Muthiah Flashcards

Question

What is the best fluid to give patients in sepsis? Why?

Answer 1

- _Balanced fluids_: avoid the biochemical effects of normal saline -\> giving these instead of NS may be a good thing 1. Probably won’t be on test, but just in case, choose **LACTATED RINGERS** 2. Reduced peri-operative mortality & ICU morbidity - _Normal saline_ (NS): can cause hyperchloremia & metabolic acidosis bc pH is only 5.4 1. Alterations in renal blood flow 2. Potentially important effects on immune function

Answer 2

- Levophed better than Dopamine - **Wean Levophed first** - Once \> 20 mics/min – add Vasopressin - Then: stepwise reduction in Vasopressin

Answer 3

The presence of organ dysfunction

Answer 4

Hypotension not responding to fluid resuscitation

Answer 5

Profound initial immune activation

Answer 6

Lymphocytes and GI epi cells -\> this is why patients start to develop infections with bugs found in the gut

Answer 7

Crystalloids (saline/lactated ringers)

Answer 8

- For sepsis treatment: 1. Feeds 2. Analgesics 3. Sedation protocol 4. Thrombo-embolism prophylaxis 5. Head of bed elevated \> 30^o 6. Ulcer prophylaxis 7. Glucose control

Answer 9

Improves mortality

Answer 10

- Sepsis is associated with profound immune activation - Pro-inflammatory cytokine levels are elevated along with neutrophilic leukocytosis

Answer 11

- _Primary Pulmonary HTN_ (PPH) – IPAH (idiopathic pulmonary arterial hypertension) 1. No identifiable reason - _Secondary Pulmonary HTN_ 1. Some other condition, i.e., left heart failure (pulm venous HTN -\> back pressure on the arteries) - After dx, most people _die within 3-5 years_ (mostly young F)

Answer 12

- Post-capillary HTN rules out IPAH b/c this means the PAH is most likely attributable to left heart failure - Pre-capillary HTN only -\> PAH

Answer 13

- Mean _PAP \>25mmHg at rest_ \>30mmHg w/exercise 1. Schwann-Ganz catheter (RH catheterization) the *only* direct way to measure pulm HTN 2. Mean PAP usually 10-15 mm Hg (\>2x here) - _Mean PCWP_ _& LVEDP \<15_ mmHg (ruling out LH failure b/c common) 1. INC LVEDP is gold standard for dx left heart failure (can do left heart catheterization, but dangerous, so PCWP is a surrogate) - Unclear etiology; absence of demonstrable cause - _REMEMBER_: systemic BP 120/80 (mean 65-70), PCWP = pulm cap wedge pressure, LVEDP = LV end diastolic pressure

Answer 14

- _Parenchymal lung disease_: alveolar hypoxia can stimulate vasoconstriction - Chronic thromboembolic disease: _CTEPH_ - Left-sided valvular disease - _Myocardial disease_: left ventricular failure - _Congenital heart disease_: R to L shunting - Systemic connective tissue disease - Primary if you don't find any of these

Answer 15

- _Groups 1-5_: things to know are in BOLD 1. Group 1: mutation-related (**idiopathic**, heritable, BMPR2), drug-, toxin-induced, HIV, CT disease -\> look phenotypically the same A. _Plexiform lesions_: endothelial proliferations in pulmonary circulation, causing occlusion of the arteries (seen in all conditions in group 1) 2. Group 2: PAH due to heart disease 3. Group 3: PAH due to lung disease 4. Group 4: **CTEPH** 5. Group 5: multifactorial etiology

Answer 16

- **Plexiform lesion**: single pulmonary arteriole

Answer 17

- INC in intimal thickness, fibroblasts, collagen, very small lumen -\> obviously going to INC the pressure, so RV has to work harder, leading to RHF (i.e., lower extremity edema symptoms)

Answer 18

- **Plexiform lesion**: proliferation may be monoclonal 1. PPH 2. Familial PPH 3. HIV-associated P HTN 4. L-R shunts 5. Toxins (Fen-phen, Aminorex, etc.) 6. HHT (hereditary hemorrhagic telangiectasia) w/PHT 7. CTEPH 8. Mitral stenosis

Answer 19

- Genetics + environmental trigger + imbalance of vascular effectors - **Vascular factors**: 1. _Prostacyclin and TXA2_ (platelet factor) 2. _ET-1_: most potent vasoconstrictor 3. _NO_: locally produced, very short half-life (DEC in NO synthase) 4. _Serotonin_: platelet aggregator, pulm vasoconstrictor 5. _VEGF_: overexpressed in plexiform lesions 6. _Anorexiants_: appetite suppressants (i.e., phen-phen associated with PAH in small minority of pts; mitral valve thickness and disease) 7. _CNS stimulants_, including cocaine -\> heart failure or brain hemorrhage first 8. _Adrenomedullin_: vasodilator peptide

Answer 20

- _Auto-immune_: scleroderma, SLE, MCTD, RA (Raynaud's) - _HIV_: 0.5%; _HHV-8_ (not sure why) -\> always do good hx and HIV test - _Portal HTN_ (~5%): relieve portal HTN, and 2/3rd’s of these pts get improvement in their PAH - _Thrombocytosis_: excess serotonin and TXA2 -\> platelet plugs and vasoconstriction - _Hemoglobinopathies_ (about 10% of sickle cell): may have to do with free heme (NO scavenger), which eats up NO - _Hereditary hemorrhagic telangiectasia_ (HHT; 15%) **- KNOW: systemic sclerosis, HIV, and sickle cell**

Answer 21

- Familial predisposition: observed in 6 - 10 % - _Autosomal dominant_ with incomplete penetrance - A responsible gene (PPH1) - _chromosome 2_ at locus 2q33 - Results in defective function of the bone morphogenetic protein receptor type II (**BMPR2**) - Asymptomatic carriers of PPH1 have abnormal pulmonary vascular responses to exercise

Answer 22

- Made by vascular endothelium - Catalyzed by nitric oxide synthase - Promotes vasodilation and inhibits smooth-muscle growth - _Endothelium from PPH patients showed negligible immunohistochemical staining for nitric oxide synthase_

Answer 23

- _Fen-phen_: especially in patients whose BMI is a little higher (they are not going to volunteer this information)

Answer 24

- _Potent vasoconstrictor & mitogen for smooth-muscle cells_ - Produced by vascular endothelium - Localizes to muscular pulmonary arteries of patients with PAH

Answer 25

- Specific _endothelial growth stimulant_ - Induced by various cytokines including PDGF &TGFβ - Expressed by endothelial cells in **plexiform lesions** - Role in pathogenesis is still speculative

Answer 26

- Stored mainly in platelets - Associated with _pulm vasoconstriction and proliferation of smooth muscle cells_ - Plasma serotonin concentrations are higher than normal in PPH - SSRI’s: small INC in PAH, but still not evidence-based

Answer 27

- Control the _cell-membrane potential and the release of calcium_ via sarcolemmal voltage-gated channels - In PPH pulmonary artery smooth muscle cells have low mRNA for the potassium channels and low channel current, with a resultant _increase in intracellular calcium_ - **Blocked by the appetite suppressants** -\> thought this would help with therapeutic modalities, but not yet

Answer 28

- Mean age at dx: 36 (typically F in 20's or 30's); but can present at any age (Muthiah had a 72 y/o pt) - Diagnosis often delayed bc pts present with non-specific symptoms: 1. Fatigue 2. Exertional dyspnea (tx as asthma for a year sometimes) 3. Exertional chest pain 4. Exertional Syncope 5. Edema - Treated as something else before dx of PAH entertained

Answer 29

- Detailed H and P; high index of suspicion (rare, but bad) - **Things to look for**: 1. _Dyspnea_ of variable severity 2. _Apical impulse shifted outwards_: same ICS, but in the axillary line (down and out LV, out RV) 3. Parasternal heave: 2-3 fingers in L parasternal region (going to lift your fingers) 4. Palpable P2: can hear accentuated P2 (loud) 5. _Accentuated P2_; lungs may be clear 6. Widely split S2 7. SEM L 2nd ICS 8. PFTs w/mildly DEC DLCO w/o evidence of airway obstruction or decreased lung volumes

Answer 30

- Nothing seems to stop disease course -\> **PROGRESSIVE** - PVR: pulmonary vascular resistance - If sedentary lifestyle, may not have symptoms for awhile - Once RV starts to decompensate, PAP may come down -\> _PVR is what you are going to be looking for_ - CO stays okay in pre-compensation stage, but with symptoms and uncontrolled pulmonary pressure, CO starts to fall consistently

Answer 31

- **Echo** (TTE: transthoracic echo) - About 95% confidence -\> if it looks like it, then do **R heart catheterization to confirm** - Pulmonary angiography: required when you are thinking about chronic thromboembolic PH - CT scan: when you think it is associated with interstitial lung disease (or if looking for a PE -\> helical CT) - THIS WILL PROBABLY BE IN THE BOARDS

Answer 32

- **R. heart catheterization**: to confirm the diagnosis (do this bc also can be caused by left heart failure, so you have to check PCW pressure to make sure it is \<15) - RV systolic pressure should be \<15-20

Answer 33

- **PCWP**: when left heart fails, left atrial pressure increase, but difficult and more invasive to do left heart cath, so you check pulmonary cap wedge pressure (PCWP) as an indirect measurement of L atrial pressure (_Schwan Ganz catheter_) - If \<15, then patient does not have LHF (PAH, not PVH) - PVH = pulmonary venous HTN

Answer 34

- Vasoreactive pts have a relatively (or much) **better prognosis** (only about 5-6% of pts) compared to pts w/o vasoreactivity 1. _Vasoreactivity_: pulmonary vasculature constricted -\> if I give vasodilators, will it give in to these - _Inhaled NO_ is probs the best agent to test vasoreactivity

Answer 35

- **Nitric oxide** (NO) - Sometimes use adenosine: very important vasodilator, but short-acting, and can have unstable shelf-life

Answer 36

- Echo is usually the first diagnostic test -\> **good screen** - _Will show_ _evidence of_: 1. Right heart chamber enlargement 2. Paradoxical motion of the IVS 3. Tricuspid insufficiency – 4V²+ RA Pressure - Look for tricuspid insufficiency: there will be tricuspid regurgitant jet (measured using echo -\> formula above; don’t need to remember the equation, but _know that this jet is used to measure pulmonary artery pressure_)

Answer 37

- CBC, CMP, TFTs (to test for hyperthyroidism), HIV - CXR - Connective tissue serology (ANA,Scl- 70, Anti-RNP) - PFTs, _exercise oxymetry_: only 2 conditions that can cause exercise desaturation in early stages -\> PAH and pulmonary fibrosis - _Echocardiography_ - V/Q scanning or CT angiography - Sleep studies - Complete _cardiac catheterization_ - **Go through most of these**

Answer 38

**Normal FVC, FEV-1, and TLC with reduced DLCO** - _Pulmonary vascular disease pattern_ (lung is normal; really a vascular disease, like PE) 1. Isolated reduction in DLCO, unless some other comorbidity - _Causes of reduction in DLCO_: PAH, anemia, early/late stage emphysema (significantly DEC), chronic bronchitis (mildly decreased)

Answer 39

- **Isoprostenol**: IV; pretty unstable in ambient temperature (has to be refrigerated) 1. Short half-life, so need an IV pump (venous access via indwelling catheter) 2. Acute interruptions can lead to rebound increase in PAH -\> if pump malfunctions, pt can drop dead - _Class II or III,_ can start with _Bosentan_: endothelin-1 receptor antagonist available as a pill

Answer 40

Normal CXR

Answer 41

PPH CXR: proximal enlargement of the vasculature

Answer 42

- _Tall p wave_: p-pulmonale -\> R. atrial enlargement (if M-shaped or bifid, it looks like mitral or left atrial enlargement) - Evidence of _R ventricular hypertrophy_: dom R wave in V1 (and aVR), dom S wave in V5-6 - _R ventricular strain pattern_: ST depression and T wave inversion in the right precordial (V1-4) and inferior (II, III, aVF) leads - _S1Q3T3_: bottom left -\> acute = PE, chronic = PAH - Reference: http://lifeinthefastlane.com/ecg-library/basics/right-ventricular-hypertrophy/

Answer 43

- Typical PFT from pt with PAH - FVC and FEV-1 normal, but _DLCO reduced_

Answer 44

- _~5 percent of PAH pts are responders_, defined as: 1. **\>20% reduction in PAP & PVR** 2. INC or unchanged CO 3. Minimally reduced or unchanged systemic blood pressure & SVR 4. \>10mmHg drop in MPAP (should drop to \<40mmHg) - **Inhaled NO**: selective for the pulm vascular bed 1. Binding w/Hgb in pulm caps makes it physiologically inactive 2. _Fall in PAP in response to inhaled NO is a good indicator the pt will respond to CCB's_ 3. Often better tolerated dx agent than IV vasodilators

Answer 45

- _Start with echo_, then depending on how pt looks, you can go through the rest of the work-up as needed

Answer 46

- _CCB's_: huge doses; most patients not compliant (for WHO III or IV, wait for RV failure, and start Ipoprostenol infusions) - _Bosentan/Ambrisentan/Macitentan_: can be given orally - _Sildenafil_: Viagra (PDE-5 INH that INC NO locally in pulmonary vasculature) - _Treprostinil_: prostacyclin analog (like Ipo; better shelf life and doesn’t have to refrigerated; oral form now too) 1. Iloprost: inhaled, short half-life (9x per day) 2. Epoprostenol - _Riociguat_: INC cGMP by stimulating Guanylate Cyclase - Adjuvant therapy - Advantage of different MOA’s is that you **can use them in combination**

Answer 47

- **MOA**: potent vasodilator that acts via receptors linked to adenylate cyclase -\> **v****asodilation 2^o to INC IC cAMP** 1. INH platelet aggregation and smooth m proliferation - Delivered by **portable infusion pump**: both responders and non-responders show improvements in exercise tolerance, hemodynamics, and survival 1. Begin at doses of 1-2 ng/kg/min, and INC by 1 to 2 ng/kg/min every 1-2 days as tolerated 2. Most pts require dose INC of 1-2 ng/kg/min every 2-4 weeks in order to sustain clinical improvement - **Side effects**: jaw pain, diarrhea, arthralgias, infection, _thrombosis_, pump malfunction, interruption of the infusion

Answer 48

- Phase III trial: improved 6-min walk distance (Sildenafil showed similar walking improvements), INC CO, DEC mean PAP, and DEC PVR - **AE's**: elev of serum aminotransferase levels, teratogenic, interaction with Cyclosporine

Answer 49

- Several studies suggest they may _improve survival_ - Pts with PPH at INC risk for intrapulmonary thrombosis and VTE, due to: 1. Sluggish pulmonary blood flow (clots can form behind plexiform lesions) 2. Dilated right heart chambers 3. Venous stasis 4. Sedentary lifestyle - Anticoagulant of choice is **Warfarin** (goal INR of 2)

Answer 50

- Variable -\> depends on the: 1. Severity of hemodynamic derangement 2. Response to vasodilator therapy - **Echocardiographic findings** associated w/poor outcome: 1. Larger R atrial size 2. Degree of septal shift in diastole (hypertrophied R. heart starts to shift septum to left side) 3. Presence of a pericardial effusion - Patients with PAH are _at risk for both progressive right heart failure and sudden cardiac death_ - CPR after CV collapse (code) in generally unsuccessful - **Mean survival of ~ 3 yrs** from diagnosis, but pts with severe PAH or Rt HF tend to die within one year (once RV failure sets in, hard to get these pts to turn back around) - Functional classes I and II tend to live far longer than those who fall into classes III and IV

Answer 51

- _Hypoxemia at rest or during activity_, due to a reduced CO, ventilation-perfusion inhomogeneity, or R-to-L shunting through a patent foramen ovale 1. Try to break hypoxia-induced vasoconstriction 2. Supplemental _oxygen_ should be provided in this setting - _Diuretics_ can be given for control of edema-\> can get these pts from class IV to class II sometimes (but preload dependent, so take it slow) 1. Avoid excessive preload reduction - _Digoxin_ may be of some benefit with right ventricular dysfunction - controversial

Answer 52

- Coumadin, O2 (because they will desaturate when they walk), Digoxin, Aldactactone, Diuretic - CCB (seldom used), Bosentan/Ambri/Macitentan, Epoprostenol (IV), Iloprost (inhaled), Treprostinil (IV), Sildenafil, Riociguat 1. Expensive - Transplantation – probably will cure PAH, but doesn’t make pts live much longer -\> does improve quality of life (8-10% peri-operative mortality) 1. Some may live up to 10 more years though

Answer 53

- Insidious onset, progressive disease -\> high index of suspicion necessary - _Poor prognosis_: ≤3year survival if untreated 1. Epoprostenol, Bosentan proven to improve survival 2. Anticoagulation also may add to survival - Oral ET antagonists may be an attractive choice - Inhaled Iloprost: also an attractive alternative - Macitentan/Riociguat – recently approved - Future (Already here!): **combination therapy** - Lung Transplantation in the appropriate setting

Answer 54

- Distance b/t spinous processes and the clavicles equal on both sides = not rotated - _NOTE_: if rotated, it can look like there are hilar infiltrates even though there are not

Answer 55

- This will be the view for patients that cannot stand up - One disadvantage is that the heart will look larger than it actually is (see attached image -\> AP view on the right)

Answer 56

Line is the minor fissure - normal CXR

Answer 57

- Major fissure the diagonal, and the horizontal is the minor fissure -\> helps you identify which lobe is infiltrated - Only a major fissure in the left lung

Answer 58

- White-outs: pathognomonic for air-space disease - _Air bronchograms_ (attached image): pathognomonic for air-space disease -\> classic in pneumonia

Answer 59

Air bronchograms (air-space disease)

Answer 60

- _White-out_: air-space disease - Looks like _left side pleural effusion_ as well (possible) - line on the left

Answer 61

- Pneumococcal pneumonia - Mostly neutrophils - Lower respiratory specimen bc minimal epithelial cells (light-colored ones)

Answer 62

- Cardiomegaly with perihilar infiltrates (aka, central or bilateral alveolar) - Leads: AP view

Answer 63

- Lasix for CHF patient - _Note_: transudative edema will clear much faster than exudative

Answer 64

- "Bat wing" infiltrate -\> pulmonary edema

Answer 65

- _Cephalization_: rarely seen bc these pts present later - _Cardiomegaly_ - _Perihilar infiltrates_ - _Peribronchial cuffing_: looks like bronchus is surrounded by edema from side view - _R. pleural effusion_ (more common on R side when unilateral, but most commonly bilateral) - _Enlarged azygos vein_ - _Kerley B lines_ (lymph lines -\> transporting fluid when pts have chronic, not acute, pulmonary edema)

Answer 66

- Cardiomegaly -\> sign of CHF

Answer 67

- Fluid in the fissures - Can be initial manifestation of CHF, but by no way the most common

Answer 68

- Pulmonary hemorrhage, and in this case, renal (b/c Goodpasture's)

Answer 69

- _Pulmonary edema_: fluid - _Pneumonia_: exudate, or WBC's 1. Usually going to be pulm edema or pneumo -\> think about white count, fever, etc. to distinguish bt the two - _Pulmonary hemorrhage_: blood - Tumor/bronchoalveolar cell _carcinoma_: looks like pneumo, but older pt w/o fever who won't respond to tx - Idiopathic

Answer 70

- Reticulonodular pattern - Reticular: criss-crossed lines + nodular: dots = interstitial disease: sarcoidosis

Answer 71

- Reticulonodular pattern - Reticular: criss-crossed lines + nodular: dots = interstitial disease: sarcoidosis

Answer 72

- Classic presentation of **sarcoidosis**: bilateral hilar adenopathy (enlarged lymph nodes) 1. Should be at the bottom of your dx list, however, bc it is one of exclusion (think: lymphoma, histo, TB, etc.) - Paratracheal or bilateral hilar adenopathy with or w/o reticular infiltrates

Answer 73

- Classic presentation of **sarcoidosis**: bilateral hilar adenopathy (enlarged lymph nodes) 1. This should be at the bottom of your dx list, however, because it is a dx of exclusion (think: lymphoma, histo, TB, fen-phen use, etc.) - Paratracheal or bilateral hilar adenopathy with or w/o reticular infiltrates

Answer 74

- Lymphoma - Histo - Fen-phen use - TB - Castleman's - HIV: pts with bilateral hilar adenopathy -\> think TB - Sarcoidosis: at the bottom of the list because it is a diagnosis of exclusion

Answer 75

- Well-formed, non-caseating granuloma -\> sarcoid

Answer 76

- Usually means advanced stage of interstitial disease - Air with cystic spaces separated by coarse reticular network - Grossly distorted parenchyma - _Examples_: IPF, RA lung

Answer 77

- IPF - Upper lobes less involved than lower lobes in this example

Answer 78

- Similar chest radiographs for COPD/chronic bronchitis 1. most pts have both - Hyper-inflated lungs - INC compliance and airway resistance - Flattened hemi-diaphragms - Narrow, vertical heart (in the absence of CHF) - Increased "lung markings" - Bullous disease

Answer 79

- Flattened hemi-diaphragms - Characteristic of COPD

Answer 80

Bullous emphysema

Answer 81

- **Bronchiectasis**: _persistent dilatation of terminal bronchi_ with destruction of the elastic and muscle tissue of the bronchial wall - Plain CXR: bronchial wall thickening, parallel lines (tram lines), sometimes cysts

Answer 82

Cystic bronchiectasis

Answer 83

- Most common is a _NORMAL CXR_ 1. Atelectasis may be present (and pleural effusions, when present, are small) 2. Portion of lung not getting blood flow will tend to divert air, probably via bronchospasm - In exam, if pt has acute onset SOB and no ronchi and normal breath sounds on both sides, then they have PE

Answer 84

- PE in left lower lobe, so elevated hemi-diaphragm due to atelectasis

Answer 85

- _Hampton's hump_: infarcted part of the lung - Pretty rare -\> probably won't be tested on this

Answer 86

- **Westermark's sign** - _Don’t see vasculature_ at all -\> R. pulmonary trunk embolus - We would also suspect pneumothorax (collapsed lung) in this case 1. Know it’s not this because listen to the pt and hear good, bilateral lung sounds -\> listening to lungs or ultrasound could help - Why doesn’t the lung infarct? Dual blood supply

Answer 87

- _Signs of benignity_: 1. Well-defined (circumscribed) nodules 2. No assoc lymph node or mediastinal masses 3. No satellite lesions 4. Calcified nodules - _SPN's_: 3 cm's in size or less, and 30-40% are malignant 1. Smaller = nodules and larger = masses - **MUST KNOW THESE**

Answer 88

- _Dense_ - _Popcorn_ - _Lamellar_: onion-skinning - Some central can also be benign (less strong sign; top right example in attached image) - _Note_: spiculated or changing would be signs of malignancy

Answer 89

Popcorn calcification

Answer 90

- Spiculated nodules: larger on one side? - Non-calcified nodules - Associated mediastinal or lymph node masses - Presence of cavitation: blood supply not enough to keep up with fast growth, so necrosis -\> usually squamous cell carcinoma - Large nodules: in general, 3-4 cm, suspect malignancy

Answer 91

- _Biopsy_: surgical excision, transbronchial sampling during fiberoptic bronchoscopy, trans-thoracic needle aspiration - _Sputum cytology_ (low yield): do this in patients with hemoptysis, esp. those that are poor bronchoscopy candidates 1. Can help to avoid a procedure

Answer 92

- If there is fat in the nodule, it is a HAMARTOMA - Omstel units: water = 0 (things that float on water have negative value)

Answer 93

Well-circumscibed nodule (probably benign)

Answer 94

Right atrium (NOT the right ventricle)

Answer 95

- **Silhouette sign** - Can't see the right heart border -\> infiltration of the lung, changing contrast between heart and lung 1. _Right middle lobe infiltrative process_ - If there were no left heart border, this would suggest an invasive process in the lingula - If you are not able to see the hemi-diaphragm, the infiltrate is in the lower lobe - THIS WILL BE ON THE EXAM

Answer 96

- Carina is splayed -\> cardiomegaly - Left atrial enlargement: described as an orange w/in the heart

Answer 97

- Left: _pleural effusion_ (white out) 1. _Meniscus sign_: crescent-shaped inclusion of air surrounded by consolidated lung tissue 2. The larger the effusion, the more likely the mediastinum is going to be pushed to opposite side A. If it shifts to the same side, you are going to assume there is some kind of atelectasis as well (like in this case) B. Left lung looks hyperinflated here - Right: _hydropneumothorax_ -\> air and fluid (could be blood as well, or pyo, but not as common) in the pleural space (air:fluid straight line)

Answer 98

- _Pneumothorax_: 80-90% collapse of the left lung, but compared to Westermark's sign, we are able to see the lung that has collapsed - Pleural pressure has increased, so there is no more negative pressure holding the lung open

Answer 99

Large pneumothorax (pt w/bad emphysema)

Answer 100

Lateral view of pneumothorax (more air in front, and maybe up in the apex as well)

Answer 101

Ideally-placed chest tube -\> negative suction to take the air out, allowing the lung to completely expand (post-pneumothorax, for example)

Answer 102

- _Respiratory_: hypoxic (respiratory failure will actually include ventilator failure) - _Ventilatory_: hypercapnic (decrease in alveolar respiration) - Clearly, these are often going to coexist, but we talk about them as separate issues 1. Can be acute (hours to days) or chronic, or even acute on chronic (i.e., COPD exacerbation)

Answer 103

- Hypoxemic failure - Ventilation/Perfusion (V/Q) mismatch: in airway obstruction (COPD), gas exchange not happening effectively even though it may look like pt is moving air - Shunt - Exacerbated by low mixed venous O2 (SvO2) - Hypercapnic failure - Decreased minute ventilation (MV) relative to demand, e.g., narcotics (hypoventilation) - Increased dead space ventilation

Answer 104

- _Normal A-a gradient_: 1. Hypoventilation 2. Decreased PiO₂ - _Increased A-a gradient_: 1. V/Q mismatch 2. R-to-L shunt 3. Diffusion limitation

Answer 105

- Central hypoventilation - Neuropathies - Muscle (pump) failure 1. Muscular dystrophies 2. Myopathies 3. Myasthenia gravis - Airway Obstruction

Answer 106

- Relatively large changes in O2 saturation do not dramatically change PO₂until you get to a PO₂ of about 40 or O₂ saturation of 70% 1. For example, a minimal increase in O2 sat from pO2 of 60 to 100 due to hemoglobin loading

Answer 107

- TAP: 1. Temperature 2. Acidosis 3. Phosphate – 2,3-DPG 4. CO2 - Decreases affinity for, and unloads oxygen

Answer 108

- Hypothermia (DEC temperature) - Alkalosis (INC pH) - Fetal hemoglobin - CO - These all cause increased affinity for O2

Answer 109

- Pt will present with dyspnea and/or hypoxia 1. _Acute_: think PE, acute MI (silent -\> happen more often in F, and pts with uncontrolled diabetes) - **Things to do**: 1. _History and physical_: JVD, S3, pulm crackles 2. Vital signs, incl pulse oximetry 3. CXR 4. _EKG_: pts w/heart transplants may have MI and not know it bc denervated -\> always do EKG on these patients when they come in short of breath A. Also in pts w/suspected heart failure 5. ABG 6. CBC 7. _Electrolytes_: e.g., bicarbonate -\> if it is \>30, you can begin to suspect these pts are retaining CO2 A. Pts retaining CO₂ more likely to get into trouble 8. _Sputum and blood cultures_: look for neutros 9. _UA_: sepsis can cause resp failure (look for leukocyte esterase, nitrites to see if UTI -\> esp. important in F, older M w/BPH, pts with catheters) 10. _Helical CT vs. V/Q scan_: to avoid contrast (due to allergy or kidney damage), use V/Q scan A. _Helical CT_: now test of choice if looking for PE bc global view (if you can’t find a PE, you can probably find out what is wrong) B. _PE_: demonstrate V/Q mismatch 11. _Pulmonary function tests (PFT’s)_: don’t do these on pts in acute situations, but rather for chronic conditions like COPD or asthma 1. _6-minute walk test_: see how far patients can walk in 6 seconds

Answer 110

Supplemental O₂

Answer 111

- _V/Q mismatch_: readily corrects w/O₂ supplementation - _Note_: shunt would NOT correct with O₂

Answer 112

- To see how far patients can walk in 6 seconds 1. Tests for interstitial disease and pulmonary arterial HTN (goal-directed therapy) -\> these are the only 2 conditions w/desaturation on exercise in their early stages 2. If this continues to drop, these patients have the worst prognosis

Answer 113

- Send them to the **cath lab to break up the clot** - _Heparin_ helps prevent clots, but does not bust them up (if high suspicion, and no contraindications, start on anticoagulant while waiting for helical CT) - _TPA_ will activate fibrinolytic process to help bust up clot -\> bleeding is a big problem, so don’t want to use TPA on all patients; _may be contraindicated_ 1. *Only use this in pts with acute PE and shock*

Answer 114

- Bronchodilators: Epinephrine, Theophylline, Albuterol - Beta 2 agonists: 1. SABA: Albuterol 2. LABA's: Formoterol or Salmeterol -\> don't use these for rescue, even though Formoterol is fast-acting - Anticholinergic agents: Ipratropium

Answer 115

- _Albuterol and Ipatropium_: 5 to 15 min. - _Formoterol_: fairly rapid onset of action, but still not used as a rescue inhaler

Answer 116

- Asthma, COPD exacerbations - Anaphylaxis - Acute bronchitis - Toxic inhalations

Answer 117

- Bronchodilators - _Hydration_: losing insensible water via breathing, so hydration is important for these patients (can lose a lot of water; sometimes up to 3 liters) - _Systemic corticosteroids_: reduce inflammation - Treat the precipitating cause - _Infection/AB's_: err on side of caution by tx w/ AB's if you are not sure if an infection is viral or bacterial - **What if pt continues to get worse or get tired**: 1. _BiPAP_ -\> non-invasive positive pressure that doesn’t involve putting anything in pt. (mask you can put PEEP on -\> pressure support for when pt takes a breath, _DEC work of breathing_, & keeping airways open when the pt is breathing out) A. Decreases mortality by 30% 2. If this doesn’t work, and pt. continues to retain CO2 and have bad O2 saturation, then _intubate_ A. Rarely intubate patients with COPD - **How do you know if the patient is getting tired?** 1. Looks apprehensive 2. Experienced nurse: “He is not looking good” 3. Increased somnolence (sleepy, drowsy: CO₂ is a narcotic) 4. Decreasing RR or respiratory excursions 5. _Borderline O₂ sats_: may not be present while giving supplemental oxygen 6. _What is the ABG likely to reveal_? INC CO₂-\> need to IMPROVE VENTILATION

Answer 118

- Assist breathing - Mechanical ventilation - Non-invasive (BiPAP) vs. endotracheal intubation

Answer 119

B.The amount of oxygen that is dissolved in plasma (PaO2)

Answer 120

Alveolar hypoventilation

Answer 121

- In chronic hypercapnia, PCO2 may rise in response to supplemental oxygen for 3 reasons: 1. _Worsening V/Q mismatch_: supplemental O2 abolishes hypoxic-induced vasoconstriction of the pulmonary vasculature 2. Release of hypoxic vasoconstriction in poorly ventilated areas of lung caused by INC in PaO2 3. _Consequence_: increased blood flow to low V/Q areas and a worsening of V/Q inequality which exaggerates the degree of CO2 retention

Answer 122

- In hypoxic pts some CO2 is bound to hemoglobin as carboxyhemoglobin - Supplemental oxygen raises both PaO2 and SaO2 - CO2 must be displaced from hemoglobin (carboxyhemoglobin becomes oxyhemoglobin) - CO2 can only dissolve in blood, raising PCO2 - **Succinctly**: deoxygenation of blood INC its ability to carry CO2; conversely, oxygenated blood has a reduced capacity for carbon dioxide

Answer 123

- The COPD V/Q inequality, along with the ‘Haldane effect’ are the most significant causes of hypercapnea; therefore continue 40% O2 - _Haldane effect_: deoxygenation of blood INC its ability to carry CO2; conversely, oxygenated blood has a reduced capacity for carbon dioxide

Answer 124

**E. The pathognomonic EKG finding of S1Q3T3 is seen only in a minority of patients** ## Footnote - About 10% from upper extremities, but INC due to obesity, lying in bed, IV’s from central venous catheters - Bronchospasm and wheezing *can be seen* because platelet products can provoke bronchoconstriction - Reason for hypoxemia is dead space ventilation - Anticoagulation therapy SHOULD BE initiated -\> can save patient’s lives - _S1Q3T3 is evidence of R ventricular strain_

Answer 125

- Lung has dual blood supply - PA bringing in de-oxygenated blood, and veins take the oxygenated blood back to the left heart

Answer 126

- YES -\> causes vital signs to go out of whack - We have rapid response teams for acute onset SOB

Answer 127

- Annual incidence more than 500,000 - 11% die suddenly (autopsy -\> saddle emboli) - 67% not diagnosed during life (autopsy) - Undiagnosed PE has a mortality of 30% to 55% 1. Diagnosed PE has a mortality \< 10% -\> _diagnosis saves lives_

Answer 128

- \> 90% from _deep vein thrombosis_ (DVT) in the legs 1. Pelvic veins in some (i.e., post-surgical) 2. Upper extremity veins in others (central venous catheters) - _Non-blood clot emboli_: 1. _Air_: from central venous lines (60-100 cc’s of air to kill the patient -\> avoid this by placing patient in trendelenburg position) 2. _Tumor_: renal cell carcinoma 3. Amniotic fluid 4. Talc 5. _Fat_: bone break (typically in elderly)

Answer 129

- _Virchow's triad_: 1. Stasis 2. Endothelial damage 3. Hypercoagulable state (e.g., trauma or surgery)

Answer 130

**B. Factor V Leiden** ## Footnote - _Factor V Leiden_: resistance to activated protein C (a natural anti-coagulant) 1. Homozygotes are most affected 2. Prothrombin gene mutation also a risk factor 3. Anti-cardiolipin Ab’s 4. Protein C or S deficiency 5. Antithrombin III deficiency - Chemo not a risk factor, but cancer causes hypercoagulable state, especially adenocarcinomas - Exertion not associated with VTE - Estrogen is associated, but progesterone is not - High altitude can cause pulmonary HTN, but not VTE

Answer 131

- Immobility - Bed rest - Anesthesia - Congestive heart failure/cor pulmonale - Prior venous thromboembolism - Central venous catheters

Answer 132

- **Heritable**: 1. _Factor V Leiden mutation_ 2. Prothrombin G20210A mutation 3. Protein C & Protein S deficiency 4. Antithrombin III deficiency 5. Dysfibrinogenemia 6. Homocystinemia 7. INC levels of factor VIII (newer info) - **Acquired**: 1. _Estrogen use_: also INC during pregnancy (so hormonal changes while prego a factor) 2. _Malignancy_ 3. Thrombocytosis: INC availability of platelets 4. Disseminated intravascular coagulation (DIC) 5. _Heparin induced thrombocytopenia_ (HIT): if PLT count drops after starting heparin therapy (or clot forms), suspect HIT -\> problem is if pt now has a clot or is going to, and need an anti-coagulant (will have to be something other than heparin) A. Anti-platelet 4 antibodies (high sensitivity and low specificity) 6. _Antiphospholipid antibody syndrome_: can be a stand-alone syndrome (aka, anti-cardiolipin) 7. _Nephrotic syndrome_: loss of proteins (anti-coags lost in the urine, so pt more prone to VTE) 8. Paroxysmal nocturnal hemoglobinuria (PNH)

Answer 133

- Homocystinemia - Autoimmune injury - Trauma - Surgery - Malignancy, and treatment for malignancy

Answer 134

- Size of the embolus -\> larger embolus = more problems - Cardiopulmonary status/reserve: has a lot to do with how the patient presents - Neurohormonal substances

Answer 135

- _Increased pulmonary vascular resistance_: 1. Vascular obstruction 2. Neurohumoral agents: serotonin, endothelin -\> vasoconstriction, & further INC vascular resistance - _Impaired gas exchange_: 1. Increased alveolar dead space ventilation from vascular obstruction (V/Q mismatch) 2. Impaired carbon monoxide transfer (low DLCO) due to loss of gas exchange surface 3. Right-to-left shunting (in massive PE) - Alveolar hyperventilation due to reflex stimulation of irritant receptors (J receptors) - Increased airway resistance due to broncho-constriction (resulting in wheezing) - Decreased pulmonary compliance due to lung edema, lung hemorrhage, or loss of surfactant - All of this can make your patient present with **SOB** after a pulmonary embolism

Answer 136

- _Vasodilatation of uninvolved vasculature_ 1. Pressure may not change at all, esp. if pt has healthy lungs - _Helps DEC the INC in pulm vascular resistance_ (PVR) 1. 1. If you block R pulm artery, pulm vascular resistance barely goes up bc, in general, about 25-30% of pulm capillaries aren’t participating (until you are exerting yourself, for example) - _Also improves V/Q relationship in uninvolved areas_ - This _improves overall oxygenation_ 1. May not be very hypoxic -\> pt may be tachypnic and tachycardic (hyperventilating)

Answer 137

- Trachea is index of upper mediastinal position: 1. Pleural pressures on either side determine the position of mediastinum -\> will shift to side with relatively higher (-) pressure relative to the other - _Deviated towards diseased side_: 1. Atelectasis 2. Agenesis of lung 3. Pneumonectomy 4. Pleural fibrosis - _Deviated away from diseased side_: 1. Pneumothorax 2. Pleural effusion 3. Large mass

Answer 138

- Increase in minute ventilation (tachypnea) - V/Q inequality (hypoxemia -\> wide A-a) - Shunting (in massive PE) - _Gas exchange abnormalities_: 1. Hypocapnia: because J receptors activated and hyperventilating 2. Hypoxemia 3. Wide (PA-Pa)O2 –\> A-a gradient

Answer 139

- Severe ALI involving DAD, INC microvascular permeability and non-cardiogenic pulmonary edema - Acute refractory hypoxemia - High mortality: 40-60% - Bilateral, diffuse alveolar infiltrates (classic x-ray image attached)

Answer 140

- Acute onset of resp failure (\<1 week) - Bilateral infiltrates on CXR - _No evidence of volume overload_ (new addition to the criteria) - PaO2/FiO2 \< 300

Answer 141

- _Activation of inflammatory mediators_ and cellular components -\> damage to cap endo and alveolar epi 1. Neutros (instead of macros) predominate in BAL of these patients due to inflammation - _INC permeability_ of alveolar capillary membrane - _Influx of protein-rich edema fluid_ and inflammatory cells into air spaces - _Dysfunction of surfactant_: alveolar collapse -\> very little gas exchange, but blood still coming into lungs 1. If this happens to the whole lung, top to bottom, the patient will die (usually only about 80-90%, so patients end up on mechanical ventilation)

Answer 142

- **Direct lung injury**: 1. Pneumonia/aspiration of gastric contents or other causes of chemical pneumonitis (inhaled smoke from a fire) 2. Pulmonary contusion, penetrating lung injury 3. _Fat emboli_: e.g., long bone fracture -\> more common w/elderly than young people bc young people have more marrow and less fat 4. Near drowning 5. Inhalation injury - **Indirect lung injury** 1. _Sepsis_: inflammation spreads via cytokines, and 100% of blood goes through lungs, so they are affected by sepsis (more than kidneys, even) 2. Severe trauma w/ shock hypoperfusion 3. Drug OD 4. Cardiopulmonary bypass 5. _Acute pancreatitis_: inflammation that can spread to lung, kidneys 6. Tansfusion of blood products 7. TRALI: transfusion-related lung injury

Answer 143

- Consolidation usually most prevalent in posterior, or dorsal part of the lung -\> excess lung water in the back of the patient when they are lying down (gravity) - _Lying prone can help reduce mortality_ (rather than supine) -\> diverts blood from poorly aerated to better aerated areas 1. Can help improve gas exchange

Answer 144

- Exudative: 1-4 days - Proliferative: 4-8 days - Fibrotic: \>8 days - Recovery

Answer 145

- Chronic liver disease - Non-pulmonary organ dysfunction - Sepsis - Advanced age

Answer 146

- Based on CXR, PaO2/FiO2, PEEP, and respiratory compliance - Add all of the points and divide by 4 1. Mild-moderate: 1 - 2.5 2. Severe: 2.5 - 4 - Probably will not be tested on this -\> know the concept, but not necessarily how it is calculated

Answer 147

**Increase the PEEP** (+ end expiratory pressure) ## Footnote - To _redistribute (NOT reduce) the lung water_, pushing it away from the alveoli, and back into the non-alveolar portion of the interstitium 1. Not going to stop the flow of air - _INC tidal volume doesn’t work_; can be detrimental bc the more you stretch your cells, the more they are going to get inflamed - Want to avoid O2 toxicity (i.e., from free radicals) - If you vasodilate portions of the lungs that are better aerated, you can improve function -\> you can do this by giving _inhaled NO_ (not shown to improve mortality, but can improve oxygenation; cost $300 per hour)

Answer 148

**Recruiting atelectatic alveoli and increasing FRC** ## Footnote - Residual volume + expiratory reserve volume = FRC; better the FRC, the better the reserve when you hold your breath - Pregnant women/obese patients, saturation drops when you intubate due to low FRC 1. Better to have high FRC 2. Pregnant women also have increased risk of PE

Answer 149

They are normal

Answer 150

D. High grade inflammation

Answer 151

D. Absence of evidence of Volume overload ## Footnote - Adaptive repair: can happen in younger patients, but some older patients will have lasting fibrosis

Answer 152

B. Deployment of lower TV than usual (6 cc /Kg predicted body weight) ## Footnote - This will ABSOLUTELY be on the boards - _Peak pressure_: highest pressure that you see during inhalation in the respiratory system (flow + resistance) 1. _Plateau pressure_: pressure taken when you pause at full inspiration 2. If both peak and plateau pressures are high, then the problem is with compliance 4. Peak high, plateau normal, resistance problem

Answer 153

B. After two weeks of ARDS onset ## Footnote -

Answer 154

C. Acute decrease in pulmonary compliance ## Footnote - Increased lung water or consolidation will cause this

Answer 155

- Subcutaneous emphysema - Interstitial emphysema following inflammation rupture (due to necrosis?)

Answer 156

B. Multi-organ failure ## Footnote - Because you can't control inflammation -\> give corticosteroids to help control this - This will probably be on USMLE - Decreasing tidal volume helps limit further damage to the lungs

Answer 157

- Gravity-dependent consolidation in ARDS - You can improve aeration of the dependent portions by having the patient lie prone

Answer 158

E. Pneumonia -\> most likely etiologic agent is strep pneumo

Answer 159

G. Strep pneumo

Answer 160

C. Shunt ## Footnote - Hypoxemia is not going to completely shut off this blood flow, but rather just limit it (shunt + V/Q mismatch)

Answer 161

- Medical emergency -\> support breathing: intubation, mechanical vent, BiPAP - Tx underlying cause and give corticosteroids (most likely) to reduce inflammation and limit further damage to the lungs - Infection surveillance - Prone ventilation to redistribute lung water, and take weight off of the lungs (decreases mortality) 1. Diuresis as needed to decrease lung water and avoid volume overload - Preventive care in ICU for: DVT, GI, infection

Answer 162

As soon as the injury happens

Answer 163

**Sepsis** ## Footnote - Sepsis-associated ARDS mortality has decreased only minimally (predictor of bad outcomes)

Answer 164

- Chronic inflammatory disorder of airways characterized by _episodic, reversible bronchospasm_ resulting from exaggerated bronchoconstrictor response to various stimuli 1. Airway inflammation contributes to _airway hyper-responsiveness_, airflow limitation, resp symptoms, and disease chronicity -\> AIRWAY REMODELING 2. Earlier stages completely reversible (but less so with more attacks) - Eosinophils, mast cells, T-cells - There is a _link between obesity and asthma_ - Can't be cured, but can be controlled

Answer 165

- 2-7% of pop 1. We all have bronchospasm, but this protective mech goes overboard in asthma pts - 30-50% of children outgrow asthma - 20-30% of adult-onset asthma will have remission: may have no stimulus - Incidence more in F, but childhood prev more in M - _Black race associated with higher rate of death_ (more arsenic-arsenic instead of arsenic-glycine) - Significant morbidity and mortality: attached graph shows INC prevalence (although _deaths have been going down_ in the US since 2000 due to beta-agonist + inhaled corticosteroid therapy)

Answer 166

- Extrinsic: atopic/allergic - Intrinsic: idiosyncratic/non-allergic - Drug-induced: ASA, NSAIDS - Occupational - Cough-variant - Exercise-induced bronchospasm (EIC) - ABPA: anti-fungals seem to have no effect -\> fleeting infiltrates bc coughed up and go somewhere else

Answer 167

- Dx: intermittent vs. persistent - Follow-up: controlled, partially controlled, uncontrolled

Answer 168

- Intermittent: as-needed Albuterol (rescue medicine) - Persistent disease: requires controllers 1. Mild: inhaled corticosteroids 2. Moderate: inhaled steroids, LABA's 3. Severe: inhaled steroids, LABA's, LTA's - _Note_: LABA's associated with increased mortality, so use with caution (black box warning, but clinicians still use these; make sure you f/u w/pt every 6 months, and more closely if you note any changes)

Answer 169

- Most common type of asthma, common in children - _IgE-mediated_ response to _enviro allergens_ (dust mites, cockroaches, animal protein, dusts, pollens, fungi, food) 1. Acute response (minutes after exposure) 2. Late response (hours after exposure) - Elevated serum IgE: significant (\>40% or 2000; usually low, e.g., 40-50) - _Family history_ - _Control by_: reducing exposure to house mites, cockroaches, pets, and mold -\> _cleaning up the envo_ critical to control

Answer 170

- Triggered by respiratory infection - Adult-onset - Non-allergic mediated -\> serum IgE not elevated - skin antigen test usually negative - Family history non-contributory - Intrinsic asthma tends to be more year round than extrinsic asthma

Answer 171

- YES - Moving to a different location can help alleviate asthma symptoms - For example, moving away from the pollen in Memphis to Denver -\> get these people away from the allergen, and make the air less dense, e.g., by breathing a helium/oxygen mix, which eases the patient’s breathing

Answer 172

- 15-20% of patients with asthma - Psychosomatic, but not a manufactured attack

Answer 173

- Aspirin, NSAIDS - Affects adults -\> do really well when you put them on LT antagonists - Samter's Syndrome: 1. Asthma 2. Aspirin sensitivity (flushing, angioedema, urticaria) 3. Nasal polyps

Answer 174

- Most common occupational disease - Exposure to fumes, organic and chemical dusts, gases at workplace - Occurs after _repeated exposure and sensitization_ - 2-10% of adult-onset asthma due to occupational asthma - Mechs include _IgE and non-IgE_ mediated reactions - _Typical scenario_: every evening, the person has asthma, but they are better on the weekends or when on vacation

Answer 175

- Asthma symptoms occur usually immediately after exercise - Symptoms and _lung function changes usually peaks 5-10 minutes after exercise_ - **Cooling and mucosal drying of airways** during exercise thought to trigger mast cells to release histamine - _Pre-treatment with B-agonist or cromolyn_ is effective - Also slow warm up period helps - Most patients with asthma will have an exercise-induced component (i.e., worse symptoms with exercise)

Answer 176

- Not all that wheezes is asthma and not all asthma wheezes - Cough may be the only presenting symptom of asthma without variable airflow obstruction - History of _chronic cough with irritants_ (i.e. cigarette smoke, fumes, exercise) - _Diagnosis may be a positive clinical response to tx_ - _Methacholine inhalation_ challenge test may aid defining the diagnosis

Answer 177

- Asthma symptoms that predominantly occur at night during sleep - Common between midnight to 8AM **thought to be due to decline of circulating catecholamines and cortisol** 1. Cortisol peak around 6-8 AM, and trough around 12 AM

Answer 178

- Asthma due to specific fungi, Aspergillus fumigatus - IgE-mediated reaction and _type III IgE mediated response_ - **Criteria** necessary for diagnosis: 1. Poorly controlled asthma 2. Eosinophilia 3. A. fumigatus positive skin antigen test, IgG Ab 4. IgE \> 1000ng/ml 5. Proximal bronchiectasis (see attached image) 6. Fleeting chest infiltrates 7. Peripheral eosinophilia with chest infiltrates 8. Mainstay of treatment is prednisone

Answer 179

- Airway hyperresponsiveness- exaggerated bronchoconstrictive response by the airways to a variety of stimuli (aeroallergens, cold air, environmental irritants, viruses, ozone, sulfur dioxide); _airflow obstruction_ 1. Airway Inflammation 2. Epithelial Injury 3. Neural Mechanisms 4. Intrinsic Airway Smooth Muscle Function - Increase in goblet cells, mucous production, and peribronchial fibrosis -\> _all at the expense of the lumen_

Answer 180

- _Eosinophils_: steroids - Basophils - _Mast cells_: cromolyn - CD4/TH2 lymphos - Major basic protein - Eosinophilic cationic protein - _Histamine_: H1 blockers - _LT's_: LTRA's - _IgE_: Omalizumab - _Vagal afferent_: anti-cholinergic - _IL-5_: Mepolizumab - PAF

Answer 181

- Epi injury in asthma: disruption of the epi with _loss of ciliated cells to complete denudation of the epithelium_ - INC permeability to inhaled allergens, irritants, and inflammatory mediators ultimately promoting hyperresponsiveness - Transudation of fluids and increased mucous and respiratory secretions

Answer 182

- ANS regulates airway tone, airway secretions, blood flow, microvascular permeability and release of inflammatory cells - Asthma patients have **elevated parasympathetic tone and reflex bronchoconstriction** - Partially responsible for bronchospasm due to inhaled irritants

Answer 183

- Determined by the diameter of the airway lumen, which can be altered by: 1. Edema 2. Mucous 3. Airway smooth m contraction and hypertrophy 4. Inflammatory cell infiltration 5. Airway remodeling - **Airway remodeling causes permanent narrowing of airways due to subepithelial fibrosis**

Answer 184

Bronchoconstriction after allergen challenge

Answer 185

KNOW THIS TABLE. Please. Thanks

Answer 186

- _Symptoms_: wheezing, chronic cough, nocturnal cough/wheeze, chest tightness, sputum production 1. May be exacerbated by allergens, GERD, URI, exercise - SOB or wheezing that is seasonal/after exposure to allergens (may be more year-round in intrinsic) - Relief when medication is used - Viral tracheobronchitis may cause a post- infectious bronchial hyperresponsiveness for up to 6 weeks - Can actually make a dx of asthma based on symptoms

Answer 187

- Accessory muscle use on presentation (SCM and intercostal muscle retractions, pulsus paradoxus, signs of R heart strain, i.e., p-pulmonale on EKG), hypoxemia, hypercapnia - _Death from asthma usually related to diffuse mucous plugging of airways_

Answer 188

- _Peak flow meter_ – diurnal variation of PEFR \>20% is considered diagnostic 1. Normal: highest PEFR at 4PM and lowest at 4AM. 2. **Thought to be due to decline of circulating catecholamines and cortisol** (JUST KNOW THIS) - _Spirometry_ – reduction of FEV1, FEV1/FVC, FEF25-75 that reverses with bronchodilators 1. _Reversibility criteria_: 12% improvement AND 200cc increase in FEV1 and/or FVC - _Lung volumes_ – _evidence of hyperinflation_ suggested by elevated RV, FRC, RV/TLC, TLC - _Gas exchange_ – _DLCO is normal_; occasionally may be even be elevated

Answer 189

- Normal CXR vs. asthma attack - Count ribs when looking for hyperinflation

Answer 190

Looks like it

Answer 191

Peak and scoop improve with bronchodilators

Answer 192

- Give patient gradually increasing concentrations of methacholine, and do spirometry looking at FEV-1 until there is a 20% drop (at which point you stop the test) - PC = provocative concentration (the lesser it takes to cause bronchospasm, the higher the airway reactivity) -\> positive test is less useful - NEGATIVE TEST RULES OUT ASTHMA bc high negative predictive value (this WILL BE ON EXAM)

Answer 193

- Changes in humidity and barometric pressure - _Allergens_: house dust mites, cockroaches, molds, pets, pollen, food (eggs, nuts, milk), aspirin, NSAIDS - Occupational fumes, gases, dust (ozone, sulfur dioxide) - Viral URI’s, Sinusitis - _GERD_: common cause of chronic cough, as well as difficult to control asthma - Hormonal: Menses, Hyperthyroidism, Pregnancy - Psychological factors - Cigarette smoking

Answer 194

- _Patient education w/action plan_ to manage asthma - Objective measures of lung function to monitor and assess the disease severity and control: _PFT's_ - _Pharmacologic therapy_: anti-inflammatory, inhaled beta agonist, leukotriene inhibitors, immunotherapy, antibiotics (if infection was a trigger) 1. Relievers: SABA, SAMA 2. Controllers: inhaled corticosteroids, inhaled LABA, leukotriene modifiers, systemic steroids, anti IgE, and anti-IL-5 3. Make sure you teach pt how to use inhaler

Answer 195

- Asthma is an inflammatory disorder - Prevalence of asthma may be increasing - There are different types of asthma -\> causes are multi-factorial and triggers are numerous - Airway hyperresponsiveness is due to several mechanisms causing airflow obstruction - _Diagnosis_: compatible symptoms and lung function tests (PEFR, Pulmonary Function Test) - Methacholine challenge test has a high NPV - _Management of asthma_: good patient education and appropriate pharmacologic treatments 1. ICS -\> LABA-\> LTRA 2. LABA are associated with increased Mortality – use cautiously, with regular follow up

Muthiah Flashcards

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