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OMS III > IM Pulm > Flashcards

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
Q

never use LABA

A

first or alone

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26
Q

zafirlukast is hepatotoxic and has been associated with

A

churg-strausss syndrome

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27
Q

adverse effects of inhale dsteroids are

A

dysphonia and oral candidiasis

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28
Q

adverse effects of systemic corticosteroids

A

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

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29
Q

high dose inhaled steroids rarely lead to the adverse effects associated with

A

prednisone

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30
Q

Antiocholinergics in asthma

A

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.

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31
Q

influenza and pnuemococcal vaccine are given in all

A

asthma pts

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32
Q

what is the best indication of the severity of his asthma

A

respiratory rate, if during an acute exacerbation

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33
Q

The severity of an asthma exacerbation is quantified by:

A

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

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34
Q

asthma predisposed to

A

pneumothorax

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35
Q

treatment for acute asthma exacerbation

A

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

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36
Q

Magnesium helps relieve

A

bronchospasm, magnesium is used only in acute, severe asthma exacerbation not responsive to several rounds of albuterol while waiting for steroids to take effect

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37
Q

the following are not effective in acute exacerbations:

A 
theophylline
cromolyn and nedocromil (best with exrinsic allergies like hay fever)
leukotriene modifiers
omalizumab
salmeterol
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38
Q

if a pt having an acute exacerbation does not respond to oxygen, albuterol, and steroids or develops…

A

respiratory acidosis (increased pco2), the pt may have to undergo endotracheal intubation for mechanical ventilation. these pts should be placed in the icu

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39
Q

COPD

definition

A

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.

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40
Q

COPD

etiology

A

tobacco smoking leads to almost all copd. tobacco destroys elastin fibers

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41
Q

COPD in a young nonsmoker

A

alpha-1 antitrypsin deficiency

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42
Q

COPD

presentation

A

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

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43
Q

COPD

best initial test

A

cxr:

increased ap diameter

air trapping and flattened diaphragm

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44
Q

COPD

most accurate diagnostic test

A

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

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45
Q

COPD

reversibility with inhaled bronchodilators

A

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

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46
Q

full reversibility in response to bronchodilators is defined as greater than

A

12% increase and 200 ml increase in FEV1

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47
Q

COPD

reversibility with inhaled bronchodilators

arterial blood gas

A

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

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48
Q

COPD

reversibility with inhaled bronchodilators

CBC:

A

may have an increase in hematocrit from chronic hypoxia

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49
Q

COPD

reversibility with inhaled bronchodilators

EKG:

A

R atrial hypertrophy and R ventricular hypertrophy

atrial fibrillation or multifocal atrial tachycardia (MAT)

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50
Q

COPD

reversibility with inhaled bronchodilators

echocardiography

A

R atrial and R ventricular hypertrophy

pulmonary htn

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51
Q

COPD

treatment

improves mortality and delays progression of disease

A

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

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52
Q

COPD

treatment

definitely improves symptoms (but does not decrease disease progression or mortality)

A

saba (albuterol)

anticholinergic agents: tiotropium, ipratropium

steroids

laba (slameterol)

pulmonary rehabilitation

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53
Q

asthmatics not controlled with albuterol

A

give inhaled steroid

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54
Q

COPD not controlled with albuterol

A

give an anticholinergic (tiotropium) or inhaled steroids

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55
Q

COPD possible improves sx

A

theophylline

lung volume reduction surgery

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56
Q

COPD no benefit

A

cromolyn

leukotriene modifiers (montelukast)

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57
Q

with COPD when all medical therapy is insufficient the answer is

A

refer to transplantation

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58
Q

inhaled anticholinergics are most effective in

A

COPD

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59
Q

O2 use

COPD

A

pO2

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60
Q

treatment of acute exacerbations of chronic bronchitis

A

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

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61
Q

AECB treatment is identical to

A

asthma treatment but with less proven benefit

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62
Q

treatment of acute exacerbations of chronic bronchitis

Most effective

A

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

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63
Q

treatment of acute exacerbations of chronic bronchitis

second line agents

A

doxy

bactrim

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64
Q

Criteria for oxygen use in COPD

A

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%

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65
Q

although the hypoxic drive elimination concept

A

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

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66
Q

the idea of eliminatign hypoxic drive

A

is not accurate. dyspneic, hypoxic patients with COPD must get oxygen

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67
Q

Bronchiectasis

definition

A

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

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68
Q

Bronchiectasis

etiology

A

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
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69
Q

Bronchiectasis

Presentation/what is the most likely diagnosis

A

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
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70
Q

it is impossible to diagnose Bronchiectasis w/out

A

an imagin study of the lungs such as a CT scan

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71
Q

Bronchiectasis

best initial test

A

a cxr that shows dilated thickened bronchi, some times with tram-tracks which is the thickening of the bronchi

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72
Q

Bronchiectasis

most accurate test

A

high-resolution CT

sputum culture is the only way to determine the specific bacterial etiology of the recurrent episodes of infection

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73
Q

Bronchiectasis

treatment

A
  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
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74
Q

Allergic Bronchopulmonary Aspergillosis (ABPA)

definition/etiology

A

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

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75
Q

Allergic Bronchopulmonary Aspergillosis (ABPA)

what is the most likely diagnosis

A

look for an asthmatic pt with recurrent episodes of brown-flecked sputum and transient infiltrated on cxr

cough, wheezing, hemoptysis, and sometiems bronchiectasis occur

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76
Q

Allergic Bronchopulmonary Aspergillosis (ABPA)

diagnostic tests

A

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

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77
Q

Allergic Bronchopulmonary Aspergillosis (ABPA)

treatment

A
  1. oral steroids (prednisone) for severe cases; inhaled steroids are not effective for ABPA
  2. itraconazole orally for recurrent episodes
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78
Q

an inhaler cannot deliver a high enough dose of steroids to be effective in

A

Allergic Bronchopulmonary Aspergillosis (ABPA)

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79
Q

Cystic fibrosis

etiology

A

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

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80
Q

neutrophils in cf dump ton of

A

dna into airway secretions, clogging them up

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81
Q

lung disease accounts for 95% of deaths in

A

CF

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82
Q

Cystic fibrosis

presentation

A

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

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83
Q

Cystic fibrosis GI involvement

A

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

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84
Q

Cystic fibrosis

gu involvement

A

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

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85
Q

Cystic fibrosis

diagnostic tests

A

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

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86
Q

Cystic fibrosis

additional diagnostic tests

A 
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

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87
Q

Cystic fibrosis

sputum culture

A

nontypable h flu
psuedomonas auruginosa
staph aureus
burkholderia cepacia

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88
Q

Cystic fibrosis

treatment

A
  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
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89
Q

community-acquired pnuemonia

definition

A

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

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90
Q

community-acquired pnuemonia

etiology

A

strep pneumo is the most common cause of CAP. netiher the environemental reservoir of s pneumo nor its method of acquistion is known

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91
Q

CAP and COPD

A

h flue

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92
Q

CAP and recent viral infection

A

s aureus

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93
Q

CAP and alcoholism and diabetes

A

klebsiella pneumonia

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94
Q

CAP and poor dentition and aspiration

A

anaerobes

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95
Q

CAP and young healthy pts

A

mycoplasma pnueomoniae

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96
Q

CAP and hoarseness

A

chlamydophilia pnuemoniae

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97
Q

CAP and contaminated water sources air con and ventilation systems

A

legionella

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98
Q

CAP and birds

A

chlamydia psittaci

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99
Q

CAP and anials at the time of giving birth vets and farmers

A

coxiella burnettii

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100
Q

CAP

Presentation

A 
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
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101
Q

CAP

severe infection vital signs

A

tachycardia
hypotension
tachypnea
mental status

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102
Q

chest pain from pneumonia

A

is often pleuritic, changing with respiration

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103
Q

dyspnea, high fever, and an abnormal cxr distinguish

A

pneumonia from bronchitis

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104
Q

hemoptysis from necrotizing disease “currant jelly” sputum

A

klebsiella pneumonia

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105
Q

foul-smelling sputum, rotten eggs

A

anaerobes

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106
Q

dry cough, rarely severe, bullous myringitis

A

mycoplasma pneumoniae

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107
Q

gi symptoms (pain diarrhea) or CNS sx such as ha and confusion

A

legionella

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108
Q

aids with less than 200 CD4 cells

A

pneumocystis

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109
Q

Infections with a dry or nonproductive cough

A 
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

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110
Q

specific sputum colors

A

are useless in determining etiology

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111
Q

CAP

diagnostic tests

A

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

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112
Q

CAP

CXR

A

b/l interstitial infiltrates are seen with:

mycoplasma
viruses 
coxiella
pneumocystis
chlamydia

same organisms as nonproductive cough, xrays lag behind clinical findings

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113
Q

CAP

the first cxr can be negative in at least

A

10-20% of cases or pneumonia

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114
Q

CAP

sputum gram stain is adequate if there are

A

more than 25 white blood cells and fewre than 10 epithelial cells

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115
Q

CAP

ct and mri

A

show greater definition of abnormlalities found on a chest xray but will still not be able to determine a specific microbiologic etiology

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116
Q

with infections dieases the radiology test

A

is never the most accurate test

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117
Q

CAP

blood cultures

A

are positive in 5-10% of cases, usually with s pneumo

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118
Q

CAP

tests done in severe disease with an unclear etiology or those not responding to treatment

A

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

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119
Q

it is impossible to make a specific diagnosis of the cause of pneumonia based on

A

hx and physical

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120
Q

new large effusions secondary to pneumonia should be

A

tapped

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121
Q

Mycoplasma pneumoniae

diagnostic test

A

pcr
cold agglutins
serology
special culture media

122
Q

chlamydophila pneumoniae

diagnostic test

A

rising serologic titers

123
Q

legionella

diagnostic test

A

urine antigen

culture on charcoal yeast extract

124
Q

chlamydia psittaci

diagnostic test

A

rising serologic titers

125
Q

coxiella burnetti

diagnostic test

A

rising serologic titers

126
Q

pneumocystis jiroveci (PCP)

diagnostic test

A

brochoalveolar lavage (BAL)

127
Q

mycoplasma and chlamydophila are rarely confirmed

A

bc they are simply treated empirically

128
Q

CAP

it is the severity of disease not the etiology that drives

A

initial therapy

129
Q

CAP

outpatient treatment

A

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
Q

CAP

inpatient treatment

A

Resp fqs: levo or moxifloxaxin

or

ceftriaxone and azithromycin

131
Q

hypoxia and hypotension as single factors are a reason to

A

hospitalize a pt

132
Q

CAP

reasons to hospitalize

A

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
Q

notic that the cxr does not guide what in CAP

A

admission

134
Q

xray cannot tell severity of

A

hypoxia

135
Q

CAP

Curb65=

A

admission

Confusion
Uremia
Resp distress
BP low
Age>65
136
Q

infected pleural effusion or empyemawill respond most rapidly to

A

drainage by chest tube or thoracostomy

137
Q

exudate VS transudate

A

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
Q

CURB 65

0-1 point

A

send home

139
Q

CURB 65

> or equal to 2 points

A

admission

140
Q

pleural effusion with a large meniscus sign

A

only a fluid sample from thoracentesis can determine the specific cause

141
Q

effusion should be freely

A

mobile and form a layer when the pt lies on he rside

142
Q

hydropnuemothorax is both

A

abnormal air and lfuid in the pleural space, must drain with a chest tube

143
Q

consultation is almost never

A

the right answer

144
Q

pneumococcal vaccination

A

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
Q

other reasons to vaccinate against pnuemococcal

A

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
Q

do healthcare workers need pneumococcal vaccine?

A

no

147
Q

Healthcare Associated or hospital acquired Pneumonia

A

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
Q

piperacillin and ticarcillin are always used in

A

combination with a betalactamas inhibitor such as tazobactam or clavulanic acid

149
Q

Ventilator Associated Pneumonia (VAP)

definition

A

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
Q

Ventilator Associated Pneumonia

what is the most likely diagnosis

A

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
Q

Ventilator Associated Pneumonia

diagnostic tests

A

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
Q

Ventilator Associated Pneumonia

tracheal aspirate

A

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
Q

Ventilator Associated Pneumonia

bronchoalveolar lavage (BAL)

A

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
Q

Ventilator Associated Pneumonia

protected brush specimen

A

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
Q

Ventilator Associated Pneumonia

video assisted thoracoscopy (VAT)

A

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
Q

Ventilator Associated Pneumonia

open lung biopsy:

A

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
Q

subcutaneous emphysema

A

air abnormally leaking into the soft tissue of the chest wall, may be caused by chest tube placement

158
Q

Ventilator Associated Pneumonia

treatment

A

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
Q

culturing an et tube is like culturing urine with a foley catheter in place

A

it will always grow something bc of colonization

160
Q

no daptomycin for

A

lungs!!

daptomycin is inactivated by surfactant

161
Q

change the initial therapy for VAP

A

if a specific etiology is identified

162
Q

imipenem

A

can cause seizures

is excreted thorugh the kidneys

renal failure causes a rise in impienem levels leading to toxicity

163
Q

carbamazepine is no more effective

A

than phenytoin at stopping seizures

caused by imipenem?

164
Q

lung abscess

etiology

A

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
Q

aspiration pneumonia happens in the upper lobe

A

when lying flat

166
Q

lung abscess

what is the most likely diagnosis

A

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
Q

lung abscess

diagnostic test

A

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
Q

lung abscess

treatment

A

clindamycin or penicillin are best to cover a lung abscess

169
Q

sputum culture is wrong answer for diagnosing a

A

lung abscess

all sputum has anaerobes from mouth flora

170
Q

chest cavity consistent with an abscess

A

thick wall and an air fluid level

171
Q

Pneumocystis Pneumonia

etiology

A

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
Q

Pneumocystis Pneumonia

what is the most likely diagnosis

A

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
Q

Pneumocystis Pneumonia

diagnostic testing

A

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
Q

a normal LDH means you should not answer what as the omst likely diagnosis

A

pcp

175
Q

you cannot distinguish pcp from mycoplamsa chlamydophila or viruses by xray alon. however in hiv, pcp is most likely with

A

interstitial infiltrates

176
Q

Pneumocystis Pneumonia

treatement

A

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
Q

Pneumocystis Pneumonia

grading

A

severe - pO2 less than 70 or an A-a gradient above 35

mild - mild hypoxia

178
Q

adverse effects of Bactrim

A

rash

bone marrow suppression

179
Q

if pt has g6pd deficiency and Pneumocystis Pneumonia give what instead of clindamycin and primaquine ifcant give bactrim

A

pentamidine

180
Q

antiretrovirals during acute opportunistic infection

A

no they can exacerbate it

181
Q

Pneumocystis Pneumonia prophylaxis

A

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
Q

always choose therapy based on

A

efficacy not adverse effects

183
Q

dapsone is ci in those with

A

g6pd

184
Q

azithromycin for prophylaxis in what for aids

A

atypical mycobacteria when cd4 is below 50u/l

185
Q

TB

overview

A

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
Q

almost all pts with tb have one or more risk factors like:

A

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
Q

TB

presentation/ what is the most likely diagnosis

A

look for a person wtih one of the previously listed risk factors presenting with fever, cough, sputum, weight loss, hemoptysis, and night sweats

188
Q

you cannot answer tb without

A

clear risk factor

cavity on cxr

or a positive smear

189
Q

TB

diagnostic tests

A

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
Q

ppd skin testing in TB

A

never the best test for TB in a symptomatic pt

191
Q

TB treatment

A 
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
Q

when is treatment for TB extended to longer than 6 months

A

osteomyelitis
miliary tb
meningitis
pregnancy or any other time pyrazinamide is not used

193
Q

TB

toxicity of therapy

A

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
Q

Rifampin

toxicity -

management -

A

toxicity - red color to body secretions

management - none, benign finding

195
Q

isoniazid

toxicity -

management -

A

toxicity - peripheral neuropathy

management - use pyridoxine to prevent

196
Q

Pyrazinamide

toxicity -

management -

A

toxicity - hyperuricemia

management - no treatment unless symptomatic

197
Q

Ehtambutol

toxicity -

management -

A

toxicity - optic neuritis/color vision

management - decrese doe in renal failure

198
Q

TB

use of steroids

A

glucocorticoids decrease the risk of contstictive pericarditis in those with pericardial involvement. they also decrease neurologic compication in TB meningitis

199
Q

what should pregnant pts not receive with TB

A

pyrazinamide or streptomycin

200
Q

Latent TB (PPd testing and treatment)

indications for PPd testing

A

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
Q

Latent TB (PPd testing and treatment)

what is considered a positive test?

A

only induration is counted towards a positive test, erythema is irrelevant

202
Q

Latent TB (PPd testing and treatment)

what is considered a positive test?

induration larger than 5 mm

A

hiv pts

glucorticoid users

close contacts of those with active tb

abnormal calcifications on cxr

organ transplant reicpients

203
Q

Latent TB (PPd testing and treatment)

what is considered a positive test?

induration larger than 10 mm

A

recent immigrants (past 5 years)

prisoners

healthcare workers

close contacts of someone with tb

hematologic malignancy, alcoholics, dm

204
Q

Latent TB (PPd testing and treatment)

2 stage testing

A

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
Q

Latent TB (PPd testing and treatment)

treatment for a positive ppd or igra

A

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
Q

everyone with a postiive ppd test should have

A

cxr to exclude active disease

207
Q

if the first ppd test is positive

A

a second test is not necessary

208
Q

once the ppd is positive

A

it will always be positive in the future

209
Q

previous bcg has not effect on what

A

ppd recommentation, if the ppd is positive the pt ust tak inh for months even if they have had bcg

210
Q

Solitary pulmonary nodule

benign

A

<30

no change in size

nonsmoker

smooth border

small,<1cm

normal lung

no adenopathy

dense, central calcification

normal pet scan

211
Q

Solitary pulmonary nodule

malignant

A

> 40

enlarging

smoker

spiculated (spikes)

large,>2 c

atelectasis

yes adenopathy

sparse, eccentric aclcification

abrnormal pet scan

212
Q

best initial step in all lung lesion

A

copare the size with old xrays

213
Q

biopsy what lung lesions

A

all enlargins

particularly if they are papidly enlarging

214
Q

Solitary pulmonary nodule

mangement of high probability lesions

A

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
Q

Solitary pulmonary nodule

management of intermediate probability lesions

definition

A

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
Q

Solitary pulmonary nodule

management of intermediate probability lesions

sputum cytology

A

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
Q

Solitary pulmonary nodule

management of intermediate probability lesions

bronchosocpy or thansthoracic needle biopsy

A

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
Q

Solitary pulmonary nodule

management of intermediate probability lesions

positron emission tomgraphy

A

(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
Q

Solitary pulmonary nodule

management of intermediate probability lesions

videa ssisted thoracic surgery (VATS)

A

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
Q

most common adverse effect of transthoracici biopsy

A

pneumothorax

221
Q

pet is most accurate with

A

larger lesion >1cm

222
Q

interstitial lung disease

definition

A

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
Q

interstitial lung disease

etiology

A

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
Q

Specific causes of pulmonary fibrosis

A

idiopathic, interstitial pulmonary fibrosis

radiation

drugs: bleomycin, busulfan, amiodarone, methylsergide, nitrofurantoin, cyclophosphamide

225
Q

coal workers pneumoconioses

A

coal

226
Q

silicosis

A

sandblasting, rock mining, tunneling

227
Q

asbestosis

A

shipyard workers, pipe fitting, insulators

228
Q

byssinosis

A

cotton

229
Q

berylliosis

A

electronic manufacture

230
Q

bagassosis

A

moldy sugar cane

231
Q

interstitial lung disease

presentation

A

dyspnea, worsening on exertion

fine rales or crackles on examination

loud p2 heart sound

clubbing of the fingers

232
Q

interstitial lung disease

diagnostic tests

A

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
Q

inflammatory infiltration with white cells

A

is reversible whereas fibrosis is irreversible

234
Q

severe long standing interstitial fibrosis produces thick walls between alveoli that give the appearance of

A

honeycombing

235
Q

interstitial lung disease

treatment

A

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
Q

Sarcoidosis

definition/etiology

A

more common in african american women. it is an idiopathic inflammatory disorder predominantly of th elungs but can affect most of th ebody

237
Q

Sarcoidosis

most likely dx

A

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
Q

Sarcoidosis

also presents with

A

parotid gland enlargement

facial palsy

heart block and restrictive cardiomyopathy

cns involvement

iritis and uveitis

239
Q

biopsy shows granulomas in

A

berrylliosis

240
Q

answer sarcoidosis when

A

a cxr or ct shows hilar adenopathy in a generally healthy african american woman

241
Q

although liver and kidney granulomas are very common on autopsy they are

A

rarely symptomatic

242
Q

Sarcoidosis

diagnostic tests

A

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
Q

what does bronchoalveolar lavage show in sarcoidosis

A

increased helper cells

244
Q

Sarcoidosis

treatment

A

prednisone is the clear drug of choice. few pts fail to respond.

asymptomatic hilar adenopathy dies not need to be treated

245
Q

Thromboembolic disease

definition

A

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
Q

Thromboembolic disease

etiology

A

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
Q

Thromboembolic disease

presentation/what is the most likely dx

A

look for the sudden onset of sob with clear lungs on examination and a normal cxr

248
Q

other findings in PE

A

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
Q

most questions about pe concern

A

diagnostic testing and treatment

250
Q

Thromboembolic disease

diagnostic tests

A

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
Q

main issues to know in pe is

A

what is the most common finding

and

what is the most common abnormality when there is an abnormality?

252
Q

Thromboembolic disease

cxr

A

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
Q

Thromboembolic disease

EKG

A

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
Q

Thromboembolic disease

ABG

A

hypoxia and respiratory alkalosis (high PH and low p C02 with a normal chest xray is extremely suggestive of PE

255
Q

the most common wont answer to choose on a pe ekg is

A

S1, Q3, T3

256
Q

what do you do when you havent dont a spiral ct but initial labs and hx suggest pe

A

enoxaparin

257
Q

Thromboembolic disease

spiral CT scan

A

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
Q

Thromboembolic disease

ventilation/perfusion

A

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
Q

v/q is first only in

A

pregnancy

260
Q

thromboembolic disease

D-dimer

A

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
Q

thromboembolic disease

lower extremity doppler study:

A

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
Q

Spiral Ct (negative)>v/q or le doppler (negatige)>

A

withhold therapy with heparin

263
Q

thromboembolic disease

angiography

A

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
Q

adverse effects of angiography

A

allergy renal toxicity and death

265
Q

d dimer is the answer for pe when

A

the pretest probability of pe is low and you need a simple noninvasive test to exclude thromboembolic disease

266
Q

the cxr must be normal for what in pe

A

the v/q scan to have any degree of accuracy. do a spiral ct if the cxr is abnormal

267
Q

le dopplers are a good test if what in pe

A

if the v/q and spiral ct do not give a clear dx

268
Q

when testing for pe angiography

A

is rarely done

269
Q

thromboembolic disease

treatment

A

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
Q

when do you use an ivc filter in thromboembolic disease

A

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
Q

when are thrombolytics the right answer in thromboembolic disease?

A

hemodynamically unstable pts (e.g. hypotension systolic <90 and tachy)

acute rv dysfunction

272
Q

what is the time limit for thrombolytics in pe

A

there is none, unlike iwth mi

273
Q

when are direct acting thrombin inhibitors (argatroban, lepirudin) the answer in thromboembolic disease?

A

heparin induced thrombocytopenia (fondaparinux is an inhibitor that is an alternative to heparin)

274
Q

fondaparinux can be used if there is

A

HIT

275
Q

when is aspirin the answer in thromboembolic disease?

A

never

276
Q

virchows triad

A

stasis of blood flow
immobilitty
CHF
recent surgery

endothelial injury
trauma
surgery
recent fx

hypercoagulability
factor Vleidin mutation
any alignancy leads to DVT

277
Q

Pulmonary HTN

definition

A

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
Q

Pulmonary HTN

etiology

A

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
Q

Pulmonary HTN

presentation

A

dypsnea and fatigue

syncope

chest pain

wide splitting of S2 from pulmonary htn with a loud p2 or tricuspid and pulmonary valve insufficiency

280
Q

it is impossible to know that pumonary htn is causing the dyspnea w/o

A

tests

281
Q

Pulmonary HTN

diagnostic tests

A

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
Q

Pulmonary HTN

cxr and ct

A

best initial tests showing dilation of the proximal pulmonary arteries awith narrowing or pruning of distal vessels

283
Q

Pulmonary HTN

right heart or swan ganz catheter

A

most accurate test and the most precise method to measure pressures by vascular reactivity

284
Q

Pulmonary HTN

ekg

A

right axis deviation, right atrial and ventricular hypertrophy

285
Q

Pulmonary HTN

echocardiography

A

RA and Rv hypertrophy. doppler estimates pulmonary arter (PA) pressure

286
Q

Pulmonary HTN

treatment

A
  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
Q

wha tis the only think that can cure idiopathic pulmonary htn

A

lung transplantation

288
Q

Obstructive sleep apnea

etiology

A

obesity is most common cause

289
Q

Obstructive sleep apnea

symptoms

A

daytime somnolence

snoring

ha

impaired memory and judgement

depression

htn

erectile dysfunction

bull neck

290
Q

Obstructive sleep apnea

testing

A

most accurate test is polysomnography (sleep study) which shows multiple episodes of apnea. arrhythmias and erytrhocytosis are common

291
Q

with increased bicarb sleep apnea becomes

A

obesity/hypoventilation syndrome

292
Q

Obstructive sleep apnea

treatment

A

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
Q

Acute Respiratory distress Syndrome

definition

A

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
Q

Acute Respiratory distress Syndrome

etiology

A

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
Q

Acute Respiratory distress Syndrome

diagnostic tests

A

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
Q

pO2/FIO2<300

A

ards

297
Q

pO2/FIO2<200

A

moderatly severe ards

298
Q

pO2/FIO2<100

A

severe

299
Q

ARDS

treatment

A

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
Q

no treatment is proven to reverse

A

areds, dont gorget to treat the underlying cause

OMS III (21 decks)

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