

exertional syncope

110
Q

nebulizers are preferred for what

A

severe asthma or COPD

111
Q

down side of dry powder inhalers?

A

theyre irritating and require high airflow

112
Q

MOA of B2 agonist?

A

increase cAMP –> smooth muscle relaxation and inhibits release from mast cells

113
Q

what contributes to the safety of b2 agonists

A

they have low affinity for b1 (cardiac) receptors

114
Q

when do u use SABAs

A

txt of acute bronchospasms in asthma and COPD (initially and in all stages of asthma txt)

115
Q

why cant u give LABAs by themselves

A

bc they have no direct anti inflammatory effect and can increase risk of fatal asthma attack (they facilitate anti inflammatory actions of ICS )

116
Q

what do u give LABAs with

A

ICS or LAMA

117
Q

what accounts for LABA duration of action

A

slow release from lipid membranes

118
Q

most common b2 agonist side effect

A

tremor

119
Q

other side effects of b2 agonists?

A

cardiovascular stimulation (rare), hypokalemia (watch K+ sparring) and hyperglycemia

120
Q

what cortical arousal pathway does B2 take to cause CNS stimulation

A

locus ceruleus–> NE–> cerebral cortex (restlessness)

121
Q

which asthma drug has a black box warning of asthma related death

A

products thathave laba alone

122
Q

which LABA has a nebulization solution available

A

formoterol (salmeterol is a DPI)

123
Q

which LABA has a faster onset of action

A

Formeterol is faster than salmeterol (both have 12 hr duration)

124
Q

in anaphylaxis ___ can be added after emergency epinephrine

A

inhaled SABA

125
Q

which beta agonists have tablet formulations

A

albuterol and terbutaline (not recommended bc of side effects unless children or ppl that cant take the other forms)

126
Q

Ipratropium is a (type of drug)

A

SAMA (the other iums are LAMAs: tiotropium and aclidinium bromide)

127
Q

muscarinic antagonists MOA

A

prevent bronchoconstricting effects of ach on m3 muscarinic receptors. reduce parasympathetic tone

128
Q

what do you comine muscarinic antagonists for maximal airway dilation

A

beta agonists

129
Q

from most likely to least likey what are the muscarinic antagonists side effects

A

dry mouth, constipation or difficulty urinating, increased HR (ocular effects possible if sprayed to eye accidentally)

130
Q

SAMA principal use

A

COPD, can use in asthma if SABA intolerant, best if used in SABA /SAMA combo in both COPD and severe asthma

131
Q

SAMA ROA

A

MDI or nebulization

132
Q

LAMA principal use

A

long term management of stable copd

133
Q

diff between SAMA and LAMA?

A

LAMA has greater selectivity for M3 receptor (less side effects), and longer duration of action

134
Q

what combo is given for stable severe copd

A

LAMA/LABA soft mist inhaler (once daily–> great adherence)

135
Q

name the two systemic glucocorticoids

A

prednisone and methylprednisone (all the other -sone are ICS)

136
Q

what drug is used for initial traditional daily maintenace for persistent asthma

A

ICS (combined w SABA as needed)

137
Q

are ICS fast acting

A

no, the improvement is delayed up to one week (no immediate benefit)

138
Q

when do you give systemic glucocorticoids

A

in severe asthmatic attacks and COPD exacerbations

139
Q

how long can you give oral prednisone, why?

A

for 1-2 weeks, if longer they can cause hypothalamic pituary adrenal axis suppression

140
Q

which is the only individual drug available as a solution for nebulization

A

budesonide

141
Q

when do you use LABA/ICS combinations

A

in asthma control for better symptom control (but u still need to use SABA)

142
Q

when do you use ICS/LAMA/LABA 3x combos

A

fda indication for COPD (incorporates all possible mechanisms for maximal reduction of airway resistance)

143
Q

when do you use theophylline

A

in asthma when pt cant use inhaled agents

144
Q

Roflumilast mechanism of action

A

PDE4 inhibitor (anti-inflammatory)

145
Q

when do you use roflumilast

A

to reduce frequency of exacerbations of COPD (not used for asthma)

146
Q

Roflumilast side effects

A

nausea, diarrhea , weight loss and headache

147
Q

what is montelukast approved for

A

prophylaxis and maintenance of asthma, may be used in children 6-12

148
Q

montelukast is very effective for

A

aspirin exacerbated respiratory disease (AERD)

149
Q

montelukast common side effect

A

dyspepsia (pain in upper abdomen)

150
Q

omalizumab is restricted for whaat pt

A

severe asthma w evidence of allergic sensitization (hx of severe exacerbation respond best)

151
Q

benralizumab targets what receptor

A

IL-5 receptor in eosinophilic asthma

152
Q

what is the most common sympton of PE

A

dyspnea at rest or w exertion, pleuritic pain (most symptoms vary some are asymptomatic)

153
Q

pulmonary manifestations of pulmonary embolism?

A

may be normal, but consistent with consolidation (esp when assoc w infarct)

154
Q

lower extremity findings of PE?

A

swelling, redness, warmth

155
Q

what syndrome is assoc w higher risl for venous thromboembolism (VTE)

A

antiphospholipid antibody syndrome

156
Q

most common genetic cause of VTE?

A

factor V leiden mutation

157
Q

^what other mutations

A

prothrombin, antithrombin III, protein C and protein S

158
Q

what score do u use to catergorize PE

A

wells score (low risk less than 2, high risk more than 6)

159
Q

Aa gradient in PE?

A

elevated

160
Q

what acid base disorder in PE

A

alkalosis bc tachypnea (also hypoxemia)

161
Q

PE V/Q ration?

A

increased, normal ventilation but no perfusion (bc clot0

162
Q

a normal D dimer can exclude ___ in a low risk pt

A

pulmonary embolus, intermediate and high risk need to be worked up)

163
Q

what two things do you look for in PE x ray

A

hamptons hump ( pulmonary infarct), westermarks sign (pleural effusion)

164
Q

gold standard for PE suspicion

A

CTPA

165
Q

what diagnostic test can identify source of PE

A

doppler (also used if CTPA cannot be performed)

166
Q

when do you use V/Q for PE and what do u see

A

if pt cant do CTPA , mismatch defect: ventilation but no perfusion

167
Q

if a pt has both decreased ventilation and perfusion on V/Q they most likely have

A

lobar pheumonia

168
Q

EKG on PE?

A

tachycardia and nonspecific St wave changes, right ventricular strain pattern if big clot

169
Q

txt for PE

A

anticoagulants: heparin then transition to oral anticoagulants like factor XA inhibitors (xaban) and direct thrombin inhibitor)

170
Q

why is warfarin not preferred over the other oral anticoagulants

A

it is diffucult to manage bc it requires monthly INR check ups, it also interacts with meds and leafy green vegetables

171
Q

how long should anticoagulant therapy last in a patient with a first thromboembolic event occurring in the setting of reversible risk factors

A

long term therapy for 3 months

172
Q

when should you give lifelong anticoagulation if not contraindicated

A

in patients who have recurrent VTE or irreversible risk factors

173
Q

when should you consider thrombolytic therapy

A

in hemodynamically unstable patients systolic BP <90 mmHg and respiratory distress/failure, or patients with right ventricular strain pattern on echo

174
Q

abs contraindications of thrombolytic therapy?

A

prior ICH, cerebrovascular lesion, malignant neoplasm, stroke, aortic dissection

175
Q

when would you use an IVC filter?

A

to treat PE in patients with a contraindication to anticoagulation (active bleeding like GI, CNS bleed, recent CNS surgery)

176
Q

pregnancy ___ the risk of VTE

A

increases (has nonspecific symptoms like low O2 levels post partum)

177
Q

if you suspect VTE in a pregnant person what test should you order

A

lower extremity doppler if positive patient should be anticoagulated (if negative do an X-ray)

178
Q

what should you do if a pregnant patient has an abnormal chest x ray

A

CTPA (dont do V/Q bc its sensitivity decreases with abormal chest x ray)

179
Q

what is the best anticoagulant to use during pregnancy

A

LMWH throughout pregnancy and for 4-6 weeks post partum (IVC if anticoagulation contraindication)

180
Q

how should you treat primary spontaneous pneumothorax

A

surgical treatment because recurrence rate is very high

181
Q

what does iatrogenic pneumothorax mean and what are three examples

A

its secondary to diagnostic or therapeutic medical intervention (close proximity to the lungs): thoracocentesis, bronchoscopy and central line placement

182
Q

pneumothorax usually develops at ___

A

rest

183
Q

which pneumothorax is thought to arise from thoracic endometriosis

A

catamenial pneumothorax

184
Q

what is the common presentation of catamenial pneumothorax

A

seen in women aged 30-40 and symptoms present within 48 hrs of menstruation , right side most common

185
Q

which condition is assoc with chylothorax and causes spontaneous pneumothorax

A

lymphangioleiomyomatosis : characterized by thin walled cysts in women of child bearing age

186
Q

pneumothorax has ____ tactile fremitus

A

decreased

187
Q

what can be mistaken for a pneumothorax and lead to unnecessary intervention

A

a vertical skin line

188
Q

what diagnostic test can distinguish between large bulla and pneumothorax

A

CT

189
Q

how do you manage small pneumothoraxes

A

observation w x rays, they heal spontaneously. u might need o2 to expedite resorption

190
Q

what do you use to repair underlying defect in patients w PSP

A

video assisted thoracoscopic surgery (VATS)

191
Q

what is pleurodesis and what is it usually used for

A

the pleura stick together by using talc to induce inflammation, used with pt with nonresolving pleural effusions

192
Q

what is pneumomediastinum usually caused by and how do you treat

A

most commonly due to secondary to pneumothorax, can also be due to rupture of esophagus. treat underlying cause and manage conservatively

193
Q

primary stressor causing altitude illness, how maby feet leads to it?

A

hypoxemia, 8,000 ft or higher

194
Q

what is the most common form of altitude illness, symptoms and how do you resolve

A

acute mountain sickness, malaise, resolves 24-72 hrs after acclimatization

195
Q

when does high altitude cerebral edema occur, what symptoms?

A

in indiv with AMS or HAPE in elevation over 10,000 ft. encephalopathic symptoms: medical emergency

196
Q

which altidude illness has breathlessness at rest and pink frothy sputum

A

high altitude pulmonary edema

197
Q

the difference between PiO2 and PaO2 ___ at high altitudes because of increased ventilation

A

narrows

198
Q

arterial oxygen saturation (SaO2) is well maintained while awake until ____

A

3000 meters

199
Q

what is the txt of choice in HAPE, what else can you use

A

descent txt of choice, u can use acezolamide, difedipine and dexamethasone until descent is possible or prophylactically

200
Q

what is the most common cause of COPD exacerbation

A

infection (tracheobronchitis) get a gram stain

201
Q

in what stage can exacerbation of asthma occur

A

any stage!

202
Q

what are signs of a severe asthma exacerbation

A

tachypnea, tachycardia, accessory muscle use, unable to speak in full sentences and pulsus paradoxus

203
Q

how could you identify status asthmaticus

A

lack of response to SABAs

204
Q

how do you identify COPD exacerbation

A

dyspnea/ cough that worsens over 14 days

205
Q

wht other differential should you consider in COPD exacerbation

A

pneumonia, take a chest x ray

206
Q

what is the target O2 sat for a pt w exacerbation

A

92% and above

resp 2 exam 1 (2 decks)

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