IM Pulm Flashcards

1
Q

Asthma

definition

A

asthma, or reactive airway disease, is an abnormal bronchoconstriction of the airways. Asthma is a reversible obstructive lung disease, which is the main difference between this disorder and chronic obstructive pulmonary disease (COPD)

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2
Q

Asthma

etiology

A

etiology is unknown, association with atopic disorders and obesity

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3
Q

Asthma

causes of acute exacerbations include:

A

allergens like pollen, dust mites, cockroaches, and cat dander

infection and cold air

emotional stress or exercise

catamenial (related to menstrual cycle)

aspirin, nsaids, bblockers, histamine, any nebulized medication, tobacco smoke

GERD

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4
Q

Asthma

presentation

A

the clear presence of wheezing with the acute onset of sob, cough, and chest tightness make a what is the most likely diagnosis question. increased sputum production is common although a fever is not always present

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5
Q

asthma prevalence, incidence, and hospitalization rates are all

A

increasing

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6
Q

which of the following is most likely to be associated with/found in this pt?

asthma

A

symptoms worse at night

nasal polyps and sensitivity to aspirin

eczema or atopic dermatitis on physical examination

increased length of expiratory phase of respiration

increased use of accessory respiratory muscles (intercostals)

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7
Q

the oral temperature may not be accuratly measured in pts that are

A

breathing fast. mouth breezing cools the thermometer

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8
Q

the answer to the best initial test question in asthma is based on the

A

severity of presentation

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9
Q

make sure you can understand the sound of

A

wheezing

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10
Q

Asthma

diagnostic tests

best initial test in an acute exacerbation:

A

peak expiratory flow or arterial blood gas. peak flow can be used by the pt to determine function

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11
Q

CXR in asthma

A

most often normal, but may show hyperinflation

it is usually used to:
exclude pneumonia as a cause of exacerbation
exclude other disease such as pneumothorax or CHF in cases that are not clear

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12
Q

asthma can present exclusively as a

A

cough

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13
Q

asthma

most accurate diagnostic test

A

pulmonary function testing. spirometry will show a decrease in the ration of forced expiratory volume in 1 second (fev1) to forced vital capacity (FVC). the FEV1 decreases more than the FVC.

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14
Q

most accurate diagnostic test in a person with asymptomatic asthma

A

20% decrease in FEV1 wiht the use of methacholine or histamine

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15
Q

pulmonary function testing in Asthma

A

decreased fev1 and decreased fvc with a decreased ration of fev1/fvc

increase in fev1 of more than 12% and 200ml with the use of albuterol

decrease in fev1 of more than 20% with the used of methacholine or histamine

increase in the diffusion capacity of the lung for carbon monoxide (DLCO)

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16
Q

with asthma RTFs are normal in between

A

exacerbations

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17
Q

In asthma ACH and histamine

A

provoke bronchoconstriction and an increase in bronchial secretions. methacholine is an artificial form of ach used in diagnostic testing

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18
Q

additional testing options for asthma

A

CBC may shoe an increased eosinophil count

skin testing is used to identify specific allergens that provoke bronchoconstriction

increased IgE levels suggest an allergic etiology. IgE levels may also help guide therapy such as the used of the anti-IgE medication omalizumab. increased ige levels are also associated with allergic bronchopulmonayr aspergillosis

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19
Q

Asthma treatment

step 1

A

always start the treament of asthma with an inhaled short acting beta agonist (SABA)

examples of SABA are:
albuterol
pirbuterol
levalbuterol

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20
Q

Asthma treatment

step 2

A

add a long-term control agent to a SABA. low-dose inhaled corticosteroids (ICS) are the best initial long term control agent

examples of ICS are:
beclomethasone
budesonide
flunisolide
fluticasone
mometasone
triamcinolone

alternate long term agents are:
cromolyn and nedocromil to inhibit mast cell mediator release and eosinophil recruitment
theophylline
leukotriene modifiers: montelukast, zafirlukast, or zileuton (best with atopic pts)

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21
Q

Asthma treatment

step 3

A

add a long-acting beta agnoist (laba) to a SABA and ICS, or increase the dose of ICS

LABA medications are salmeterol or formoterol

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22
Q

Asthma treatment

step 4

A

increase the dose of the ICS to maximum in addition to the LABA and SABA

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23
Q

Asthma treatment

step 5

A

omalizumab may be added to the SABA, LABA, and ICS in those who have an increased IgE level

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24
Q

Asthma treatment

step 6

A

oral corticosteroids such as prednisone are added when all the other therapies are not sufficient to control sx

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25
never use LABA
first or alone
26
zafirlukast is hepatotoxic and has been associated with
churg-strausss syndrome
27
adverse effects of inhale dsteroids are
dysphonia and oral candidiasis
28
adverse effects of systemic corticosteroids
should be used as a last resort bc they can cause: osteoporosis cataracts adrenal suppression and fat redistribution hyperlipidemia, hyperglycemia, acne, and hirsutism (in women) thinning of skin, striae, and easy bruising
29
high dose inhaled steroids rarely lead to the adverse effects associated with
prednisone
30
Antiocholinergics in asthma
the role of ipratropium and tiotropium in asthma management is not clear. anticholinergic agents will dilate bronchi and decrease secretions. they are very effective in COPD.
31
influenza and pnuemococcal vaccine are given in all
asthma pts
32
what is the best indication of the severity of his asthma
respiratory rate, if during an acute exacerbation
33
The severity of an asthma exacerbation is quantified by:
decreased peak expiratory flow (PEF) ABG with an increased A-a gradient the PEF is an approximation of the FVC. there is no precise normal value. it is based predominantly on height and age, not weight. the PEF is used in acute assessment by seeing how much difference there is from the pts usual PEF when the pt is stable. CXR is used to see if there is an infection leading to the exacerbation
34
asthma predisposed to
pneumothorax
35
treatment for acute asthma exacerbation
oxygen albuterol steroids the best initial therapy is oxygen combined with inhaled short acting beta agonists such as albuterol and a bolus of steroids. corticosteroids need 4 to 6 hours to begin work, so give them right away. epinephrine injections are not more effective than albuterol and have more adverse systemiceffects. ipratropium should be used, but does not work as rapidly as albuterol epinephrine is rarely used and only as a drug of last resort. magnesium has some modest effect in bronchodilation. magnesium is not as effective as albuterol, ipratropium, or steroids, but it does help
36
Magnesium helps relieve
bronchospasm, magnesium is used only in acute, severe asthma exacerbation not responsive to several rounds of albuterol while waiting for steroids to take effect
37
the following are not effective in acute exacerbations:
``` theophylline cromolyn and nedocromil (best with exrinsic allergies like hay fever) leukotriene modifiers omalizumab salmeterol ```
38
if a pt having an acute exacerbation does not respond to oxygen, albuterol, and steroids or develops...
respiratory acidosis (increased pco2), the pt may have to undergo endotracheal intubation for mechanical ventilation. these pts should be placed in the icu
39
COPD definition
COPD is the presence of sob from lung destruction decreasing the elastic recoil of the lungs. most of the ability to exhale is from elastin fibers in the lungs passively allowing exhalation. this is lost in COPD, resulting in a decrease in FEV1 and FVC with an increase in the toal lung capacity (TLC). COPD is not always associated with reactive airway disease such as asthma although both are obstructive disease.
40
COPD etiology
tobacco smoking leads to almost all copd. tobacco destroys elastin fibers
41
COPD in a young nonsmoker
alpha-1 antitrypsin deficiency
42
COPD presentation
sob worsened by exertion intermittent exacerbation with increased cough, sputum, and sob often brought on by infection barrel ches from increased air trapping muscle wasting and cachexia
43
COPD best initial test
cxr: increased ap diameter air trapping and flattened diaphragm
44
COPD most accurate diagnostic test
PFT: decreased fev1, fvc, and fev1/fvc ration under 70% increased tlc bc of an increase in residual volume decreased dlco (emphysema, not bronchitis) incomplete improvement with albuterol little or no worsening with methacholine
45
COPD reversibility with inhaled bronchodilators
pts with COPD have a broad range of response to inhaled bronchodilators such as albuterol. this ranges from no reversibility to complete reversibility. about 505 will have some degree of response. plethysmography will show an increase in residual volume
46
full reversibility in response to bronchodilators is defined as greater than
12% increase and 200 ml increase in FEV1
47
COPD reversibility with inhaled bronchodilators arterial blood gas
acute exacerbations of COPD are associated with increased pCO2 and hypoxia. respiratory acidosis may be present if there is insufficient metabolic compensation and the bicarbonate level will be elvated to compensate. in between exacerbation, not all those with COPD will retain CO2
48
COPD reversibility with inhaled bronchodilators CBC:
may have an increase in hematocrit from chronic hypoxia
49
COPD reversibility with inhaled bronchodilators EKG:
R atrial hypertrophy and R ventricular hypertrophy atrial fibrillation or multifocal atrial tachycardia (MAT)
50
COPD reversibility with inhaled bronchodilators echocardiography
R atrial and R ventricular hypertrophy pulmonary htn
51
COPD treatment improves mortality and delays progression of disease
smoking cessation oxygen therapy for those with pO2 less than or equal to 55 or saturation less than or equal to 88%; mortality benefit is directly proportional to the number of hours that the oxygen is used influenza and pnuemococcal vaccines
52
COPD treatment definitely improves symptoms (but does not decrease disease progression or mortality)
saba (albuterol) anticholinergic agents: tiotropium, ipratropium steroids laba (slameterol) pulmonary rehabilitation
53
asthmatics not controlled with albuterol
give inhaled steroid
54
COPD not controlled with albuterol
give an anticholinergic (tiotropium) or inhaled steroids
55
COPD possible improves sx
theophylline lung volume reduction surgery
56
COPD no benefit
cromolyn leukotriene modifiers (montelukast)
57
with COPD when all medical therapy is insufficient the answer is
refer to transplantation
58
inhaled anticholinergics are most effective in
COPD
59
O2 use COPD
pO2
60
treatment of acute exacerbations of chronic bronchitis
the management of acute episodes of increased sob is similar to the treatment of acute asthma exacerbations. the use of bronchodilators and corticosteroid therapy is combined with antibiotics antibiotics are generally used in acute exacerbations of chronic bronchitis (AECB) because infection is by far the most commonly identified cause
61
AECB treatment is identical to
asthma treatment but with less proven benefit
62
treatment of acute exacerbations of chronic bronchitis Most effective
Although viruses cause 20% to 50% of episodes, coverage should be provided against Strep Pneumo, H flu, and moraxella cararrhalis Macrolides: zpak, clarithromycin Cephalosporins: cefuroxime, cefixime, cefaclor, ceftibuten Amoxicillin/clavulanic acid quinolones: levofloxacin, moxifloxacin, gemifloxacin
63
treatment of acute exacerbations of chronic bronchitis second line agents
doxy bactrim
64
Criteria for oxygen use in COPD
oxygen decreases mortality, Criteria are: pO2 below 55 mm Hg or oxygen saturation below 88% or if there are signs of right sided heart disease/failure or an elevated hematocrit: pO2 less than 60 mm Hg or oxygen saturation below 90%
65
although the hypoxic drive elimination concept
is not correct, you would still avoid reflexively placing a pt with COPD on a ver high flow 100% nonrebreather mask. use only as much osgycen as is necessary to the rasie the pO2 above 90% saturation
66
the idea of eliminatign hypoxic drive
is not accurate. dyspneic, hypoxic patients with COPD must get oxygen
67
Bronchiectasis definition
an uncommon disease from chronic dilation of the large bronchi. this is a permanent anatomic abnormality that cannot be reversed or cured. bronchiectasis is uncommon bc of better control of infections of th elung which lead to the weakening of the bronchial walls
68
Bronchiectasis etiology
the single most common cause of bronchiectasis is cystic fibrosis, which accounts for half of cases ``` other causes: infections, tb pneumonia, abscess foreign body or tumors allergic bronchopulmonary aspergillosis (abpa) collagen-vascular disease such as RA ```
69
Bronchiectasis Presentation/what is the most likely diagnosis
recurrent episodes of very hgih olume purulent sputum production is the key to the suggestion of the diagnosis. hemoptysis can occure. dyspnea and wheezing are present in 75% of cases. ``` other findings are: weight loss anemia of chronic disease crackles on lung exam clubbing is uncommon dyskinetic cilia syndrome ```
70
it is impossible to diagnose Bronchiectasis w/out
an imagin study of the lungs such as a CT scan
71
Bronchiectasis best initial test
a cxr that shows dilated thickened bronchi, some times with tram-tracks which is the thickening of the bronchi
72
Bronchiectasis most accurate test
high-resolution CT sputum culture is the only way to determine the specific bacterial etiology of the recurrent episodes of infection
73
Bronchiectasis treatment
1. chest physiotherapy (cupping and clapping) and postural drainage are essential for dislodging plugged-up bronchi 2. treat each episode of infection as it arises. use the same antibiotics as for exacerbations of COPD. the only difference is that inhaled antibiotics seem to have some efficacy and a specific microbiologic diagnosis is preferred since mai (mycobacterium avium intracellulare) can be found 3. rotate antibiotic, 1 weekly each month 4. surgical resection may be indicated
74
Allergic Bronchopulmonary Aspergillosis (ABPA) definition/etiology
abpa is a hypersensitivity of the lungs to fungal antigens that colonize the bronchial tree. ABPA occurs almost exclusively in pts with asthma and a history of atopic disorders
75
Allergic Bronchopulmonary Aspergillosis (ABPA) what is the most likely diagnosis
look for an asthmatic pt with recurrent episodes of brown-flecked sputum and transient infiltrated on cxr cough, wheezing, hemoptysis, and sometiems bronchiectasis occur
76
Allergic Bronchopulmonary Aspergillosis (ABPA) diagnostic tests
peripheral eosinophilia skin test reactivity to aspergillus antigens precipitating antibodies to aspergillus on blood test elevated serum IgE levels pulmonary infiltrates on cxr or CT
77
Allergic Bronchopulmonary Aspergillosis (ABPA) treatment
1. oral steroids (prednisone) for severe cases; inhaled steroids are not effective for ABPA 2. itraconazole orally for recurrent episodes
78
an inhaler cannot deliver a high enough dose of steroids to be effective in
Allergic Bronchopulmonary Aspergillosis (ABPA)
79
Cystic fibrosis etiology
Cystic fibrosis is an autosomal recessive disorder caused by a mutation in the genes that code for chloride transport. this is known as the cystic fibrosis transmembrane conductance regulator (CFTR). mutations in the CFTR gene damage chloride and water transport across the apical surface of epithelial cells in exocrine glands throughout the body. this leads to abnormally thick mucus in the lungs, as well as damage to the pancrease, liver, sinuses, intestines, and gu tract. they all clog up damaged mucus clearance decreases the ability to get rid of inhaled bacteria
80
neutrophils in cf dump ton of
dna into airway secretions, clogging them up
81
lung disease accounts for 95% of deaths in
CF
82
Cystic fibrosis presentation
over 1/3 of CF pts are adults. look for a young adult with chronic lung disease (cough, sputum, hemoptysis, bronchiectasis, wheezing, and dyspnea) and recurrent episodesof infection. sinus pain and polyps are common
83
Cystic fibrosis GI involvement
meconium ileus in infants with abdominal distention pancreatic insufficiency (in90%) with steatorrhea and vitamin ADE and K malabsorption recurrent pancreatitis distal intestinal obstruction biliary cirrhosis
84
Cystic fibrosis gu involvement
men are often infertile, 95% have azoospremia, with the vas deferns missing in 20%. women are infertil bc chronic lung disease alters the menstural cycle and thick cervical mucus blocks sperm entry
85
Cystic fibrosis diagnostic tests
the most accurate test is an increased sweat chloride test. pilocarpine increases ach levels which increases sweat production. chloride levels in sweat above 60meq/l on repeated testing establishes the diagnosis Genotyping is not as accurate as finding an increased sweat chloride level. this is bc there asre so many different types of mutations leading to CF
86
Cystic fibrosis additional diagnostic tests
``` cxr and ct have no single abnormality that confirm diagnosis but may show bronchiectasis pneumothorax scarring atelectasis hyperinlfation ``` ABG may show hypoxemia and in advanced disease a resp acidosis pfts show mixed obstructive and restrictive patterns; decrease in fvc and total lung capacity; and decreased diffusing capacity for carbon monoxide
87
Cystic fibrosis sputum culture
nontypable h flu psuedomonas auruginosa staph aureus burkholderia cepacia
88
Cystic fibrosis treatment
1. abs are routine, same ones as bronchiectasis, inhaled aminoglycosides are seen only in CF 2. inhaled recombinant deoxyribonuclease (rhDNase), this breaks down the DNA in resp mucus that clogs up the airways 3. inhaled bronchodilators like albuterol 4. pneumococcal and influenza vaccination 5. lung transplantation is used only in advanced disease not responsive to herapy 6. ivacaftor increases activity of cftr in some pts
89
community-acquired pnuemonia definition
defined as pneumonia occuring before hospitalization ot within 48 hours of hospital admission. CAP is the most common infectious cause of death int he US, and is the only infectious disease that is among the top 10 causes of death nationwide
90
community-acquired pnuemonia etiology
strep pneumo is the most common cause of CAP. netiher the environemental reservoir of s pneumo nor its method of acquistion is known
91
CAP and COPD
h flue
92
CAP and recent viral infection
s aureus
93
CAP and alcoholism and diabetes
klebsiella pneumonia
94
CAP and poor dentition and aspiration
anaerobes
95
CAP and young healthy pts
mycoplasma pnueomoniae
96
CAP and hoarseness
chlamydophilia pnuemoniae
97
CAP and contaminated water sources air con and ventilation systems
legionella
98
CAP and birds
chlamydia psittaci
99
CAP and anials at the time of giving birth vets and farmers
coxiella burnettii
100
CAP Presentation
``` fever cough dyspnea (severe infection) hemopstysis dullness to percussion if effusion bronchial breath sounds and egophony from consolidation of air spaces rales ronchi and crepitations abdominal pain or diarrhea from lower lobe infection chills or rigors from bacteremia chest pain from pleura inflammation hypothermia is just as bad as fever ```
101
CAP | severe infection vital signs
tachycardia hypotension tachypnea mental status
102
chest pain from pneumonia
is often pleuritic, changing with respiration
103
dyspnea, high fever, and an abnormal cxr distinguish
pneumonia from bronchitis
104
hemoptysis from necrotizing disease "currant jelly" sputum
klebsiella pneumonia
105
foul-smelling sputum, rotten eggs
anaerobes
106
dry cough, rarely severe, bullous myringitis
mycoplasma pneumoniae
107
gi symptoms (pain diarrhea) or CNS sx such as ha and confusion
legionella
108
aids with less than 200 CD4 cells
pneumocystis
109
Infections with a dry or nonproductive cough
``` mycoplasma viruses coxiella pneumocystis chlamydia ``` usually involve the interstitial space and more often leave the air spaces of the alveoli empty, which is why there is less sputum production
110
specific sputum colors
are useless in determining etiology
111
CAP diagnostic tests
best initial test is cxr sputum gram stain and culture are best ways to tre and determine a specific microbial etiology atypical pneumonia refers to an organism not visible on gram stain and not culturable on standard blood agar (mycoplasma, chlamydophila, legionella, coxiella, and other viruses) leukocytosis is often present but is nonspecific
112
CAP CXR
b/l interstitial infiltrates are seen with: ``` mycoplasma viruses coxiella pneumocystis chlamydia ``` same organisms as nonproductive cough, xrays lag behind clinical findings
113
CAP the first cxr can be negative in at least
10-20% of cases or pneumonia
114
CAP sputum gram stain is adequate if there are
more than 25 white blood cells and fewre than 10 epithelial cells
115
CAP ct and mri
show greater definition of abnormlalities found on a chest xray but will still not be able to determine a specific microbiologic etiology
116
with infections dieases the radiology test
is never the most accurate test
117
CAP blood cultures
are positive in 5-10% of cases, usually with s pneumo
118
CAP tests done in severe disease with an unclear etiology or those not responding to treatment
thoracentesis - can determine empyema if diagnosis is unclear, drain empyema (like an abscess, infected pleural effusion) empyema - look for ldh above 60% of serum level and protein avoe 50% of serum level. a white cell coutn above 1000/ul or PH<7.2 is suggestive of infection bronchoscopy - rarely needed, used if need to go to ICU, when initial testing like sputum and culture do not yield an organism and the pts condition is worsening despite empiric therapy. an exception is pneumocystis pneymonia in which onnivasive testing reraely reveals a dx and precise confirmation of the etiology is critical to guide therapy
119
it is impossible to make a specific diagnosis of the cause of pneumonia based on
hx and physical
120
new large effusions secondary to pneumonia should be
tapped
121
Mycoplasma pneumoniae diagnostic test
pcr cold agglutins serology special culture media
122
chlamydophila pneumoniae diagnostic test
rising serologic titers
123
legionella diagnostic test
urine antigen | culture on charcoal yeast extract
124
chlamydia psittaci diagnostic test
rising serologic titers
125
coxiella burnetti diagnostic test
rising serologic titers
126
pneumocystis jiroveci (PCP) diagnostic test
brochoalveolar lavage (BAL)
127
mycoplasma and chlamydophila are rarely confirmed
bc they are simply treated empirically
128
CAP it is the severity of disease not the etiology that drives
initial therapy
129
CAP outpatient treatment
previously healthy or no antibiotics in the pat 3 monthsand mild symptoms > macrolide (azithromycin or clarithromycin)hyp or doxycycline comorbidities or abs int eh past 3 months > resp fluoroquinolone (levofloxacin or moxifloxacin)
130
CAP inpatient treatment
Resp fqs: levo or moxifloxaxin or ceftriaxone and azithromycin
131
hypoxia and hypotension as single factors are a reason to
hospitalize a pt
132
CAP reasons to hospitalize
those with severe disease have a combination of: hypotension (systolic below 90 mm HG) rr above 30 per minute or pO2 less than 60 mm Hg, PH below 7.35 elevated BUN above 30 mg/dl, sodium less tahn 130 mmol/l, glucose above 250 mg/dl pulse above 125 per minute confusion temp above 104 deg age 65 or older, or commorbidities such as cancer, COPD, CHF, renal failure, or liver disease
133
notic that the cxr does not guide what in CAP
admission
134
xray cannot tell severity of
hypoxia
135
CAP Curb65=
admission ``` Confusion Uremia Resp distress BP low Age>65 ```
136
infected pleural effusion or empyemawill respond most rapidly to
drainage by chest tube or thoracostomy
137
exudate VS transudate
pleural effusion with pH o<7.2 suggests empyema and needs chest tube drainage. LDH >60% of serum (0.6) or protein >50% of serum (0.5) suggest an exudate. Exudates are cuased by infection and cancer
138
CURB 65 0-1 point
send home
139
CURB 65 > or equal to 2 points
admission
140
pleural effusion with a large meniscus sign
only a fluid sample from thoracentesis can determine the specific cause
141
effusion should be freely
mobile and form a layer when the pt lies on he rside
142
hydropnuemothorax is both
abnormal air and lfuid in the pleural space, must drain with a chest tube
143
consultation is almost never
the right answer
144
pneumococcal vaccination
everyone aboe 65 should receive vaccination with the 13 polyvalent vaccine. followed in 6-12 months with the 23 polyvalent vaccine. in additon those with chronic heart, liver, kidney, or lung disease (including asthma) should also be vaccinated as soon as their underlying disease is apparent if first dose given before 65, give another dose 5 years later
145
other reasons to vaccinate against pnuemococcal
function or anatomic asplenia (sickle cel) hematologic malignancy (leukemia, lymphoma) immunosuppression: dm, alcoholics, corticosteroid users, AIDS or HIV positive CSF leaks or cochlear implant
146
do healthcare workers need pneumococcal vaccine?
no
147
Healthcare Associated or hospital acquired Pneumonia
defined as a pneumonia developing more than 48 hours after admission or after hopsitalization in the last 90 days. higher incidence of gram neg bacilli like ecoli or pseudomonas macrolides are not acceptable instead use: antipseudomonal cephalosporins: cefepime or ceftazidime or antipseudomonal penicillin: piperacillin/tazobactam or carbapenems: imipenem, meropenem, or doripenem
148
piperacillin and ticarcillin are always used in
combination with a betalactamas inhibitor such as tazobactam or clavulanic acid
149
Ventilator Associated Pneumonia (VAP) definition
mechanical ventilation interferes with normal mucociliary clearance of the respiratory tract such as the ability to cough. postiivte pressure is temendously damaging to the normal ability to clear colonization Ventilator Associated Pneumonia has an incidence as high as 5% per day int he first few days on a ventilator
150
Ventilator Associated Pneumonia what is the most likely diagnosis
bc of multiple conuterncurrent illnesses such as CHF, even a diagnosis of VAP can be hard to establish look for: fever and or rising wbcs new infiltrate on cxr purulent secretion coming from the et tube
151
Ventilator Associated Pneumonia diagnostic tests
bc of coloniztion of the et tube, sputum culture is worthless, dx of specific etiology is difficult. in order from least accurate but easiest to do to most accurate and hardest to do: tracheal aspirate bronchoalveolar lavage protected brush specimen video-assisted thoracoscopy open lung biopsy
152
Ventilator Associated Pneumonia tracheal aspirate
a suction catheter is palced in the et and aspirates the contents below the trachea when the catheter is past the end of the et tube
153
Ventilator Associated Pneumonia bronchoalveolar lavage (BAL)
a bronchoscope is placed deeper into the lungs where there are not supposed to be any organisms. can be contaminated when passed throught he nasopharynx
154
Ventilator Associated Pneumonia protected brush specimen
the tip of the bronchoscope is covered when passed thorugh the nasopharynx then ucovered only inside the lungs much more specific bc of decreased contamination
155
Ventilator Associated Pneumonia video assisted thoracoscopy (VAT)
a scope is placed htrough the chest wall and a sample of the lung is biopsied. this allows a large piece of lung to be taken without the need for cutting the chest open (thoracocotomy). it is like sigmoidoscopy of the chest
156
Ventilator Associated Pneumonia open lung biopsy:
the momst accurate diagnostic test of VAP, but with much greater morbidity and potential complication of the procedure bc of the need for thoracotamy
157
subcutaneous emphysema
air abnormally leaking into the soft tissue of the chest wall, may be caused by chest tube placement
158
Ventilator Associated Pneumonia treatment
combine 3 different drugs 1. antipseudomonal beta lactam cephalosporin (ceftazidime or cefepime) or penicillin (piperacillin/tazobactam) or carbapenem (imipenem, meropenem, or doripenem) Plus 2. second anti pseudomonal agent aminoglycoside (gentamicin or tobramycin or amikacin) or fluoroquinolone (cipro or levo) Plus 3. methicillin- resistant antistaph agent Vancomycin or linezolid
159
culturing an et tube is like culturing urine with a foley catheter in place
it will always grow something bc of colonization
160
no daptomycin for
lungs!! daptomycin is inactivated by surfactant
161
change the initial therapy for VAP
if a specific etiology is identified
162
imipenem
can cause seizures is excreted thorugh the kidneys renal failure causes a rise in impienem levels leading to toxicity
163
carbamazepine is no more effective
than phenytoin at stopping seizures caused by imipenem?
164
lung abscess etiology
rare bc of prompt treatment of aspiration pneumonia occurs only with a large volume of aspiration of oral/pharyngeal contents, usually with poor dentition, and not treated stroke with loos of gag reglex seizures intoxication et tube
165
aspiration pneumonia happens in the upper lobe
when lying flat
166
lung abscess what is the most likely diagnosis
look for a person with one of the risk factors presenting a chronic infection (etiologies) developing over several weeks with large volume sputum that is fould smelling bc of anaerobes, weight loss is common
167
lung abscess diagnostic test
cxr is best initial test and will show a cavity possible with an air gluid level chest ct is more accurate than cxr but only a lung biopsy can establish the specific etiology
168
lung abscess treatment
clindamycin or penicillin are best to cover a lung abscess
169
sputum culture is wrong answer for diagnosing a
lung abscess all sputum has anaerobes from mouth flora
170
chest cavity consistent with an abscess
thick wall and an air fluid level
171
Pneumocystis Pneumonia etiology
the agent causing pcp has been renamed P. Jiroveci instead of P carinii. PCP occurs alomst esclusively in pts with AIDS whose CD4 cell count has dropped below 200u/l and who are not on prophylactic therapy
172
Pneumocystis Pneumonia what is the most likely diagnosis
look for a pt with AIDS presenting with dyspnea on exertion, dry cough and fever. the question will often suggest or directly state that the CD4 count is low (below 200u/l and that he pt is not on prophylaxis
173
Pneumocystis Pneumonia diagnostic testing
the best initial test can be either a cxr showing b/l interstitial infiltrates or an arterial blood gas looking for hypoxia or an increased A-a gradient. LDH levels are always elevated. the most accurate test is a bronchoalveolar lavage. sputum stain for pcp is quite specfic if it is positive there is no need to do further testing a negative sputum stain means you should answer bronchoscopy as the best diagnostic test
174
a normal LDH means you should not answer what as the omst likely diagnosis
pcp
175
you cannot distinguish pcp from mycoplamsa chlamydophila or viruses by xray alon. however in hiv, pcp is most likely with
interstitial infiltrates
176
Pneumocystis Pneumonia treatement
bactrim is the best initial therapy for both best initial therapy and prophylaxis. add steroid to decrease mortality if th epxp is severe atovaquone can be used as an alternative to bactrim if the pcp is mild if bactrim toxicity switch to: clindamycin and primaquine or pentamidine
177
Pneumocystis Pneumonia grading
severe - pO2 less than 70 or an A-a gradient above 35 mild - mild hypoxia
178
adverse effects of Bactrim
rash bone marrow suppression
179
if pt has g6pd deficiency and Pneumocystis Pneumonia give what instead of clindamycin and primaquine ifcant give bactrim
pentamidine
180
antiretrovirals during acute opportunistic infection
no they can exacerbate it
181
Pneumocystis Pneumonia prophylaxis
start treatement to prevent pcp in those with aids whose cd4 count is below 200u/l 1. bactirm if there is a rash or neutropeina form bactrim use: 2 atovaquone or dapsone aerosol pentamidine is not used as second line therapy for prophylaxis bc it has less effiicacy then those listed above
182
always choose therapy based on
efficacy not adverse effects
183
dapsone is ci in those with
g6pd
184
azithromycin for prophylaxis in what for aids
atypical mycobacteria when cd4 is below 50u/l
185
TB overview
continues to diminsh in the US. 2/3rds of domestic TB cases occur in those who are recent immigrants from countries with poor control including those who have been preciously vaccinated with bcg. this is why previous bcg vaccine has no impact or effect on recommendation for treatment of latent tb (positive ppd)
186
almost all pts with tb have one or more risk factors like:
recent immigrants (in the past 5 years) prisoners hiv positive healthcare workers lcose contacts of someone with tb steroid use hematologic malignancy alcoholics dm
187
TB presentation/ what is the most likely diagnosis
look for a person wtih one of the previously listed risk factors presenting with fever, cough, sputum, weight loss, hemoptysis, and night sweats
188
you cannot answer tb without
clear risk factor cavity on cxr or a positive smear
189
TB diagnostic tests
the best initial test is an cxr as well as with all respiratory infections sputum stain and culture specifically for acid fast bacilli (mycobacteria) must be done 3 times to fully exclude TB pleural biopsy is the single most accurate diagnostic test
190
ppd skin testing in TB
never the best test for TB in a symptomatic pt
191
TB treatment
``` when the semar is positive begin therapy with 4 drugs: Rifampin Inh pyrazinamide ethambutol ``` you do not need the ethambutolif it is known at the beginning of therapy that the organism is sensitive to all TB medications ethambutol is given as part of 4 drug empiric therapy prior to konwing the sensitivity of the organism aftreu using ripe for the first 2 months . stop ethambutol and pyrazinamide and continue rifampin and inh for the next 4 motnhs the standard of care is 6 total months of therapy
192
when is treatment for TB extended to longer than 6 months
osteomyelitis miliary tb meningitis pregnancy or any other time pyrazinamide is not used
193
TB toxicity of therapy
all of the TB medications cause hepatotoxicity but do not stop them unless the tansaminases rise to 3 to 5 times the upper limit of normal
194
Rifampin toxicity - management -
toxicity - red color to body secretions management - none, benign finding
195
isoniazid toxicity - management -
toxicity - peripheral neuropathy management - use pyridoxine to prevent
196
Pyrazinamide toxicity - management -
toxicity - hyperuricemia management - no treatment unless symptomatic
197
Ehtambutol toxicity - management -
toxicity - optic neuritis/color vision management - decrese doe in renal failure
198
TB use of steroids
glucocorticoids decrease the risk of contstictive pericarditis in those with pericardial involvement. they also decrease neurologic compication in TB meningitis
199
what should pregnant pts not receive with TB
pyrazinamide or streptomycin
200
Latent TB (PPd testing and treatment) indications for PPd testing
the PPd is not a general screening test for the whole population only those in the risk groups previously described whould be screened. ppd testing is not useful in those who are symptomatic or those with abnormal cxr, these pts need acid fast sputum testing
201
Latent TB (PPd testing and treatment) what is considered a positive test?
only induration is counted towards a positive test, erythema is irrelevant
202
Latent TB (PPd testing and treatment) what is considered a positive test? induration larger than 5 mm
hiv pts glucorticoid users close contacts of those with active tb abnormal calcifications on cxr organ transplant reicpients
203
Latent TB (PPd testing and treatment) what is considered a positive test? induration larger than 10 mm
recent immigrants (past 5 years) prisoners healthcare workers close contacts of someone with tb hematologic malignancy, alcoholics, dm
204
Latent TB (PPd testing and treatment) 2 stage testing
if the pt has never had a ppd skin test before, a second test is indicated within 1 to 2 weeks if the first test is negative. this is bc the first test may be falsely negative. if the second test is negative, it means the pt is truly negative. if the second test is postiive, it means the first test was a false negative intereron gamma realsea ssay (IGRA) is a blood test equal in significance to ppd to excldue tb exposure, there is no cross reaction with bcg
205
Latent TB (PPd testing and treatment) treatment for a positive ppd or igra
after active tb has been excluded with a cxr pts hould receive 9 months of inh. a positive ppd confers a 10% lifetime risk of tb, INH results in a 90% reduction in this risk, after inh the lifterime risk goes down to 1%. the ppd test should not be repeated once it i spoitivie, use pyridoxine (B6) with inh those at hig risk such s healthcare workers should have a ppd done every year to screen for conversion omst of the risk of developing active tb lies withing the first 2 years after conversion
206
everyone with a postiive ppd test should have
cxr to exclude active disease
207
if the first ppd test is positive
a second test is not necessary
208
once the ppd is positive
it will always be positive in the future
209
previous bcg has not effect on what
ppd recommentation, if the ppd is positive the pt ust tak inh for months even if they have had bcg
210
Solitary pulmonary nodule benign
<30 no change in size nonsmoker smooth border small,<1cm normal lung no adenopathy dense, central calcification normal pet scan
211
Solitary pulmonary nodule malignant
>40 enlarging smoker spiculated (spikes) large,>2 c atelectasis yes adenopathy sparse, eccentric aclcification abrnormal pet scan
212
best initial step in all lung lesion
copare the size with old xrays
213
biopsy what lung lesions
all enlargins particularly if they are papidly enlarging
214
Solitary pulmonary nodule mangement of high probability lesions
when many of the features described under malignant in the previous table are present, the answer is to resect )remove) thelesion. when many feeatures of malignancy are present, sputum cytology, needle biopsy, and pet scanning should not be done bc a negative test is liekly a false negative. if resection is one of the choices then it is the best answer
215
Solitary pulmonary nodule management of intermediate probability lesions definition
you may notice there are some gray or inconclusive aspects of the solitary pulmonary nodule in the previous table sugh as the gap in age ranges or size, this is the definition of intermeidate probability
216
Solitary pulmonary nodule management of intermediate probability lesions sputum cytology
sputum cytology: if the question says cytoloy is poitive this is highly specific and the most appropriate next step in mamangeemnt is resection of the lesions, a negative cytology does not exclude malignancy.
217
Solitary pulmonary nodule management of intermediate probability lesions bronchosocpy or thansthoracic needle biopsy
bronchoscopy or transthoracic needle biopsy: these are the most appropriate next step in most pts with intermediate probability of malignancy. use bronchoscopy for central lesions and transthoracic biopsy for peripheral lesions
218
Solitary pulmonary nodule management of intermediate probability lesions positron emission tomgraphy
(pet scan) this is a way of telling whether the content of the lesion is malignant without a biopsy. malignancy has increased uptake of tagged glucose. the sensitivity of pet scan is 85% to 95% a negative scan points swaya from malignancy
219
Solitary pulmonary nodule management of intermediate probability lesions videa ssisted thoracic surgery (VATS)
VATS is both more senitive and more specific than all the othe rforms of testing. frozen section in the operating room allows for immediate conversion to an open thoracoscopy and lobectomy if malignacy is found
220
most common adverse effect of transthoracici biopsy
pneumothorax
221
pet is most accurate with
larger lesion >1cm
222
interstitial lung disease definition
pulmonary fibrosis is thickening of the interstitial septum of the lung between the arteriolar space and the alveolus. fibrosis interegeres with gas exchange in both direction
223
interstitial lung disease etiology
fibrosis can be idiopathic or seconary to a large number of inflammatory conditions, radiation, drugs, or from inhalations of txoins. all of the thicken the septum only some have white cell infiltrates iwth lymphocytes or neutrophils. chornic conditions lead to fibrosis and thickening. it is also known as idiopathic fibrosing interstitial pneumonia
224
Specific causes of pulmonary fibrosis
idiopathic, interstitial pulmonary fibrosis radiation drugs: bleomycin, busulfan, amiodarone, methylsergide, nitrofurantoin, cyclophosphamide
225
coal workers pneumoconioses
coal
226
silicosis
sandblasting, rock mining, tunneling
227
asbestosis
shipyard workers, pipe fitting, insulators
228
byssinosis
cotton
229
berylliosis
electronic manufacture
230
bagassosis
moldy sugar cane
231
interstitial lung disease presentation
dyspnea, worsening on exertion fine rales or crackles on examination loud p2 heart sound clubbing of the fingers
232
interstitial lung disease diagnostic tests
best initial tes is a cxr high resolution ct scan is more accurate then a cxr lung biopsy is the most accurate test echo will often show pulmonary htn and possible right vent hypertrophy pfts: restrictive lung disease with decrease of everything proportionately the FEV1, FVC, TLC, and residual volume will all be decreased, but since everything is decreased the FEV/FVC ration will be normal. the dlxo is decreased in proportion to the severity of the thickening of the alveolar septum
233
inflammatory infiltration with white cells
is reversible whereas fibrosis is irreversible
234
severe long standing interstitial fibrosis produces thick walls between alveoli that give the appearance of
honeycombing
235
interstitial lung disease treatment
most types of interstitial lung diseases are untreateable if the biopsy shows white cell or inflammatory infiltrate, prednisone should be used. of all the causes of pneumoconioses, berylliosis is the most likely to respond to treatement with steroids. this is due to the presence of granulomas, which are a sign of inflammation
236
Sarcoidosis definition/etiology
more common in african american women. it is an idiopathic inflammatory disorder predominantly of th elungs but can affect most of th ebody
237
Sarcoidosis most likely dx
look for a young african american woman with shortness of breath on exertion and occasional fine rales on lung exam, but without the wheezing of asthma. erythema nodosum and lymphadenopathy, either on examination or especially on cxr
238
Sarcoidosis also presents with
parotid gland enlargement facial palsy heart block and restrictive cardiomyopathy cns involvement iritis and uveitis
239
biopsy shows granulomas in
berrylliosis
240
answer sarcoidosis when
a cxr or ct shows hilar adenopathy in a generally healthy african american woman
241
although liver and kidney granulomas are very common on autopsy they are
rarely symptomatic
242
Sarcoidosis diagnostic tests
cxr is best initial test, hilar adenopathy is present in 95% of pts. parenchymal involvement is also present in combination with lymphadenopathy lymph node biopsy is the most accurate test. the granulomas are noncaseating elevated ace -60% hypercalciuria - 20% hypercalcemia - 5% (granulomas in sarcoidosis make vit D PFTs- restricitve lung disease (decreased FEV1, FVC, and TLC with a normal FEv1/FVC ration
243
what does bronchoalveolar lavage show in sarcoidosis
increased helper cells
244
Sarcoidosis treatment
prednisone is the clear drug of choice. few pts fail to respond. asymptomatic hilar adenopathy dies not need to be treated
245
Thromboembolic disease definition
pulmonary emboli (PE) and deep venous thrombosis (DVT) are essentially treated as a spectrum of the same disease. PE derives from DVT of the large vessels of the legs in 70% and pelvic veins in 30%, but since the risks and the treatment are the same they can be discussed at the same time
246
Thromboembolic disease etiology
DVTs arise bc of stais from immobility, surgery, trauma, joint replacement, or thrombophilia such as factor V leiden mutation and antiphospholipid syndrome. malignancy of any kind leads to DVT
247
Thromboembolic disease presentation/what is the most likely dx
look for the sudden onset of sob with clear lungs on examination and a normal cxr
248
other findings in PE
tachypnea, tachycardia, cough, and hemoptysis unilateral leg pain from DVT pleuritic chest pain from lung infection fever can arise from any cause of clot or hematoma extremely severe emboli will produce hypotension
249
most questions about pe concern
diagnostic testing and treatment
250
Thromboembolic disease diagnostic tests
there is no uncomlicated diagnostic test for a pe. cxr, ekg, and abg are athe best initial tests. angiography is the most accurate test, but can be fatal in 0.5% of cases. after doing an ABG cxr and ekg the best next step is most often a CT angiogram
251
main issues to know in pe is
what is the most common finding and what is the most common abnormality when there is an abnormality?
252
Thromboembolic disease cxr
usually normal in pe the most common abnormality is atelectasis, wedge shape infarction, pleural based lesion (hampton hump), and oligemia of one lobe (westermark sign) are much less common than simple atelectasis
253
Thromboembolic disease EKG
usually shows sinus tachycardia. the most common abnormalitiy is nonspecific St-T wave changes. only 5% will show right axid deviation, RV hypertrophy or right bundle branch block
254
Thromboembolic disease ABG
hypoxia and respiratory alkalosis (high PH and low p C02 with a normal chest xray is extremely suggestive of PE
255
the most common wont answer to choose on a pe ekg is
S1, Q3, T3
256
what do you do when you havent dont a spiral ct but initial labs and hx suggest pe
enoxaparin
257
Thromboembolic disease spiral CT scan
also called a ct angiogram, the spiral ct has become the standard of care in tems of diagnostic testing to confirm the presence of a PE after the xray, ekg, and abg are done. the specificity is excellent (over 95%). sensitive for clinically significant lots varies from 95-98%
258
Thromboembolic disease ventilation/perfusion
high probability scans have no clot (false positive) in 15%. low probability scans have a clot (false negative) in 15%. a completely normal scan essentially excludes a lcot
259
v/q is first only in
pregnancy
260
thromboembolic disease D-dimer
theis test is very sensitive (better than 97% negative predictive balue) but the specificity is poor since any cuase of clot or increased lbeeding can elevate the d-dimer level. a negative test excludes a clot, but a positive test doesnt mean anything
261
thromboembolic disease lower extremity doppler study:
if the le doppler is positive no further testing is needed. only 70% of pes originated in the legs, so it will miss 30% of cases. you do not need a spiral Ct or v/q scan to confirm a pe if there is a clot in the legs bc they will not change therapy. the pt will still need heparin and 6 months of warfarin.
262
Spiral Ct (negative)>v/q or le doppler (negatige)>
withhold therapy with heparin
263
thromboembolic disease angiography
the most accurate test with nearly 100% specificity and a falst negative rate under 1%. there is a 0.5% mortality, which is high if you consider the tens of thousands of tests a year that would need to be done to exclude PE in all cases.
264
adverse effects of angiography
allergy renal toxicity and death
265
d dimer is the answer for pe when
the pretest probability of pe is low and you need a simple noninvasive test to exclude thromboembolic disease
266
the cxr must be normal for what in pe
the v/q scan to have any degree of accuracy. do a spiral ct if the cxr is abnormal
267
le dopplers are a good test if what in pe
if the v/q and spiral ct do not give a clear dx
268
when testing for pe angiography
is rarely done
269
thromboembolic disease treatment
heprain is the best initial therapy warfarin should be started at the same time a sthe heparin in order to achieve an therapeutic inr of 2-3 times normal as quickly as possible fondaparinux is an alternative to heparin rivaroxaban and dabigatran or oral agents taht do no require inrmonitoring and can be used for the treatment of pe. they reach a therapeutic effect in several hours, instead of several days like wargarin. they are used after initial therapy with low molecular weight heprarin
270
when do you use an ivc filter in thromboembolic disease
ci to the use of anticoagulants (melena, CNS bleeding) recurrent emboli while on heparin or fully therapeutic warfarin (INR of 2-3) right ventricular (RV) dysfunction with an enlarged RV on echo. in this case, disease is so severe that an IVC filter is placed bc the next emoblus, even if seemingly small, could be fatal.
271
when are thrombolytics the right answer in thromboembolic disease?
hemodynamically unstable pts (e.g. hypotension systolic <90 and tachy) acute rv dysfunction
272
what is the time limit for thrombolytics in pe
there is none, unlike iwth mi
273
when are direct acting thrombin inhibitors (argatroban, lepirudin) the answer in thromboembolic disease?
heparin induced thrombocytopenia (fondaparinux is an inhibitor that is an alternative to heparin)
274
fondaparinux can be used if there is
HIT
275
when is aspirin the answer in thromboembolic disease?
never
276
virchows triad
stasis of blood flow immobilitty CHF recent surgery endothelial injury trauma surgery recent fx hypercoagulability factor Vleidin mutation any alignancy leads to DVT
277
Pulmonary HTN definition
systolid BP>25mmhg, diastolic BP>8mmhg. any chornic lung disease leads to back pressure into the pulmonary artery obstructing flow out of the right side of the heart
278
Pulmonary HTN etiology
by definition is idiopathic. any form of chornic lung disease such as COPD or fibrosis elevates the pulmonary artery pressure. hypoxemia causes vasoconstriction of the pulmonary artery pressure. hypoxemia causes vasoconstriction of the pulmonary artery circulation as a normal reflex in the lungs to shunt blood sway from areas of the lung it considers to have poor oxygenation. this is why hypoxia leads to pulmonary htn and pulmonary htn results in more hypoxemia
279
Pulmonary HTN presentation
dypsnea and fatigue syncope chest pain wide splitting of S2 from pulmonary htn with a loud p2 or tricuspid and pulmonary valve insufficiency
280
it is impossible to know that pumonary htn is causing the dyspnea w/o
tests
281
Pulmonary HTN diagnostic tests
cxr and ct right heart or swan-ganz catheter ekg echocardiography v/q scanning identifies chronic pe as the cause of pulmonary htn cbc shows polycythemia from chronic hypoxia
282
Pulmonary HTN cxr and ct
best initial tests showing dilation of the proximal pulmonary arteries awith narrowing or pruning of distal vessels
283
Pulmonary HTN right heart or swan ganz catheter
most accurate test and the most precise method to measure pressures by vascular reactivity
284
Pulmonary HTN ekg
right axis deviation, right atrial and ventricular hypertrophy
285
Pulmonary HTN echocardiography
RA and Rv hypertrophy. doppler estimates pulmonary arter (PA) pressure
286
Pulmonary HTN treatment
1. correct the underlying cause when one is clear 2. idiopathic disease istreated, if there is vascular reactivity, with: prostacytin analogues (PA vasodilators): epoprotenol, treprostinil, iloprost, beraprost) endothelin antagonsits: bosentan, ambrisentan phosphodiesterase inhibitors: sildenaffil 3. oxygen slows progression, particularaly with COPD
287
wha tis the only think that can cure idiopathic pulmonary htn
lung transplantation
288
Obstructive sleep apnea etiology
obesity is most common cause
289
Obstructive sleep apnea symptoms
daytime somnolence snoring ha impaired memory and judgement depression htn erectile dysfunction bull neck
290
Obstructive sleep apnea testing
most accurate test is polysomnography (sleep study) which shows multiple episodes of apnea. arrhythmias and erytrhocytosis are common
291
with increased bicarb sleep apnea becomes
obesity/hypoventilation syndrome
292
Obstructive sleep apnea treatment
weigth loss and avoidance of alcohol continuous positive airway pressure (CPAP) surgical widening of the airway (uvuloplatopharyngoplasty) if this fails avoid use of sedatives oral appliances to keep the tongue out of the way
293
Acute Respiratory distress Syndrome definition
respiratory failure from over-whelming lung injury or systemic diseaseleading to severe hypoxia with a cxr suggestive of congestive failure but normal cardiac hemodynamic measurements. ARDS decreases surfactant and makes the lung cells leaky so that the alveoli fill up with fluid
294
Acute Respiratory distress Syndrome etiology
idiopathic a large number of illnesses and injuries are associated with alveolar epithelial cell and capillary endothelial cell damage sepsis or aspiration lung contusion/trauma near-drowning burns or pancreatitis
295
Acute Respiratory distress Syndrome diagnostic tests
the cxr shows b/l infiltrates that quickly become confluent (white out). air bronchograms are common ARDs is defines as haveing a pO2/FIO2 ratio below 300. the TIO2 is expressed as a decimal, so room air with 21% oxygen would be 0.21. if the pO2 is 105 on room air (21% oxygen or 0.21), then the ration of Po2/FIO2 is 500 (105/.21). if the pO2 (as measured on ABG) is 70 while breathing 50% oxygen, the ration is 70/0.5 or 140 ards is associated with normal findings on right heart catheterization, the wedge pressure is normal, but dont have to measure
296
pO2/FIO2<300
ards
297
pO2/FIO2<200
moderatly severe ards
298
pO2/FIO2<100
severe
299
ARDS treatment
low tidal volume mechanical ventilation is the best support while wiating to see if the lungs will recover. use 6 ml per kg of tidal volume. steroids are not clearly beneficial in most cases. they may help in late stage disease in which pulmonary fibrosis develops pee is used when the pt is undergoing mechanica ventilation to try to decrease the FIO2. level sof fio2 above 50% are toxic tot eh lungs. maintain the plateau pressure of less than 30cm of water. this is measured on the ventilator
300
no treatment is proven to reverse
areds, dont gorget to treat the underlying cause