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final exam Flashcards

1
Q

abx for strep pneum, legionella, mycoplasma pneum and chlaymida

A

macrolide (azithromycin)

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2
Q

drug for DRSP, enterobacteria

A

3rd gen cephalosporin (ceftriaxone)

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3
Q

drug for staph aureus

A

vancomycin

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4
Q

drug for pseudomonas

A

cefepine

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5
Q

pneumonia outpatient

A

mycoplasma penumoniae, respiratory viruses, strep penum, chlamydia pneumoniae

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6
Q

pneumonia hospital

A

s. pneum, respiratory viruses, m. pneum, h. flu

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7
Q

pneumonia ICU

A

s. pneum, legionella, gram neg bacilli, s. aureus

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8
Q

influenza pneumonia

A

nonproductive bought, rtetroorbital headaches, myalgia; bilateral interstitial infiltrate

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9
Q

suspicion for tb

A

cough for more than two weeks and compatible epidemiological history

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10
Q

what defines ARDS?

A

acute in onset
bilateral disease present on chest radiography
hypoxemia

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11
Q

4 phases of ARDS

A

1) permeability pulmonary edema (the exudative phase)–diffuse alveolar damage (hyaline membranes)
2) proliferation and fibrosis (the fibroproliferative phase)
3) recovery of lung function
4) residual lung, physical, and neuropsychological impairment

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12
Q

pathology findings of permeability edema

A

diffuse alveolar damage (diffuse refers to all parts of the alveolus not to widespread lung injury)

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13
Q

etiology of diffuse alveolar damage

A

direct lung injury or systemic disorder (viral infection, septic shock, toxic lung damage)

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14
Q

2 phases of pathology of diffuse alveolar disease

A

1) exudation

2) regeneration/resolution or fibrosis

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15
Q

where is the initial injury in diffuse alveolar damage?

A

alveolar capillary endothelium but can also be to the alveolar epithelium (cytoplasmic blabbing in both but only really necrosis and denudation of basement membrane in the epithelial not the endothelial)

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16
Q

what do you see in the early (acute or exudative) phase of DAD?

A

edema and hyaline membranes

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17
Q

what do you see in the late (proliferative or organizing) phase of DAD?

A

occurs after 1 to 2 weeks; fibrosis predominate

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18
Q

cardinal symptoms of COPD?

A

dyspnea (primarily exertional)
cough
sputum production

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19
Q

is oxygen requirement a good indicator of COPD severity?

A

NO!!! FEV1 is how we classify

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20
Q

is COPD the only leading cause of death that has increased steadily since 1970?

A

yes

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21
Q

most common cells in COPD pathogenesis?

A

macrophage, CD8 lymphocyte and neutrophil

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22
Q

severe emphysema–> clinical picture

A

pink puffer–leaning over to improve breathing

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23
Q

clinical picture of chronic bronchitis?

A

the blue bloater (coughing up so much mucus)–blue b/c hypoxic

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24
Q

when are symptoms in asthma?

A

vary day to day and often worse at night or early am

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25
Q

major cells in asthma?

A

cd4+ (th2) and eosinophils and mast cells

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26
Q

type of breathing seen in copd?

A

dynamic hyperinflation (only way to increase minute ventilation os to the inc. the rate)

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27
Q

how do you diagnose copd?

A

NOT x-ray or CT; history and PE

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28
Q

what vaccines should copd patients get?

A

influenza and pneumococcal

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29
Q

theophylline

A

bronchodilator used less commonly; little added efficacy to other bronchodilators, narrow TI esp. in the elderly (nausea, vomiting, tremor, palpitations), requires monitoring of levels

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30
Q

when should you use glucocorticoids in copd?

A

systemic steroids should be used ONLY in acute exacerbations (can be added in addition to LABA/LAMA for pts with FEV1 < 50% predicted and repeated exacerbations)

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31
Q

when should you send pts to pulm rehab in copd?

A

when their fev1 is less than 50 and they are symptomatic; may consider in pts who are symptomatic and exercise-limited even if their fev1 is more than 50

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32
Q

surgery used for copd?

A

lung volume reduction surgery–the problems suppressed lungs! (removing dead space and relieving alveolar compression and improving elastic recoil)–only can do if emphysema and focal (upper lobe)

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33
Q

acute exacerbations of copd?

A

use bpap!

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34
Q

site of obstruction in bronchial asthma

A

bronchi but also bronchioles

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35
Q

histology of bronchial asthma

A

edema and chronic inflammation in the bronchial walls, many eosinophils and excess mucus, mucus plugs contain shed epithelium and charcot-leyden crystals, goblet cell metaplasia and thickening of basement membrane, submucosal gland hypertrophy, inc. in superficial blood vessels

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36
Q

what are charcot-leyden crystals

A

found in allergic diseases (asthma)–breakdown of eosinophils

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37
Q

gross pathology of fatal asthma

A

alveolar hyperinflation and alveolar collapse (atalectasis)–thick mucous plugs in airway

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38
Q

clinical definition of chronic bronchitis

A

productive cough with a specific duration of symptoms

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39
Q

site of obstruction in chronic bronchitis

A

bronchi and bronchioles

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40
Q

histology of chronic bronchitis

A

chronic inflammation within the respiratory epithelium and submucosa; inc. goblet cells; hypertrophy/hyperplasia of bronchial submucosal glands; SQUAMOUS METAPLASIA AND/OR DYSPLASIA OF BRONCHIAL EPITHELIUM

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41
Q

mechanism of obstruction in bronchiectasis

A

1) poor airway recoil due to structural airway alterations
2) mucous plugging
3) obliteration of airways (usually distal small airways)

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42
Q

what lobes are most often affected in post-infectious bronchiectasis

A

lower lobes

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43
Q

location of widespread bronchiectasis in CF

A

upper lobe predominance but diffuse

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44
Q

site of obstruction in emphysema

A

acinus

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45
Q

mechanism of obstruction in emphysema

A

1) loss of radial traction by alteration of tethering forces on airway lumen
2) contribution of small airway disease

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46
Q

3 types of emphysema:

A

1) centrilobular (centriacinar)
2) panlobular
3) paraseptal

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47
Q

centrilobular emphysema

A

proximal acinus around bronchiole destroyed; distal alveoli spared (upper lobe predominant-smoker)
?relative lack of serum alpha1-AT to this less perfused region of the lung

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48
Q

panlobular emphysema

A

who oceans uniformly involved; predominantly lower lobe involvement (alpha-1-antitrypsinase deficiency)

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49
Q

paraseptal emphysema

A

distal acinus along interlobular septa, upper peripheral lung; associated with spontaneous pneumothorax or bulla formation in young adults

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50
Q

gender demographics of asthma

A

before puberty: men>women

after puberty: woman>men

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51
Q

3 factors of asthma

A
  1. bronchospasm
  2. hyperresponsiveness
  3. inflammation
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52
Q

2 components of asthma pathophysiology

A
  1. smooth muscle dysfunction

2. airway inflammation

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53
Q

3 stages of asthma

A
  1. rapid, spasmogenic–> mast cell-antigen reaction (direct acting mediators such as histamine, leukotrienes, and prostaglandins on the smooth muscle)
  2. late, sustained–> neutrophils
  3. subacute/chronic inflammatory–> eosinophils, monocytes
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54
Q

what sound can you hear in ILD?

A

dry velcro crackles

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55
Q

most common form of interstitial lung disease?

A

idiopathic pulmonary fibrosis (aka cryptogenic fibrosis alveolitis)

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56
Q

risk factors for idiopathic pulmonary fibrosis

A

cigarette smoking, gerd

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57
Q

hrct results with idiopathic pulmonary fibrosis

A

basal and peripheral predominance, honeycombing, minimal ground glass opacities, reticular abnormalities

58
Q

UIP pathology

A

architectural distortion, fibrosis with honeycombing, fibroblastic foci, patchy involvement, temporal heterogeneity

59
Q

conventional treatment for IPF

A

corticosteroids, azathioprine, cyclophasphamide

60
Q

new drugs for IPF

A

pirfenidone (inhibits tgf-beta induced collagen synthesis)–ppl still get worse but at a slower rate and also reduced death
nintedanib–triple tyrosine kinase inhibitor (slowed progression, didn’t show reduction in mortality)

61
Q

demographics of sarcoidosis

A

bimodal distribution with greatest peak in late 20s and then again in 50s

62
Q

hallmark on pathology of sarcoidosis

A

noncaseating granulomas

63
Q

symptoms of sarcoidosis

A

most pts are asymptomatic

64
Q

most common organ involvement of sarcoidosis

A

lung, skin, eyes, liver

65
Q

cutaneous sarcoidosis

A 
cutaneous granulomas
erythema nodosum (IC deposition)
lupus pernio (red to purple plaques on skin)
66
Q

what are the stages of sarcoidosis and what do we use to determine?

A

chest x-ray!

  1. bilateral hilar adenopathy
  2. bilateral hilar adenopathy with parenchymal infiltrates
  3. parenchymal infiltrates alone
  4. advanced fibrosis
67
Q

most common treatment for sarcoid

A

systemic corticosteroids

68
Q

how do you diagnosis usual interstitial pneumonia (UIP)

A

diagnosis of exclusion
very unusual under the age of 45 unless family history
other entities with the same histologic appearance: asbestosis, radiation injury, connective tissue disease

69
Q

histology of UIP

A

temporal heterogeneity and non-uniform patter of fibrosis that reflects chronicity; patches of normal lung and honeycomb change at the periphery
interstitium widened by dense collagen
minimal chronic interstitial inflammation
FIBROBLASTIC FOCI–suggest ongoing injury
honeycombing change is prominent at periphery and lower lobes!!!!!

70
Q

sarcoidosis histology

A

non-random distribution of granulomas–primarily along lymphatics, around bronchi and blood vessels, as well as in the interstitium

71
Q

where do you see fibrosis in sarcoid

A

upper and middle lobes (upper lobe bronchiectasis are common)

72
Q

histology seen in chronic hypersensitivity pneumonitis

A
  1. diffuse chronic interstitial inflammation, temporally uniform
  2. bronchiolar inflammation often present
    2/3 have small non-necrotizing usually interstitial granulomas
73
Q

mineral dust penumoconioses

A

can cause interstitial fibrosis and present as progressive dyspnea (asbestosis, coal worker’s pneumoconiosis, silicosis)

74
Q

what is the most common occupational disease in the world

A

silicosis

75
Q

asbestos breaks into _______

A

fibers, rather than dust

76
Q

ferruginous body

A

indigestible fibers phagocytes by macrophages and coated with iron and glycoprotein; have a translucent core
INDICATE ASBESTOS EXPOSURE NOT ASBESTOSIS!!!

77
Q

histology of asbestosis

A

initially peribronchiolar fibrosis that eventually interstitial fibrosis that is most severe in the lower lobes (b/c you are inhaling stuff)
end-stage fibrosis similar to other forms but for presence of numerous asbestos bodies

78
Q

associated lesions of asbestos exposure

A

pleural plaque on diaphragm
pleural effusion
malignant mesothelioma
bronchogenic carcioma

79
Q

definition of asbestos

A

interstitial fibrosis with the identification of numerous asbestos bodies

80
Q

bronchoalveolar lavage in sarcoidosis

A

inc. in activated T cells, cd4 cells, immunoglobulins, and igg-secreting cells, reduced number of cd8 cells, and an elevated Cd4-cd8 count!

81
Q

copd inflammation is mediated by ______

A

NEUTROPHILS (cd8+ t cells and macrophages)

82
Q

asthma inflammation is mediated by

A

HELPER T2 CELLS AND EOSINOPHILS

83
Q

anticholinergics vs. beta agonists

what works best in what

A

copd: anticholinergics
asthma: beta agonists are better

84
Q

two basic ways to promote airway smooth muscle relaxation and decrease airway constriction

A
  1. receptor blockade promotes relaxation: cysLTR and muscarinic receptor antagonists (inhibition of receptor that is coupled to a G protein that increases cytosolic calcium and promotes contraction)
  2. receptor stimulation promotes ASM relaxation: cAMP or cGMP (beta-2 agonists)–> activate PKA
85
Q

anticholinergic of choice in copd

A

ipratroprium

86
Q

methylxanthines

A

theophylline–causes bronchodilation by inhibiting phosphodiesterase thereby dec. cAMP hydrolysis

87
Q

albuterol

A

short acting beta2 agonist

88
Q

long acting beta2 agonists

A

indacaterol, salmeterol, formoterol

89
Q

anticholinergic does or does noT dec. bronchial hyper responsiveness over time?

A

DOES NOT

90
Q

what do leukotrienes do?

A

potent inflammatory mediators that promote smooth muscle contraction, induce vasopermeability, and enhance mucus secretion while decreasing mucus clearance and promoting eosinophil chemotaxis (leukotriene modifiers–have both bronchodilator and limited anti-inflammatory because they act on both beta receptor and also cysltrs)–but they are only really effective in 20-30% of pts

91
Q

what are the most potent of the inhaled steroids?

A

fluticasone and budesonide

92
Q

what is the best combination for copd?

A

ipratroprium (anticholinergic) and theophylline (phosphodiesterase inhibitor)

93
Q

what is the only therapy proven to prolong life in copd?

A

o2 therapy!

94
Q

most common pathogens in cf

A

s. aureus, p. aeruginosa, mrsa

95
Q

what is the new drug for CF called

A

kalydeco

96
Q

timing for acute sinusitis

A

less than 4 weeks

97
Q

timing for chronic sinusitis

A

greater than 12 weeks

98
Q

what is the first line tx for treating acute sinusitis

A

amoxicillin

99
Q

microbiology of acute sinusitis

A

strep pneumo, h. influ, staph aureus

100
Q

histopath for acute vs. chronic sinusitis

A

acute: exudative process, associated with hemorrhage and necrosis; NEUTROPHILS!!!
chronic: proliferative process, fibrosis of lamina propria, LYMPHOCYTES, PLASMA CELLS, EOSINOPHILS!!

101
Q

complication of ethmoid sinusitis

A

orbital extension–> periorbital cellulitis, orbital cellulitis, sub-periosteal abscess, orbital abscess, cavernous sinus thrombosis

102
Q

complication of frontal sinus

A 
cranial extension (meningitis, epidural abscess, subdural abscess, frontal lobe abscess)--> POTT's puffy tumor
inferior extension--orbital infection similar to ethmoid disease
103
Q

complication of sphenoid sinus

A

cavernous sinus extension: visual loss, cranial neuropathies, ACUTE SPHENOID SINUSITIS IS AN EMERGENCY

104
Q

protein e6 hpv

A

degrades tumor supressor gene p53

105
Q

protein e7

A

causes loss of the tumor suppressor protein rb and overexertion of p16

106
Q

monoclonal antibody against RSV

A

palivizumab

107
Q

virchow’s triad

A

1) vascular injury
2) venous stasis
3) hypercoagulability

108
Q

presence of PAH on PE?

A 
loud p2
rv lift
systolic murmur (TR)
diastolic murmur (PR)
RV S4
109
Q

presence of RV failure on PE?

A 
JVD with V wave
RV S3
hepatomegaly
edema 
ascites
110
Q

what does S3 mean?

A

heart failure!!!

111
Q

general medical management for PAH?

A

oxygen, diuretics, digoxin, warfarin and lifestyle adjustments

112
Q

what factors have increased activity in PAH?

A

endothelin

113
Q

what factors have reduced activity in PAH?

A

no and prostacyclin

114
Q

drug name for the target of the egf pathway

A

erlotinib

geftinib

115
Q

fusion gene that has been identified in non-small cell lung cancer

A

eml4/alk translocation (seen previously only lymphoma)
the normally silent anaplastic lymphoma kinase (ALK)–a tyrosine kinase is driven by the fusion with the eml4 gene
inhibition of alk in lung cancer cells carrying this fusion gene leads to apoptosis and cell death

116
Q

oral inhibitor of ALK

A

crizotinib

117
Q

what is the most common mutation seen in lung cancers?

A

kras

118
Q

two molecules in the normal pathway of T cell inhibition

A

CTLA-4 and PD-1

119
Q

anti-PD1 drug

A

nivolumab

120
Q

which arrhythmia has been shown to most commonly recur in patients with untreated obstructive sleep apnea?

A

atrial fibrillation

121
Q

the normal increase in pack during sleep is related to:

A

a decrease in the tidal volume NOT respiratory rate

122
Q

central sleep apnea is most commonly associated with….

A

severe chronic heart failure

123
Q

cheyne-stokes respiration typically occurs during which stage of sleep?

A

stages 1 and 2

124
Q

the parietal pleura is supplied by which vascular supply?

A

intercostal arteries

125
Q

hemoptysis is from which blood vessel usually?

A

bronchial arteries

126
Q

primary source of fluid production in the pleural space

A

parietal pleura

127
Q

how does the fluid in the pleural space get reabsorbed

A

stomata located in the parietal pleura (direct communication with lymphatics)

128
Q

what is the usual first test to confirm presence of pleural effusion?

A

chest x-ray

129
Q

what other imaging modality is used to evaluate pleural effusion after chest x-ray?

A

ultrasound

130
Q

when does something become an exudate

A

lights criteria: protein in the fluid:serum has to be greater than 0.5; LDH ratio has to be greater than 0.6

131
Q

when do you get decreased glucose levels in pleural fluid (<60 mg/dl)

A

infection–empyema, tb
malignancy
RA
esophageal rupture

132
Q

when do you get low pH <7.2 in pleural fluid

A

infection–empyeme, tb
malignancy
ra
esophageal rupture

133
Q

when do you get >10k cells in pleural fluid

A

infection, connective tissue dz, cancer

134
Q

what do neutrophils in the pleural fluid mean?

A

infection

135
Q

what do lymphocytes in the pleural fluid mean?

A

cancer, tb, chylothorax (high TG)

136
Q

what do eosinophils in the pleural fluid mean?

A

blood–trauma/pe; air–pneumthorax asbestos exposure, drug reaction, parasitic infectio

137
Q

different between a complicated parapneumonic effusion (CPE) and an empyema

A

both will have low ph and low glucose and high cell count with neutrophils but there will be NO bacteria in the CPE and YES BACTERIA IN THE EMPYEMA

138
Q

major cause of exudative effusion globally?

A

tb

139
Q

pleural effusions in RA

A

often painless, more often in males, subcutaneous nodules

tx: immunosuppression; occasional drainage and pleurodesis

140
Q

pleural effusions in lupus

A

often pleuritic chest pain, arthralgia of lupus

tx: immunosuppression and occasional drainage and pleurodesis

pulmonary (4 decks)

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