Pulmonary Flashcards

1
Q

air trapping signs in asthma that are ominous

A

decreased lung sounds

hyperresonance

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2
Q

dx for asthma

A

decreased PFTs (decreased FEV1/FVC
reversible - with beta agonist - albuterol
inducible - with Ach agonist

ABG - increased A-a gradient

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3
Q

If PFTs in a pt suspected of asthma next step =

A

methacholine challenge

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4
Q

stages of asthma symptoms

A

day night FEV1
I <2/wk <2/mon 80%
II <1/day <1/wk . 80%
III . >1/day >1/wk . 60-80%
IV . >1/day >1/wk . <60%
V . refractory to everything so they get oral steroids

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5
Q

stages of asthma tx

A

I - SABA
II - SABA + ICS (or leukotriene antagonist)
III - SABA + ICS + LABA
IV - SABA + ICS(increase dose) + LABA

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6
Q

LABA without ICS

A

never ever do this and leukotrine antagonist = ICS

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7
Q

basics of overall asthma tx

A

always watch pt use their med and add a spacer to make sure meds get in lungs and not just mouth

make sure pts adhere to meds

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8
Q

initial steps during an asthma exacerbation

A

O2 to maintain SpO2>90%
nebulizers (ipatropium, albuterol)
oral steroids
peak expiration flow rate

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9
Q

Following an acute asthma exacerbation what criteria allows a pt to be discharged home

A

no O2 requirement
no wheezing
peak expiratory flow rate >70%

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10
Q

following an acute asthma exacerbation what criteria puts them in the ICU

A

increased O2 demand
rising CO2 on ABG
no wheezing (cant move air)
peak expiratory flow rate <50%

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11
Q

ICU tx of an asthma exacerbation

A

ventillators
IV methylprednisone
IV magnesium is third line agent

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12
Q

salvage therapy for an asthma exacerbation

A

racemic Epi
Sub Q Epi
Mg2+

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13
Q

presentation of a pt with lung cancer

A

fever
weight loss
hemopytosis
(smoking hx)

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14
Q

initial steps to dx cancer

A

CXR

  • if neg -> paraneoplastic syndrome -> if no -> no cancer
  • if effusion -> thoracentesis -> if fluid has malignant cells —-> cancer stage 4

if non dx -> CT scan -> 1st Stage with PET scan, 2nd PFs, 3rd Tx

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15
Q

dx techniques for lung cancer

  • large proximal lesion
  • peripheral lesion
  • lesion in the middle of the lung
  • large irregular mass in lung
A
  • large proximal -bronchoscopy - EBUS (see thru walls)
  • peripheral - CT guided percutaneous biopsy (needle)
  • middle of lung - cardiothoracic surgeon - video assisted thorascopic surgery (VATS)
  • large, irregular mass in lung - resection
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16
Q

primary prevention of lung cancer

A

avoid smoking

avoid 2nd hand smoke

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17
Q

what are the requirement for cancer screening with low dose CT scans

A

55-80
30 pack per year history
quite <15 years ago

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18
Q

nodule criteria that is non cancerous

A

Size <8mm
Surface - smooth
Smoking - never
Self (age) <45

calcified

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19
Q

nodule criteria that is cancer suspicious

A

Size >2cm
Surface - spiculated
Smoking - Hx +
Self (age) - >70

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20
Q

pulmonary nodule is found next step is

A

finding old films

  • if no change –> stable
  • if new or change –>
  • —–> low risk –> serial CT scans
  • —–> high risk –> biopsy
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21
Q

small cell lung cancer basics

A

smoking Hx
centrally located

paraneoplastic syndromes - ACTH (cushing) and SIADH and Lambert Eaton syndrome

tx - chemo and radiation (responds well)

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22
Q

Sqaumous cell cancer lung cancer basics

A

smoking Hx
centrally located with necrosis and cavitation
More common than small cell cancer

paraneoplastic syndromes - PTH-related peptide (high Ca)

tx - stage related chemo, radiation, resection

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23
Q

adenocarcinoma lung cancer basics

A

MC primary lung cancer in both smokers and nonsmoker

asbesostosis (non smokers)
peripherally located - can cause pleuritic pain

tx - stage related chemo, radiation, resection

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24
Q

carcinoid lung cancer basics

A

left sided fibrosis, flushing, wheezing, diarrhea

serotinin syndrome

dx - 5-HIAA in urine

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25
Q

transudate pleural effusion pathophys

A

fluid falling out of the capillary space due to:

  • hydrostatic pressure - CHF
  • loss of oncotic pressure (hypoalbuminemia)
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26
Q

exudative pleural effusion pathophys

A

caused by inflammation - increased permeability of pleural spaces or decreased lymphatic flow from pleural surface because of damage to pleural membranes or vasculature

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27
Q

presentation of pleural effusion

A

orthopnea
dyspnea on exertion
decreased lung sounds
dullness to percussion in the area of effusion

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28
Q

CXR of pleural effusion

A

blunting of the costophrenic angle

horizontal meniscus

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29
Q

dx workup of pleural effusion imaging studies

A

Lateral Decubitus X-ray or US or CT

if small < 1cm watch and wait
if >1cm and no CHF hx –> Tap
if pt has CHF - don’t Tap –> diuresis –> if fails Tap

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30
Q

if pleural effusion suspected and septations/lobes (loculation) present next step =

A

thoracostomy (+/-) tPA –> if fails then –> thoractomy for debridment

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31
Q

thoracentesis: transudate vs exudate

lights criteria

A

LDH of fluid —> 2/3 upper nml limits
LDHfluid : LDHserum –> ( >0.6)
total protein (fluid): total protein (serum) –> ( >0.5)
[if any (1) above is + then –> exudate]

all (3) above negative = transudate

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32
Q

what tubes do you send after performing a thoracentesis

A

1) cell count with diff
2) cytology - cancer (if + stage 4)
3) ADA, glucose, pH, Total protein, LDH , TGL
4) blood cultures - gram stain culture, TB, fungi

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33
Q

breakdown of tube 1 sent s/p thoracentesis

A

PNA - leukocytosis with PMN (neutrophils)
TB - WBCs with lymphocytosis
RBC - hemothorax or cancer

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34
Q

breakdown of tube 3 sent s/p thoracentesis

A

ADA - TB

TGL - for chylothorax

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35
Q

DVT causes (vircows triad)

A

1 - venous stasis - immobility
2 - endothelial injury - central lines, plastics, smoking
3 - hypercoagable stages - hormone replacement therapy, OCPs, factor V leiden, malignancy

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36
Q

DVT presentation

A

unilateral leg swelling ( >2cm larger than other leg)

tenderness to palpation

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37
Q

dx and tx of DVT

A

US and anticoagulate

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38
Q

wedge infarct PE pathophys

A

necrosis dead lung –> hemopytosis
ischemia of pleural –> pleuritic CP

pulm HTN - due to right heart strain

0% perfusion but gas exchagne occurs 100% –> V/Q mismatch –> hypoxemia

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39
Q

platelet derived mediators pathophys on their destruction

A

vasodilation -> fluid leak out –> increased diffusion barrier for O2 which is diffusion limited -> decreased O2 –> tachypnea and tachycardia (too try and compensate by increasing CO)

but since CO2 is perfusion limited -> pt still able to breath off CO2 which will be worsened by tachypnea

due to poor hypoxia throughout lung –> massive vasoconstriction

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40
Q

ABG findings of PE

A

increased pH
decreased CO2
decreased O2

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41
Q

CXR and ECG findings in a PE with right heart strain

A

CXR - nml
ECG - S1, Q1, T3 = right heart strain
and/or elevated troponin
and/or elevated BNP

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42
Q

Wells criteria

A

<2 –> low probability –> D-dimer

> 4 –> CTA (must have good kidneys) or do V/Q

> 6 –> V/Q scan (must have nml CXR)

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43
Q

when is an IVC filter used for PE

A

when the next PE will kill the pt and/or if massive bleed (ex: GI bleed) is present and anticoagulants are C/I

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44
Q

cancer pts with PE tx

A

LMWH

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45
Q

management of an asymptomatic PE

A

home - LMWH bridge to Warfarin
no right heart strain
vital signs stable

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46
Q

management of a symptomatic PE

A

admit to floor - LMWH –> warfarin
no right heart strain
vital signs are stable

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47
Q

management of submassive PE

A

ICU - heparin drip –> warfarin
right heart strain is present
vital signs are stable

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48
Q

management of massive PE

A

ICU - TPA (if C/I –> thrombectomy)
abnormal vital signs
right heart strain is present

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49
Q

how to assess if there is right heart strain in a PE

A
elevated troponin 
or
elevated BNP 
or
2D echo - dilated RV, big RA
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50
Q

chronic thromboembolic pulmonary HTN

A

pulm HTN with multiple PEs diagnosed

tx - thrombectomy

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51
Q

COPD CXR

A

barrel shaped chest
Flat Diaphragm
increased radiolucency of lung parenchyma
elongated and narrow heart shadows

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52
Q

COPD pathophys and PFTs

A

decreased alveolar elasticity in COPD –> lung hyperinflation –> increased TLC, increased FRC, increased RV –> increased work of breathing

reduced inspiratory and expiratory flow rates

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53
Q

ADR of systemic glucocorticoids

A

leukocytosis with neutrophilic predominance
decreased lymphocytes
decreased eosinophils

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54
Q

MCC of secondary clubbing are

A

lung malignancy
cystic fibrosis
R->L cardiac shunt

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55
Q

COPD exacerbation management

A
  • O2 - SpO2 target 88-92%
  • inhaled bronchodilators
  • systemic glucorticoids
  • ABX if >1 cardinal sign
  • Oseltamavir - if evidence of influenza
  • NPPV if ventilatory failure
  • Intubate if NPPV fails or if it is contraindicated
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56
Q

cardinal signs of an infectious cause of a COPD exacerbation

A
increased dyspnea 
increased cough (frequency or severity) 
increased sputum production (change in color or volume)
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57
Q

indications for long term home O2 therapy

A

resting arterial oxygen tension (PaO2) <55mmHg
SaO2 < 88% on room air

pts with cor pulmonale or hematocrit >55% requirements

  • SaO2 <89
  • PaO2 <59
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58
Q

what are the . most common etiologies of chronic cough

A

upper airway cough syndrome (post nasal drip)
GERD
Asthma

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59
Q

When can a methachline challenge be given

A

if no bronchodilator response seen

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60
Q

Lung dz in pts with ankylosing spondylitis

A

can develop restrictive lung dz due to diminished chest wall and spinal movement

PFTs - decreased VC, decreased TCLl, nml FEV1/FVC

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61
Q

apical cavitary lesion on CXR

A

reactivation of TB

- fever, night sweats, blood tinged sputum

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62
Q

young pt with SOB, productive cough, evidence of destruction of lower lung lobes

A

alpha 1 antitrypsin deficiency

panacinar (panlobular) ephysema
<45 y/o
association with liver dz

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63
Q

clinical presentation of interstitial lung dz

A

progressive exertional dyspnea or persistent cough
half of pts have smoking hx

fine crackles heard during mid to late inspiration
possible digital clubbing

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64
Q

labs/imaging of interstitial lung disease

A

CXR - reticular or nodular opacities
CT - fibrosis, honeycombing, traction bronchiectasis
PFTs - increased FEV1/FVC
decreased DLCO2, TLC, RV

signficant hypoxemia with exertion due to V/Q mismatch —> increased Alveolar-arterial gradient (A-a)

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65
Q

idiopathic pulmonary fibrosis pathophys

A

excess collagen deposition in the extracellular matrix around the alveoli –> resultant scarring –> affected PFTs decrease

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66
Q

predisposing factors for aspiration pneumonia

A

AMS - impaired cough reflex, glottic issues
Dysphagia - due to neuro deficits
GERD
Protracted vomiting
NG-ET tubes
Large volume tube feedings in the recumbent position

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67
Q

Bilateral hilar adenopathy on CXR
increased Ca
erythema nodosum

A

Sarcoidosis

pts can also have anterior uveitis, arthralgias, arthritis, bells palsy, papilledema, peripheral neuropathy

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68
Q

emphysema presentation

pink puffer

A

pts are thin - due to increased energy during breathing which is through pursed lips
pts lean forward when sitting
using accesory muscles

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69
Q

bronchitis

blue bloater

A

overweight and cyanotic (secondary to hypercapnia and hypoxemia)

chronic cough and sputum production

inflammation of airways -> decreased O2
cyanosis and hypoxemia –> vasoconstriction in lungs -> increased resistance in pulmonary arteries -> pulmonary HTN -> RHF –> edema

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70
Q

dx workup of COPD

A

PFTs

decreased FEV1/FVC

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71
Q

tx of COPD (not an exacerbation)

A

1 - SABA
2- SABA + LAMA (tiatropium)
3 - SABA + LAMA + LABA
4 - SABA + LAMA + LABA + ICS
5 - SABA + LAMA + LABA +ICS + PDE 4inhbitor
6 - SABA + LAMA + LABA + ICS + PDE4-I + Steroids

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72
Q

tx of chronic COPD

A

Corticosteroids - inhaled, oral (prednisone), IV
(methylprednisolone)
O2 if SpO2 <88%, PaO2 <55
Prevention (vaccines: flu, streptococcal, smoking
cessation)
Dilators (Short acting - albuterol, tiatropium, long acting
LABA, LAMA, Theophyline, PDE4-I)
Experimental
Rehab

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73
Q

what 2 things decrease mortality in a COPD pt

A

O2 and smoking cessation

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74
Q

signs and symptoms of a COPD exacerbation

A

wheezing - especially on forced expiration
cough
sputum production

tachycardia, tachypnea, decreased breath sounds
prolonged expiratory time

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75
Q

pt discharged home on what meds following COPD exacerbations

A

PO steroids - prednisone

Metered dose inhalers - albuterol

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76
Q

Pathophys behind ARDS

A

noncardiogenic pulmonary edema

leaky capillaries -> crushes the alveoli –> fluid causes an increased diffusion barrier –> O2 = diffusion limited = less O2 getting in

stiff lungs, increased A-a gradient

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77
Q

presentation of ARDS

A

sick as shit patient,hypoxemic

acute hypoxemic resp failure = P/A <200

septic shock, transfusion related lung injury , near drowning victim

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78
Q

ARDS CXR

A

pulmonary edema will be evident

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79
Q

differentiating between ARDS vs HF

A

CHF - increased PCWP and decreased LV function

ARDS - decreased PCWP and nml to increased LV function

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80
Q

ARDS management

A

intubation
keep tidal volume low to reduce pressure
keep respiratory rate high so theres no accumulation of CO2

PEEP
treat underlying condition and try diuresis

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81
Q

PEEP pathophys

A

applies back pressure to maintain recruitment of alveoli which has a small diffusion barrier which allows O2 to get in easier

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82
Q

presentation of diffuse parenchymal lung disease (DPLD) also called interstitial lung disease

A

chronic and insidious development of hypoxemia
dry hacking cough
dry crackles
restrictive PFTs

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83
Q

tx of DPLD (interstitial lung dz)

A

steroids
DMARDS
biologics

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84
Q

Idiopathic causes of interstitial lung disease (DPLD)

A

< 6 wks = acute interstitial pneumonitis

> 6months = idiopathic pulmonary fibrosis

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85
Q

drug induced causes of interstitial lung disease

A
bleomycin 
amiodarone 
radiation 
nitrofurantoin 
phenytoin
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86
Q

rheumatological disease that cause interstitial lung disease

A

SLE
RA
systemic sclerosis

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87
Q

sarcoidosis interstitial lung disease

A

autoimmune, younger black women
asymptomatic bilateral hilar lymphadenopathy

insidious hypoxemia, blurred vision
heart block, bellsy palsy erythematous nodosum

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88
Q

dx of sarcoidosis

A

CXR - bilateral hilar lymphadenopathy
CT - (high resolution) - ground glass
PFTs - restrictive pattern

Biopsy = noncasseating granulomas

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89
Q

Trying to rule in cardiac sarcoidosis without pulmonary involvement work up

A

Cardiac MI followed by a biopsy of endomyocardium with sarcoid in it

conduction disturbances - heart block, arrhythmias

it is the most common cause of death

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90
Q

abestosis interstitial lung disease

A

increased cancer risk
exposure: shipyard, constructions >30yrs

CXR - pleural plaques on CXR

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91
Q

mesothelioma is dx of

A

abestosis

biopsy - barbell bodies indicative of abestosis

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92
Q

silicosis of interstitial lung disease

A

sandblasting, rock quaries, mining, glass manufacturing

upper lungs - looks like TB
pts are at increased risk for TB so need annual TB checks

egg shell calcifications - CXR

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93
Q

berryliosis interstitial lung disease

A

aeronautic professions

ppl who build or manufacture electronics

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94
Q

coal interstitial lung disease

A
coal miners 
caplan syndrome 
- arthralgias 
- pulmonary fibrosis  
----> check rhematoid factor
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95
Q

hypersensitivity pneumonitis

A

antigen mediated
person goes to work during week and has pneumonitis symptoms but these disappear over long weekend or on vacation

regional or temporal DPLD

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96
Q

intrapulmonary shunting

A

examples: pulm edema, PNA, atelectasis
increased A-a gradient
V/Q = O (no ventilation)

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97
Q

diffuse alveolar hypoventilation

A

uniform fall in ventilation throughout lung

causes: narcotic overdose and neuromuscular weakness

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98
Q

prolonged High FiO2 risks

A

oxygen toxicity - > formation of proinflammatory oxygen free radicals and predispose atlectasis as nitrogen is displaced

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99
Q

target PaO2 for COPD exacerbation

A

PaO2 55-80% once this target is reached lower FiO2 <60% which is the safe zone

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100
Q

pt with sick contact, cough, and no upper respiratory symptoms (rhinorrhea, etc) and has right lower lobe cracles on exam

A

indicates possibly pulmonary consolidation - must do CXR to r/o non viral etiology

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101
Q

pt with an underyling malignancy who presents with acute dyspnea, chest pain, tachycardia, hypoxia, and clear lungs is suggestive of

A

PE - underlying malignancy (prothrombic state)

they can present with syncope and hemodynamic collapse (RV dysfunction) if massive PE - along with RBBB on ECG

pts with PE can also develop small pleural effusions

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102
Q

new onset LBBB

A

suggest an acute MI

dyspnea/hypoxia due to pulm edema (crackles on exam)

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103
Q

MCC of orthostatic hypotension in elderly

A

hypovolemia -> due to decreased renal perfusion -> activation of renin angiotensin aldosterone system -> decreased urine sodium concentration

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104
Q

aspirin exacerbated respiratory dz

A

non IgE mediated pseudoallergic drug rxn to an imbalance between prostaglandins/ leukotrienes

pts have hx of asthma or chronic rhinosinusitis with nasal polyps

bronchospasm and nasal congestion following aspirin ingestion

tx - montelukast (leukotriene receptor antagonist)

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105
Q

goodpastures disease

A

lung affects - cough, dyspnea, hemopytosis

renal affects - nephritic range proteinuria, acute renal failure, dysmorphic red cells/red cell casts on UA

pathophys - linear . IgG antibodies along glomerular basement membrane (alpha 3 chain type IV collagen antibodies)

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106
Q

management of ARDS involves avoiding complications of mechanical ventilation such as using lung protective strategies =

A

low tidal volume ventilation –> lower pulmonary pressures –> decrease likelihood of overdistending alveoli and improve mortality

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107
Q

Pathophys behind ARDS being a complication of pancreatitis

A

increase serum [ ] of pancreatic enzymes such as phospholipase A2 –> cross pulm capillaries –> damaging lungs and cause inflammatory cascade –> leakage of blood and proteinaceous fluid into alveoli –> alveolar collapse due to surfactant loss and diffuse alveolar damage

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108
Q

complication during the post ictal state

A

hypoventilation - leading to respiratory acidosis

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109
Q

pancoast tumor (superior pulmonary sulcus tumor)

A

shoulder pain
C8-T2 neuro issues: weakness and/or atrophy of intrinsice hand muscles, pain and parethesias of 4th and 5th digit, medial forearm and arm

weight loss, supraclavicular lymph node enlargement
horners syndrome association

usually squamous cell cancers

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110
Q

primary pulmonary hypertension

presentation

A

middle aged patients
exertional breathlessness
lungs clear to auscultation

111
Q

dx of primary pulmonary hypertension

A

CXR - enlargement of pulmonary arteries with rapid tapering of distal vessels, enlargement of RV

ECG - Right axis deviation

112
Q

centrilobular emphysema

A

MC type seen in smokers
predilection for upper lung zones
destruction limited to respiratory bronchioles

113
Q

panlobular emphysema

A

pts with alpha 1 antitrypsin deficiency
destruction involves both proximal and distal acini
predilection for lung bases

114
Q

spirometry values in COPD

A

FEV1/FVC <0.70 (70%)
FEV1 is decreased

TLC is increased
residual volume is increased

115
Q

chronic bronchitis timeline

A

chronic cough productive of sputum for at least 3 months per year for at least 2 consecutive years

116
Q

alpha 1 antitrypsin pathophys

A

destruction of alveolar walls is due to relative excess in protease (elastase) which is released from PMNs and macrophages and is usually blocked by alpha 1 antitrypsin

tobacco smoke increases number of activated PMNs and macrophages as well as inhibits alpha 1 antitrypsin

117
Q

emphysema pathophys

pink puffer

A

permanent enlargement of air spaces distal to the terminal bronchioles due to destruction of alveolar walls

No change in oxygen, no hypoxemia
CO2 retention - compensate by:
- increased AP diameter (barrel chested)
- prolonged expirations

118
Q

airway obstruction spirometry values

A

nml or increased TLC with decreased FEV1 (amount of air that can be forced out of lungs in 1 sec)

the lower the FEV1 the more difficulty one has breathing

119
Q

restrictive lung dz spirometry values

A

FEV1//FVC = nml to high

TLC = low 
RV = low to normal
120
Q

COPD - affect on body pH

A

leads to chronic resp acidosis with compensatory metabolic alkalosis

also FEV1 measurements for COPD pts have the highest predictive value

121
Q

what are the only interventions in COPD known to decreased mortality

A

home oxygen therapy

smoking cessation

122
Q

what drugs are contraindicated in either a COPD exacerbation or asthma exacerbation

A

beta blockers

123
Q

complications of COPD

A

secondary polycythemia (Hct >55% in men or >47% in women)

124
Q

signs of acute severe asthma attacks

A
tachypnea 
diaphoresis 
wheezing
speaking in incomplete sentences 
use of accessory muscles
125
Q

paradoxic movement of abd and diaphragm on inspiration is a sign of

A

impending respiratory failure

126
Q

PFTs in asthma

A

decrease FEV1
decreased FVC
decreased FEV1/FVC ratio

increased FEV1 of 12% with albuterol
decreased FEV1 <20% with methacholine or histamine

127
Q

In an acute setting (ED) what is the quickest method for dx asthma when a pt is SOB

A

measuring peak flow (peak expiratory flow rate)

128
Q

during an acute asthma exacerbation if the PaO2 is nml or elevated

A

pt is getting fatigued and is no longer performing gas exchange since typically asthmatics hyperventilate and blow off CO2 so respiratory failure is imminent

129
Q

ADR of inhaled corticosteroids

A

due to oropharnygeal deposition

  • sore throat
  • oral candidiasis (thrush)
  • hoarseness

tx - using a spacer and rinsing the mouth after use

130
Q

uses for montelukast and cromolyn sodium/nedocromil sodium

A

prophylaxis for mild exercise induce asthma

131
Q

complications of asthma

A

satus asthmaticus - does not respond to standard meds

acute resp failure - due to resp muscle fatigue

pneumothroax, atelectasis, pneumomediastinum

132
Q

bronchiectasis basics

A

permanent, abnormal dilation and destruction of the bronchial walls
chronic inflammation airway

airway collapse
ciliary loss/ dysfunction leading to impaired clearance of secretion

133
Q

causes of bronchiectasis

A

recurrent infections
cystic fibrosis
kartagnener syndrome
autoimmune dzs

134
Q

clinical features of bronchiectasis

A

cough with large amounts of mucopurulent, foul smelling sputum
dyspnea
hemoptysis - due to ruptured blood vessels near bronchial wall surfaces

135
Q

dx and tx of bronchiectasis

A

dx - high res CT, obstructive PFT pattern

tx - abx, bronchial hygiene - hydration and chest physiotherapy, inhaled bronchodilators

136
Q

the main goal of treating bronchiectasis is to

A

prevent the complications of PNA and hemoptysis

137
Q

what type of dx is necessary to differentiate non small cell lung cancer to small cell lung cancer t

A

tissue diagnosis

138
Q

local invasion signs for lung cancer

A
Superior vena cava syndrome 
phrenic nerve palsy 
recurrent laryngeal nerve palsy 
horner syndrome 
pancoast tumor
139
Q

superior vena cava syndrome

A

Most commonly occurs with small cell lung cancer
facial fullness
facial and arm edema
dilated veins over anterior chest , arms and face
JVD

140
Q

phrenic nerve palsy

A

courses through the mediastinum where it can be destroyed by a tumor
hemidiaphragmtic paralysis

141
Q

recurrent laryngeal palsy

A

causes hoarseness

142
Q

tx of NSCLC and SCLC

A

NSCLC - surgery if not metastatic along with adjunct radiation

SCLC - combo os chemo and radiation surgery is not indicated as masses are unresectable

143
Q

calcification signs in lung cancer

A

eccentric asymmetric calcification - malignancy

dense central calcification - benign

144
Q

mediastinal masses

A

MCC in older pts = metastatic masses
anterior - 4 T’s = thyroid, teratogenic tumors, thymoma, terrible lymphoma
middle - lung cancer, lymphoma, aneurysms
posterior - neurogenic tumors, esophageal masses, enteric cysts, bochdalek hernia

145
Q

clinical features of mediastinal masses

A

usually asymptomatic unless compressing adjacent structures

  • cough - trachea or bronchi compression
  • dysphagia - esophagus compression
  • SVC syndrome
  • hoarseness - laryngeal
  • horners - sympathetic ganglia
  • diaphragm paralysis - phrenic
146
Q

dx of mediastinal mass

A

CT scan is test of choice

if CT suggests benign and pt is asymptomatic - observation is appropriate

147
Q

causes of transudative pleural effusions

A
CHF 
cirrhosis 
PE 
Nephrotic syndrome 
Peritoneal Dialysis 
hypoalbuminemia 
atelectasis
148
Q

causes of exudative pleural effusions

A
bacterial pneumonia 
TB (MCC in developing countries)
malignancy, Metastatic dz 
viral infection 
PE 
collagen vascular dzs
149
Q

elevated pleural fluid amylase

A

esophageal rupture

pancreatitis malignancy

150
Q

milky, opalescent fluid seen on thoracentesis drainage of pleural effusion

A

chylothorax - lymph in the pleural space

151
Q

frankly purulent fluid seen on thoracentesis

A

empyema - complication of untreated exudative pleural effusion or bacterial pna

tx - aggressive drainage of pleura and abx - recurrence rate is high if severe and persistent rib resection and open drainage might be necessary

152
Q

bloody effusion seen with thoracentesis

A

suspect malignancy

153
Q

parapneumonic effusion

A

noninfected pleural effusion secondary to bacterial pneumonia

seen as a complication of rheumatoid pleurisy
low pleural fluid glucose

pH < 7.2 - since its exudative

154
Q

if pleural fluid on thoracentesis has a glucos elevel < 60 suspect

A

rheumatoid arthritis in your differential

155
Q

tx of transudative pleural effusion

A

diuretics and sodium restriction

therapeutic thoracentesis only if massive effusion is causing dyspnea

156
Q

pneumothorax

A

air in the pleural space

2 categories: spontaneous and traumatic

157
Q

spontaneous pneumothorax

A

without trauma
primary - healthy persion, spontaneous rupture of subpleural blebs (tall, lean, men), high recurrence rate

secondary (complicated) - underlying lung dz (asthma, interstitial lung dz, CF) life threatening due to lack of pulm reserve

158
Q

presentation of pneumothorax

A

sudden onset of ipsy chest pain
dypsnea
cough

decreased breath sounds
hyperresonance over chest
decreased or absent tactile fremitus on affected side

159
Q

clinical features of a tension pneumothorax

A

hypotension - due to impaired filling of great veins
distended neck veins
trachea shifted
decreased breath sounds

160
Q

histiocytosis X

interstitial lung disease

A

caused by abnormal proliferation of histiocytes (related to langerhans cells of the skin)

smokers
dyspnea and nonproductive cough

spontaneous pneumo, lytic bone lesions, diabetes insipidus

161
Q

wegener granulomatosis

interstitial lung disease

A

characterized by necrotizing granulomatous vasculitis

upper and lower resp infections
glomerulonephritis and pulmonary nodules

+ c-ANCA

162
Q

churg strauss syndrome

interstitial lung disease

A

granulomatous vasculitis seen in pts with asthma

pulmonary infiltrates, rash, and eosinophilia
+ p-ANCA

tx - systemic glucocrticoids

163
Q

abestosis increases risk for

A

bronchogenic carcinoma and malignant mesothelioma

164
Q

causes of hypersenstivity pneumonitis

A

farmers lung - moldy hay
bird breeders lung - avian droppings

air condition lug
bagassosis lung - moldy sugar cane
mushroom workers lung - compost

165
Q

severe hypercapnia (and resp acidosis) can lead to

A

dyspnea

vasodilation of cerebral vessels (with increased intracranial pressure and subsequent papilledema, HA, and coma)

166
Q

criteria for respiratory failure

A

hypoxia - PaO2 <60mmHg

hypercapnia - PCO2 >50mmHg

167
Q

hypoxemic resp failure

A

low PaO2 with a PaCO2 that is nml or low
- present when O2 sat < 90% despite FiO2 > 0.6

Causes;
- ARDS, severe pna and pulm edema

168
Q

hypercapnic resp failure

A

failure of alveolar ventilation

decrease in mute ventilation or
increase in physiologic dead space leads to CO2 retention –> hypoxemia

Causes: CF, asthma, COPD, severe bronchitis

169
Q

ventilation is monitored by

A

PaCO2 - to decrease PaCO2 either increase RR or Tidal volume

170
Q

oxygenation is monitored by

A

PaO2 - to decrease PaO2 either decrease FiO2 or decrease PEEP

171
Q

shunting in resp failure

A

little or no ventilation in perfused areas (due to collapsed or fluid filled alveoli)

venous blood shunted into arterial circulation without being oxygenated

increased CO2 production: DKA, sepsis, hyperthermia

172
Q

causes of shunting in resp failure

A

atelectasis or fluid buildup in alveoli (pneumonia or pulmonary edema),

direct R –> L shunt

173
Q

supplemental oxygen effect on shunt in resp failure

A

hypoxia due to a shunt is not responsive to supplemental oxygen

174
Q

clinical features of respiratory failure

A

dyspnea - first symptom
maybe cough
inability to speak in complete sentences

use of accessory muscles of respiration
tachypnea, tacycardia

cyanosis
AMS

175
Q

preferred oxygen delivery system in COPD patients

A

venturi mask - since you can more precisely control oxygenation

176
Q

NPPV - noninvasive positive pressure ventilation

A

BIPA or CPAP
indicated in pts in impending resp failure in an attempt to avoid intubation and mechanical ventilation

pts must be neurologically intact, awake, cooperative and able to protect their airway

177
Q

dx of ARDS

A

CXR - bilateral infiltrates on imaging
pulm edema not explained by fluid overload or CHF

PCWP < 18mmHg

PaO2/FiO2 ration:

  • 200 to 300 - mild ARDS
  • 100 - severe ARDS
178
Q

complications of ARDS

A

permanent lung injury - lung scarring or honeycomb lung

barotrauma secondary to high pressure mechanical ventilation - pneumothorax or pneumomediastinum

renal failure - may be due to nephrotoxic medications, sepsis with hypotension

179
Q

always confirm correct ET placement by

A

listening for bilateral breath sounds
checking post intubation CXR
- tip of ET should be 2-5cm above the carina

180
Q

two major goals of mechanical ventilation

A

maintain alveolar ventilation

correct hypoxemia

181
Q

pts who require mechanical ventilation

A

significant resp distress
impaired or reduced LOC with inability to protect airway = absent cough or gag reflex

metabolic acidosis - unable to compensate with ventilation
resp muscle fatigue

significant hypoxemia = PaO2 < 70mmHg or hypercapnia PaCO2 >50mmHg

182
Q

acceptable ABG ranges with mechanical ventilation

A
PaO2 = 50 - 60 
PaCO2 = 40-50 

pH = 7.35 - 7.50

183
Q

criteria for weaning off from ventilator or extubation

A
intact cough 
PaO2/FiO2 >200 
PEEP of < 5cm 
FiO2 <40% 
RR < 35
minute ventilation < 12
184
Q

high levels of PEEP increase the risk for

A

barotrauma (injury to airway = pneumothorax)
+
decreased cardiac output (decreased venous return form increased intathoracic pressure

185
Q

complications of mechanical ventilation

A

agitation, anxiety, discomfort
difficulty with tracheal secretions

ventilator associated PNA
barotrauma

tracheomalacia (softening of the tracheal cartilage) due to prolonged presence of ET

186
Q

when a pt is ventilator dependent for 2 or more weeks a

A

tracheostomy is performed to prevent tracheomalacia

187
Q

pulmonary HTN

A

mean pulmonary arterial pressure > 25mmHg at rest

188
Q

causes of pulmonary HTN

A

passive - due to resistance in pulm venous system (LHF, mitral stenosis, atrial myxoma)

hyperkinetic (L –> R cardiac shunt, ASD, PDA)
obstruction (PE, pulm artery stenosis)
pulmonary vascular obliteration (collage vascular dz)

189
Q

pulmonary arterial HTN

A

idiopathic, familial
young or middle aged women

abnormal increase in pulmonary arteriolar resistance leads to thickening of pulmonary arteriolar walls

190
Q

clinical features of pulmonary HTN

A

dyspnea on exertion
fatigue
chest pain - exertional
syncope - exertional

191
Q

dx of Pulmonary HTN

A

loud P2
ECG - RVH and RAD
CXR - enlargend pulm arteries
echo - dilated pulm artery, dilated RA, hypertrophied RV

increase pulmonary artery pressure > 25mmHg

192
Q

dx of cor pulmonale

A

CXR - enlargement of RA, RV, and pulm arteries
ECG - RAD, RVH
echo - RV dilatation, nml LV size and function

193
Q

sources of emboli to the lungs other than the traditional traveling thrombus

A

fat embolism - long bone fx

amniotic fluid embolism - during or after delivery

air embolism - trauma to thorax, indwelling venous/arterial lines

septic embolism - IV drug use

schistosomniasis

194
Q

complications of PE

A

recurrent PEs

pulmonary HTN - in 2/3 of pts

195
Q

risk factors for PE

A

age >60
malignancy
prior DVT/PE
hereditary hypercoagulable states - factor V Leidin, protein C and S def, antithrombin III deficiency

prolonged immobilization 
obesity
major surgery (especially pelvic) 
major trauma 
pregnancy (OCPs)
196
Q

sources of emboli

A

LE - DVTs - iliofemoral DVT

UE - DVT - rare - may be seen in IV drug users

197
Q

clinical features of a PE

A

dyspnea
pleuritic chest pain
cough/ hemoptysis

tachypnea, tachycardia (leads to resp alkalosis)
rales

198
Q

dx of PE

A

CTA - showing intraluminal filling defects in central, segmental, or lubular pulmonary arteries
[cant be used if pt has renal insufficiency]

+ pulmonary angiogram - definitively proves PE

199
Q

what dx test and results can rule out a PE

A

negative (-) D-dimer and low clinical suspicion

low probability V/Q scan and low clinical suspicion

negative pulmonary angiogram (definite)

200
Q

modified wells criteria

A

symptoms and sign of DVT = 3.0
alternative dx less likely than PE = 3.0
heart rate > 100 bpm = 1.5
immobilization (>3days) or surgery in prev 4wks = 1.5
previous DVT/PE = 1.5
hemoptysis = 1.0
malignancy = 1.0

score < 5 = unlikely PE
score > 4 = PE likely

201
Q

contraindications to heparin

A

active bleeding
uncontrolled HTN
recent stroke
Heparin induced thrombocytopenia (HIT)

202
Q

tx of aspiration pneumonia

A

clindamycin (has anaerobic activity)

203
Q

differential dx of hemopytsis

A

bronchitis
lung cancer (bronchogenic carcinoma)
TB
bronchiectasis

goodpasture syndrome
Aspergilloma within cavities

204
Q

nml ABG values

A
pH = 7.35 - 7.45
PaO = 90 (decreases with age) 
PaCO2 = 35-45
205
Q

DLco mechanism

A

measures the surface area of the alveolar capillary membrane

useful in monitoring conditions such as sarcoidosis and emphysema

206
Q

causes of low DLco

A

emphysema
sarcoidosis
interstitial fibrosis
pulmonary vascular dz

lower with anemia

207
Q

causes of high DLco

A
asthma 
obesity 
intracardiac L --> R shunt 
exercise 
pulmonary hemorrhage
208
Q

if hemoptysis is severe consider

A

bronchial artery embolization or balloon tamponade of the airway

209
Q

bronchogenic cysts

A

middle mediastinum masses
benign

best seen on CT scan

210
Q

thymoma

A

anterior mediastinum mass
young male or female
strong association with myasthenia gravis

211
Q

neurogenic tumors

esophageal leiomyomas

A

located in posterior mediastinum

212
Q

indications for noninvasive positive pressure ventilation

A

COPD (severe exacerbation)
Cardiogenic pulmonary edema
acute resp failure

213
Q

contraindications for NPPV

A
inability to protect airway 
cardiac or respiratory arrest 
severe acidosis pH < 7.10 
ARDS 
recent esophageal aneursym
214
Q

pulmonary contusion
presentation
and
dx

A

< 24hrs after blunt thoracic trauma
tachycardia, tachypnea,
hypoxia

dx - rales, decreased breath sounds, CT or CXR - with patchy, alveolar infiltrates not restricted by anatomical borders

215
Q

fat embolism

A

develop resp distress
neurological abnormalities
petechial rash

following a latent period of 12-72hrs after injury

216
Q

invasive aspergillosis

risk factors and presentation

A

risk factors - immunocompromised (neutropenias, glucocorticoids, HIV)

triad - fever, cp, hemoptysis

217
Q

invasive aspergillosis

dx and tx

A

dx - CXR/ CT - pulmonary nodule with surrounding ground glass opacities (halo sign)
+ cultures
+ cell wall biomarkers (galactomannan, beta D glucan)

tx - voriconazole +/- capsofungin

218
Q

chronic aspergillosis

risk factors and findings

A

risk factors - lung dz/damage [cavitary TB]

findings = > 3months - weight loss, cough, hemoptysis, fatigue

219
Q

chronic aspergillosis

dx and tx

A

dx - cavitary lesions +/- fungus ball
+ aspergillosis IgG serology

tx - resect, azole meds, embolization if hemoptysis is severe

220
Q

what decreases the mortality rate of an acute PE

A

early and affective anticoagulation - should be initiated prior to dx tests being performed - unless a contraindication is present

221
Q

interstitial lung dz PFTs
TLC
FEV1/FVC
DLco

A

TLC - decreased
FEV1/FVC - nml or increased
DLco - decreased

222
Q

COPD PFTs
TLC
FEV1/FVC
DLco

A

TLC - increased
FEV1/FVC - decreased
DLco - decreased

223
Q

ASTHMA PFTs
TLC
FEV1/FVC
DLco

A

TLC - nml/increased
FEV1/FVC - decreased
DLco - nml/increased

224
Q

Restrictive PFTs
TLC
FEV1/FVC
DLco

A

TLC - decreased
FEV1/FVC - increased or nml
DLco - nml

225
Q

DLco in pulmonary artery HTN

A

decreased

226
Q

why is the glucose [ ] in an empyema low

A

due to high metabolic activity and/or leukocytes (and/or) bacteria in the fluid that metabolize the glucose

227
Q

3 mechanisms for transudative pleural effusion

A

increased hydrostatic pressure
decreased oncotic pressure
decreased intrapleural pressures

228
Q

compensatory metabolic alkalosis can lead to what lab affects

A

decreased Cl- concentration due to bicarbonate retention

229
Q

both nonallergic rhinitis and allergic rhinitis are managed with

A

intranasal glucocorticoids

difference between the 2 is that allergic rhinitis pts can ID their trigger and present earlier

230
Q

exudative pleural effusion mechanisms

A

increased capillary permeability
pleural membrane permeability
disruption of the lymphatic outflow

231
Q

chlorpheniramine

A

H1 antihistamine receptor blocker

decreases allergic response
anti inflammatory -> reduced nasal secretions by limited the secretory response to inflammatory cytokines

232
Q

histoplasma capsulatum

A

central, midwestern, and northeastern US

ppl who go in caves who are at increased risk for bat and bird droppings

233
Q

Coccidiomycosis

A

Arizona
CP, fatigue, cough and fever

CXR - nml unilateral infiltrate with ipsy hilar lymphadenopathy

biopsy endospores and spherules

234
Q

bronchiectasis confirmed via

A

high resolution CT scan

cough with daily mucopurelent sputum production

235
Q

empiric tx of CAP

outpatient

A

macrolide or doxycycline (healthy pt)

floroquinolone or beta lactam + macrolide (pt with comorbidities)

236
Q

empiric tx of CAP
(inpatient)
+
(inpatient in ICU)

A

inpatient - fluoroquinolone (IV) or beta lactam + macrolide (IV for both)

ICU pt - beta lactam + macrolide (IV) or beta lactam + flouroquinolone (IV)

237
Q

management of SIADH

A

fluid restriction +/- salt tablets

hypertonic (3%) saline

238
Q

granulomatosis with polyangitis

presentation

A

upper resp issues - sinusitis, saddle nose
lower resp issues - lung nodules/ cavitations
+
renal issues - rapidly progressing glomerulonephritis

skin - non healing ulcers

239
Q

granulomatosis with polyangitis

dx and tx

A

dx - CXR - necrotizing pulmonary vasculitis
ANCA - PR3, MPO
leukocytoclastic vasculitis
pauci immune GN

granulomatous vsculitis

tx - corticosteroids + immunomodulators

240
Q

CO2 retentions leads to what affect on cerebral vasculature

A

cerebral vasodilation –> seizures, stroke, AMS

241
Q

complication of pneumocysitis in HIV pts

A

SIADH - –> decreased Na which can be further worsened by nml saline bolus

242
Q

CREST syndrome

Scleroderma

A
C- calcinosis 
R- raynauds phenomenom 
E- esophageal dysmotility 
S-sclerodacytl 
T- telengiectasias
243
Q

pathophys of PAH

A

intimal hyperplasia of pulmonary arteries

progressive dyspnea, exertional syncope, lighthedness –> due to RV failure

244
Q

alveolar spaces filled with fibroblasts are consistent with

A

interstitial lung dz

245
Q

bronchial wall thickening with mucous plugs is consistent with what dx

A

bronchiectasis

246
Q

drug induced SLE meds

A

procainamide
isoniazide
hydralazine

247
Q

during an acute asthma attack if the PaCO2 begins to normalize or increase

A

it is a sign of impending resp failure because typically these pts are tachypneic and should be breathing off a lot of CO2 but now they are fatigued and their breaths are not performing gas exchange

248
Q

exercise induced asthma tx

A

SABA - such as albuterol 10-20 min before exercise

249
Q

pH of transudative pleural effusion vs exudative pleural effusion

A

transudative pleural effusion - pH 7.40 - 7.55

exudative pleural effusion - pH 7.30-.7.45

250
Q

physical exam findings of lobar pneumonia

A

increased breath sounds (Crackles and egophony)
increased tactile fremitus

dullness to percussion

251
Q

physical exam findings of a pleural effusion

A

decreased breath sounds
decreased tactile fremitus
dullness to percussion

252
Q

physical exam findings of emphysema

A

decreased breath sounds
decreased tactile fremitus
hyperresonant to percussion

253
Q

mediastinum shifting affected by atelectasis

A

mediastinum will shift towards the side with a large amount of atelectasis

decreased breath sounds
decreased tactile fremitus
dullness to percussion

254
Q

how does alveolar consolidation in PNA causes hypoxemia

A

due to R –> L intrapulmonary shunting

255
Q

dead space ventilation

A

ventilation of areas of the lung that are not perfused with blood

(ex: PE)

256
Q

high PaCO2 and low PaO2 levels are suggestive of

A

alveolar hypoventilation

257
Q

alveolar gradient formula =

A

PAO2 - PaO2

258
Q

CXR showing loculation –>

A

parapneumonic effusion and empyemas - exudative pleural effusion

high protein - <60 glucose - low pH

259
Q

development of clubbing and sudden onset joint arthropathy in a chronic smoker is suggestive of

A

hypertrophic osteoarthropathy - typically associated with cancer so need to perform a CXR to r/o malignancy

260
Q

Oxygenation of a pt with PaO <60 can be improved by

A

Increasing FiO2 - usually weaned <60% to avoid O2 toxicity

increased PEEP
- improves mortality in pts with ARDS

dont increase tidal volume as it can lead to increased risk of barotrauma

261
Q

tx of PE in pts with GFR <30

A

unfractionated heparin - preferred over LMWH

this is because in renal insufficiency there is reduced clearance of anti Xa leading to increased activity –> increased bleeding risk

262
Q

mainstay tx of COPD

A

inhaled antimuscarinic agents

263
Q

tx of post nasal drip (upper airway cough syndrome)

A

oral first generation antihistamines

264
Q

theophylline toxicity

A

CNS - HA, insomnia, Szs
GI - N/V
Cardiac - arrhythmias, palpitations

265
Q

Most Common ADR of inhaled corticosteroids therapy

A

oropharyngeal thrush (oral candidiasis)

266
Q

complications of positive pressure ventilation

A

alveolar damage
pneumothorax
hypotension

267
Q

MCC of cor pulmonale

A

COPD

268
Q

causes of increased plateau pressure

A

pneumothroax
pulm edema
PNA
atelectasis

269
Q

ADR of beta 2 agonists (albuterol)

A

reduce K+ levels by driving K+ into cells –> hypokalemia -

  • –> muscle weakness, arrhythmias,
  • –> EKG changes, tremors, palpitations, HA
270
Q

Acute PE - pressures

A

NML PCWP
increased RA pressure
increased pulmonary artery pressure

271
Q

causes of recurrent PNA in the same location

A

extrinsic bronchial compression (neoplasm, adenopathy)
intrinsic bronchial obstruction (bronchiectasis, FB)

recurrent aspirations: szs, alcohol, drug use, GERD, dysphagia

workup = CT scan

272
Q

acute bronchitis

A

cough > 5days to 3wks (+/- purulent sputum)
preceding resp illness (90% viral)

absent systemic findings (fever, chills)
wheezing or ronchi
chest wall tenderness

273
Q

dx and tx of acute bronchitis

A

CXR only if PNA suspected

tx - symptomatic tx - NSAIDs and/or bronchodilators