Respiratory

Front 1

pt with hx for DVT comes in with 2 days SOB. She is not on meds. BP is 90/50 and HR is 120.
1.what will imaging studies reveal?
2. explain physio of this
3.Tx

Back 1

1.Right Ventricular dilation and failure

-Massive PE -> RV dilation and failure -> HypOTN, tachcard, syncope, and SOB
= hemodynamic instability -> prescribe thrombolytics

Front 2

hemolytic instability + PE, what do you do

Back 2

Rx thrombolytics

Front 3

Pneumocystis jiroveci (PCP):
-how presents clinically
- on CXR
-xtrapulm involvement
- Dx

Back 3

- fever, non-productive cough, sob on exertion, wt. loss, night sweats
- perihilar b/l interstitial infiltrates espec.
-lymph nodes, spleen, liver and bone marrow
- BAL

Front 4

what should TV be in mechanically ventilated pt.s?

Back 4

6 ml/Kg of ideal body wt.

Front 5

what is ventilation defined as?
what if pt. has pH 7.5, pCO2 22, and PO2 of 121 and an appropriate TV?

Back 5

the product of RR and TV
Pt. has Resp Alk 2ndary to Hyperventilation. So, you would < the RR.

Front 6

cause of post ictal:
1, metab acidosis
2. resp acidosis

Back 6

1. lactic acid accum - don't treat will go away
2. hypoventilation or aspiration

Front 7

I.what conditions < DLCO?
II. " " > " ?

Back 7

I.1. hindrance in alveolar wall (ex. fibrosis, vasculitis (Weg or goodpast?))
2. < in total lung area (restrictive dz.)
3. uneven spread of air in lungs (ex emphysema)
4. PEmbolism (< perfusion)
5. Cardiac insufficiency
6. Pulmonary HTN
7. Bleomycin (fibrosis)
8. Anemia due to < in bld vol.
II.1. polycythemia
2. asthma (can also have normal DLCO)
3. >ed pulmonary blood vol. (ex. CHF, exercise)
4.L->R pulmonary shunting in Left heart fail

Front 8

to differentiate between asthma and COPD what do you do and what should you see?

Back 8

methacholine test
if it is asthma methacholine will cause a greater than 12% decrease in DLCO (bc in asthma lung parenchyma hasn't been destroyed)

Front 9

Tx of CAP (= <48 hours in hosp):
1. outpt.
2. In pt.

Back 9

1. previously healthy and no abx in past 3 mo.s: Mac or doxy
or
comorbidities or abx used in past 3 mo.s = respiratory fluoroquinolones ( levo or moxi)
2. azithro + ceftriaxone
or resp fluoro

Front 10

Tx of HAP (>48 hrs in hosp)

Back 10

DON'T GIVE MAC!
Antipseud beta lactam:
Antispeudo pen: TCP+tazobactam/clavulinic acid
or
Antipseudo ceph= ceftazidime, or cefepime
or
carbepenem (imipenem (SE=seizures) meropenem, doripenem)

Front 11

Tx of VAP

Back 11

1. Antipseudo beta lactam (see HAP tx)
+
2. 2nd antipseudo agent:
aminogly (GNAT) or fluoroquinolone (cipro or levo)
+
3. MRSA agent:
Vanco or linezolid

Front 12

reasons for intubation

Back 12

- pH <7.3, pCO2 > 50, pO2 <50
-SaO2 <93%
- Mental status change
-difficulty speaking

Front 13

Lung abscess Tx

Back 13

clinda or pen

Front 14

PCP PNA Tx:
1. best initial
2. if toxicity from #1
3. Prophylaxis

Back 14

1. TMP-SMX
2. -pentamidine
or
-Clinda + primaquine (unless G6PD def)
3.-TMP-SMX or
- Dapsone or Atovoquone

Front 15

what causes b/l interstitial infiltrates on cxr?

Back 15

-viral PNA, PCP, Mycoplasma, Chlamydia, coxiella, and sometimes legionella (atypicals)

Front 16

tx of viral influe

Back 16

<48 hr.s of symptoms = nasopharyngeal swab and then oseltamivir onr zanamivir (doesn't cure just shortens length of symptoms)
>48 hours just treat symptoms with analgesics, rest, hydration, antipyretic

Front 17

MC predisposing cause of acute bact. sinusitis

Back 17

viral URI

Front 18

-sinusitis dx
-most accurate test
-Tx

Back 18

-clinical dx
-sinus Bx or aspirate (don't do this unless recurrent infxn and not responding to abx)
-amoxicillin, doxy, or TMP-SMX + decongestant

Front 19

empiric Tx and cause of PNA in kids:
1. neonate
2. 1-4 mo.s
3. 4 mo.s - 4 yrs.
4. 5 - 15 yrs.

Back 19

1. Grp B strep > E coli, listeria, Chlam trach.
Tx. Amp + Gent ( +/- Vanc if MRSA is a concern. and for Chlam use erythro)
2. RSV, chlam trach, parainflu, bordetella, strep pneumo, staph. A
Tx. Mac +/- cefotaxime
3. RSV, other virus (rhino, influ, parainflu, adeno, corona)
Tx. Amox or Amp
4. strep pneu > myco, c. pneu, viruses
Tx.(1) Amox +clarithro (or erythro)
(2) Azithro
(3) amox + doxy

Front 20

Allergic bronchopulmonary aspergillosis (ABPA):
1. presentation
2. what do you see on CXR
3. main clue to make dx
4. most accurate dxic test
5. Tx

Back 20

1. similar to asthma with SOB, hemoptysis, cough, and wheezing
2. tram-track lines in bronchi (these are indicative of edema of bronchial wall and bronchiectasis)
3.elevated eosinphil count
4. elevated level of IgE, aspergillus precipitans in serum, and/or aspergillus-specific IgE and IgG
5. prednisone + itraconazole

Front 21

PCP PNA
1. CXR
2. who to suspect
3. indicative lab finding

Back 21

1. interstitial infiltrates
2. CD4 < 200 or severely immunocompromised (ex. chemo)
3. LDH > 220

Front 22

differential dx for ground glass opacities(diffuse hazy infiltrate) on CXR?

Back 22

-interstitial pna (ex PCP)
- Pulm edema
- pulm hemorrhage
- hypersensitivity pneumonitis

Front 23

1. Tx for Acute exacerbation of chronic bronchitis (AECB) (ie Acute bacteria exacerbation of COPD (ABEC))
2. Bronchiectasis
3. CF

Back 23

same causitive agents as sinusitus ( strep pneu, H. influ,
morax cat)
Same Tx for 1-3:
-Amox/clavulinic acid
or
-Macs
or
- 2nd or 3rd gen Cephs
- Respiratory fluoroquinolones

Front 24

A-a gradient = normally
pAO2=
paO2 normally
paCo2 normally
PaO2/FiO2 (ie FiO2 ratio)

Back 24

pAO2 - paO2 = 5-15 mmHg
pAO2=150 - (PaCO2/0.8)
paO2 = 90-100 mmHg
PaCO2 = 40 mmHg
PaO2/FiO2 (FiO2 is typically .21), <200 is ARDS, <300 = gas xchange deficit

Front 25

ARDS (ie shock lung)
1. cause of it
2. CXR will show
3. Dx?
4.Tx

Back 25

1. diffuse lung injury from sepsis, aspiration, trauma, pancreatitis!, or trauma ->diffuse capillary leak
2. bilat infiltrates (looks like CHF but pressures are normal)
3. presumptive dx. PaO2/FiO2 <200 and PCWP <18 mmHg
4. intubation, mech venti w/ FiO2 < 60% to maintain SaO2 >90%, and >PEEP

Front 26

Pharyngitis and tonsillar infxn Tx

Back 26

(only treat with (+) throat Cx in pharyngitis)
Amox (augmentin) or Pen
-if allergic w/ rash: cephalexin
-if anaphylaxis: clinda or Mac

Front 27

GBS muscle weakness -> resp. distress
how do you monitor resp funxn?

Back 27

serial measurement of bedside VC

Front 28

Pleural effusion:
1. what is its MCC?
2. How is transudate formed?
3. How is exhudate fomed?

Back 28

1. CHF
2.>ed hydrostatic P (seen in CHF); <ed plasma oncotic P or hypoalbuminemia (common in liver failure)
3.>ed capillary permeability as seen in inflammation

Front 29

Transudate vs. exhudative pleural effusion lab values:
<1> Labs for exhudate:
<2> also, what is pH
<3> glucose

Back 29

<1>Pleural/Serum ie PS for exhudative effusion
1. P/S protein ration > 0.5
2. P/S LDH >0.6
3. pleural fluid LDH >er than 2/3rds the upper limit of normal serum LDH
<2> Transudative pH= 7.35
Exhudative (ie inflam) <7.3
if < 7.2 then chest tube aspiration required to prevent empyema
Normal pleural fluid Ph =7.64
<3> low glucose is found in exhudative due to >ed metab activity of WBCs
[gluc] <30 : empyema or rheumatic effusion
[gluc] 30-50 : CA, SLE, Tb, or esoph. rupture

Front 30

cause of exudative pleural effusion

Back 30

- infx ( TB, PNA)
- Pulm Emb
-CA
- connective tissue dz
- iatrogenic

Front 31

Dx test of choice for PE

Back 31

helical CT angio

unless IV contrast is contraindicated ex in renal failure pt. then it is :
V/Q scan

Front 32

pt. is showing neutrophilia, and diminished eosinophils what drug can induce this?

Back 32

glucocorticoid induced neutrophilia

Front 33

Pt. comes in with exacerbated DVT and INR of 1.2 after taking hep and war tx what do you do?
What if PE?

Back 33

typically hep + warf w/ hep discontinued after 5 days once INR is 2-3.
if pt. comes back with exacerbation then bridging hep again until INR is therapeutic.
If PE then thrombolytics.

Front 34

Pt. comes in with exacerbated DVT and INR of 1.2 after taking hep and war tx what do you do?
What if PE?

Back 34

typically hep + warf w/ hep discontinued after 5 days once INR is 2-3.
if pt. comes back with exacerbation then bridging hep again until INR is therapeutic.
If PE then thrombolytics.

Front 35

criteria for long term supplemental O2 therapy

Back 35

(prolongs survival in COPD and hypoxemia)
- PaO2 </= 55, PaCO2 >/= 55, SaO2 </= 88%, erythrocytosis (hematocrit > 55%), or evidence of cor pulmonale

Front 36

Lung consolidation (ex PNA):
- breath sounds
- percussion
- fremitus

Back 36

-bronchial breath sounds (full expiratory phase),bronchphony, egophony, whispered pectoriloquy
-dull to percuss
- >ed fremitus

Front 37

pleural effusion:
-breath sound
-percussion
-fremitus

Back 37

Everything is decreased:
-<ed breath sounds
-dull to percuss
-<ed fremitus

Front 38

Ex.s of :
1. hypovent
2. low inspired O2
3. shunting
4. V/Q mismatch

Back 38

3.pulmonary edema, PNA, vasc. shunt (ex hepatopulm syndrome)
4.Pulm embolism, exacerbation of bronchial asthma, hypoxia w/ PNA

Front 39

definitive dx for bronchiectasis

Back 39

HRCT scan

Front 40

recurrent pneumonia in the same anatomic location is a red flag for ?
-next step in management
-if the above Dxic test concurs then what do you do to confirm Dx?

Back 40

lung CA. especially if pt. smokes
-CT scan
-bronchoscopic is performed if lesion has peribronchial location
vs.
CT-guided Bx is performed if lesion has peripheral location

Front 41

what does new fingernail clubbing in pt. with COPD often indicate?

Back 41

the development of lung CA

Front 42

SEs of beta 2 agonists

Back 42

<es serum potassium levels (drives K into cells) -> muscle weakness, arrhythmia, EKG changes
other side effects: tremor, headache and palpitations

Front 43

blastomycosis:
1. presentation
2. CXR
3. how manifests in body
4. what is it?
5.where is it in the country?
6. confirm Dx
7. Tx

Back 43

1.low grade fever, night sweats, productive cough, wt. loss (seen in chronic infxn, CA, or rheumatologic dz)
2. consolidation, looks like Tb
3. ulcerated skin lesions, lytic bone lesions, and lungs (BLAS = Bone, Lungs, And Skin)
4.broad based budding fungus
5. mostly in Wisconsin. Great lakes, MI and OH river valleys
6. sputum Cx
7. itraconazole or ampho B

Front 44

COPD Tx:
1. therapies proven to prolong survival
2. Tx

Back 44

1. supplemental O2 and smoking cessation
2. beta 2 agonist (albuterol) + anticholinergic (ie antimuscarinic) (ex. ipratropium)

Front 45

(HY)
Aspirin sensitivity syndrome
1. clues to Dx
2. pathogenisis
3. Tx

Back 45

1. ASA ingestion, persistent nasal blockage (polyps), and episodes of bronchocnstrxn
2. "PSEUDO-ALLERGIC RXN" = exaggerated release of vasoactive and inflam mediators in susceptible individuals
3. avoidance of NSAIDs and the use of leukotriene receptor antagonists (DOC) ex. monteleukast, zafirleukast, zileuton

Front 46

what qualifies as massive hemoptysis?
What steps to Tx?

Back 46

>100 mL of blood loss in 24hr.s
Steps:
1. intubate the pt. to protect airway
2. place bleeding lung in dependent position (ex bleeding in Rt. lung then place in Rt. lateral decubitus)
3. emergent bronchoscopy to visualize lesion and control bleeding + administer fluids.

Front 47

High clinical suspicion of PE (Algorithm)
1.
2.
3.

Back 47

1. stabalize pt.s with O2 and fluids
2. contraindications to anticoagulate?
3. * Yes -> Dxic test for PE:
+ for PE -> IVC filter
- for PE -> no further workup
* No -> start LWMH or IV hep and do Dxic test to eval for PE:
+ for PE : continue Hep and consider Qx or thrombolytics
- for PE: Stop Hep

Front 48

Mediastinum divisions and contents of each
- causes of widened mediastinum in each division

Back 48

1. Anterior mediastinum: thymus, internal mammary artery, lymph nodes
-thymoma
2. Middle: Heart in pericardium, ascending aorta, SVC, trachea and bronchi, Pulmonary artery and veins, phrenic nerves, bronchial lymph nodes
- BRONCHOGENIC CYST, aortic aneurysm/disxn, hilar lymphadenopathy, card tamp, pericard effusion
3. Posterior: esophagus, thoracic sxn of desc aorta
-esophageal rupture, neurogenic tumors (neuroblastoma, meningocele) thoracic vertebrae fractures

Front 49

HY
<ed breath sounds, dullness to percussion in right chest.
Next step?

Back 49

Thoracentesis to eval undiagnosed pleural effusion

Front 50

post op atelectasis:
1. how presents
2. prevention

Back 50

1. pain and changes in lung compliance can cause IMPAIRED COUGH AND SHALLOW BREATHING
2. pain control and incentive spirometry

Front 51

Indicators of severe asthma attack:

Back 51

normal to >ed Pco2 (from air trapping and respiratory muscle fatigue) (w/ asthma there's usually <ed Pco2 from hyperventilation), "silent" lungs, AMS

Front 52

Noninvasive positive pressure ventilation (NIPPV)
1. when do you use it?
2. contraindications?

Back 52

1. - if pt. not crashing
-for resp distress: w/ pH<7.35, or PaCO2>45 or RR>25/min
2. -septic, hypotensive or dysrhythmic pt.s (crashing): intubation

Front 53

pt. w/ raynaud's difficulty swallowing, diffuse thickening of skin w/ telangieactasia, dyspnea, nonproduct cough:
-Dx
-mechanism of pulmonary problems

Back 53

systemic sclerosis
pulmonary interstitial fibrosis

Front 54

complications of ventilation with high PEEP

Back 54

alveolar damage, tension pneum, and hypotn

Front 55

wegener's
1.ie
2. triad

Back 55

1. granulomatosis w/ polyangiitiss
2. systemic vasculitis, upper and lower airway granulomatous inflammation, and glomerulonephritis.
common external manifestations: nasal cartilage dstrxn and vasculitic cutaneous lesions (tender nodules, palpable purpura, ulcerations)

Front 56

pt w/ chronic COPD develops sudden severe dyspnea and left-sided chest discomfort, markedly decreased breath sounds over left chest.
what's the problem?

Back 56

spontaneous Pneumothorax <- rupture and air leaked into pleural space <- DILATED APICAL ALVEOLI (BLEBS) <- chronic destrxn of alveolar sacs <- chronic COPD

Front 57

septic pt. w/ respiratory failure refractory to high inspired O2 (FiO2 = 70%). what is it, what do you do?

Back 57

most likely ARDS (sepsis is a common cause).
keep FiO2<40% and >PEEP

Front 58

PNA's effect on :
1.v/q
2. A-a

Back 58

1. hypoxia <- v/q mismatch <- alveolar and interstitial inflamm
2. >ed A-a gradient

Front 59

Hypertrophic pulmonary osteoarthropathy (HPOA)
1. what is it

Back 59

1. digital clubbing + wrist and hand joint pain <- lung dz (CA, Tb, bronchiectasis, emphysema)

Front 60

CHF exacerbation
1. pathophys
2. exam findings

Back 60

1. hypocapnia and Resp Alk <-tachypnea <- pleural effusion <-fluid pools in lungs <- LV dysfnxn
2. S3 and S4, cardiomegaly, bibasilar crackles in lungs

Front 61

Atypical PNA Tx

Back 61

Mac

Front 62

Gram Neg aerobic PNA Tx

Back 62

Amp +Gent

Front 63

Anaerobic PNA Tx

Back 63

Clindamycin

Front 64

COPD vs CHF exacerbation on ABG and clinically

Back 64

CHF : Resp Alk, hypocap, and hypoxia, S3 and S4

COPD: resp acidosis and hypoxia, b/l wheezes

Front 65

exhudative pleural effusion glucose concentration
1. high or low?
2. what causes the level
3. level in empyema or rheumatic effusion?
4. level in malignancy, SLE, Esoph rupture, Tb

Back 65

1. low
2. high metabolic activity of leukocytes (and/or bacteria) in fluid decreases the [gluc]
3. <30 mg/dL
4. 30 -50 mg/dL

Front 66

intermittent asthma
1. what is it?
2. Tx

Back 66

1. daytime symptomes </= 2x/mo, normal FEV1/FVC, no daily activity limitations
2. albuteral (short acting beta 2 agonist)

Front 67

Mild persistent asthma
1. what is it?
2. Tx

Back 67

1. >2days/wk,>2x/month nighttime, normal PFTs
2. albuterol + inhaled corticoster +long-acting beta 2

Front 68

Moderate persistent
1. what is it?

Back 68

1. daily, weekly nightime, FEV1 60-80%

Front 69

Severe persistent
1. what is it?
2. Tx

Back 69

1. frequent day, frequent night, FEV1<60%
2. albuterol, long-acting beta 2 nhaler, high-dose inhaled cortico. oral prednisone can also be used.

Front 70

Indications in determining the need for chest tube placement in parapneumonic effusion (ie removal of fluid by thoracostomy)

Back 70

pH <7.2 and Glucose < 60 mg/dL

Front 71

sleep apnea can cause:

Back 71

2ndary erythrocytosis, pulmonary HTN, and cor pulmonale

Front 72

wiki's explanation of pulm shunt

Back 72

A pulmonary shunt is a right to left shunt. The shunt which means V/Q = 0 for that particular part of the lung field under consideration results in a de-oxygenated blood going to the heart from the lungs via the pulmonary veins. If giving pure oxygen at 100% for five-ten minutes doesn't raise the arterial pressure of O2 more than it does the alveolar pressure of O2 then the defect in the lung is because of a pulmonary shunt. This is because although the PO2 of alveolar gas has been changed by giving pure supplemental O2, the PAO2 ( Arterial gas pressure ) will not increase that much because the V/Q mismatch still exists and it will still add some de-oxygenated blood to the arterial system via the shunt.