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*PANCE by subspecialty > Pulmonology > Flashcards

Pulmonology Flashcards

1
Q

Treatment acute asthma exacerbation

A

BIOMES

Beta-agonists
Ipratropium
Oxygen
Mg sulfate
Epinephrine
Steroids
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2
Q

Which disease causes a low V/Q ratio?

A

V/Q mismatch is a ventilation to perfusion mismatch -

A low V:Q ratio could occur with decreased ventilation or a relative increased perfusion

Disease that could cause decreased ventilation:

Pneumonia - consolidation in alveoli
COPD - dec gas coming into alveoli b/c of mucus thickening/build up
Pulm edema - fluid overload in lungs (in alveoli)

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3
Q

What is perfusion with absolutely no ventilation called?

A

Pulmonary shunt

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4
Q

What is ventilation?

A

Ventilation is the amount of air/gas traveling into alveoli ready for gas exchange

This is abbreviated V

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5
Q

What is perfusion?

A

Amount of blood flow to the alveoli that is prepared for gas exchange as well

This is abbreviated Q

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6
Q

How does COPD affect ventilation and perfusion of the lungs?

A

Decreases ventilation because of mucus plugs in terminal alveoli (chronic bronchitis = mucus & inflammation)

LATE stage COPD also decreases perfusion b/c the capillary beds of the alveoli are destroyed

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7
Q

What is the local response to a low V:Q ratio?

A

The resultant hypoxemia = local vasoconstriction = pulmonary HTN = RAE/RVH = R-HF = cor pulmonale

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8
Q

What pulmonary diseases cause a HIGH V/Q ratio?

A

HIGH V/Q ratio = no perfusion! (denominator small)

Pulmonary embolism - clot cuts off blood supply (perfusion) to capillary beds - absolute = called dead space

Also in late stage COPD capillary beds are destroyed = decreased perfusion

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9
Q

Pathophysiology of chronic bronchitis of COPD

Causes inc or decrease V/Q?
What does it lead to terminally if not addressed?

A

“Blue bloaters”

Pathophys: Chronic inflammation, increased mucus hyper-secretion = chronic productive cough.

= Decreased ventilation (O2/air into lungs) 2/2 mucus plug in terminal alveoli = alveolar hypoxia - O2 not getting thru to alveoli efficiently = hypercapnea (too much CO2 = resp acidosis) and decreased O2 in blood - (body will make more to compensate = inc Hgb = polycythemia)

Dec O2 getting in = dec O2 in blood & inc CO2 in blood = alveolar hypoxia = pulm vessel constriction to shunt blood to healthier alveoli = inc pulm vasc pressure = pulmonary hypertension = backflow of blood to R side of heart = right sided heart failure = cor pulmonale = inc JVD

THIS IS WHY chronic bronchitis of COPD is classically a/w right heart failure 2/2 pulm HTN (cor pulmonale) & why the only medical treatment that reduces mortality is in COPD is oxygen (O2 reduces the hypoxic vasoconstriction)

Low O2 in = CYANOTIC = BLUE BLOATERS

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10
Q

Pathophysiology of emphysema?

A

Emphysema = “pink puffers”
Prominent thoracic cage, barrel-chested, cachectic (muscle wasting)….but why?

Inflammatory response from cigarette toxins (macro = cytokines = WBC-producing elastase prod) = breakdown of elastic fibers & destruction of alveolar walls = loss of alveolar integrity/recoil = AIR TRAPPING = a ton of gas left in alveoli even after you expire b/c they’re not elastically recoiling like they’re supposed to so you can’t get air out = inc end expiratory volume = BARREL CHEST - usually expiration = passive - use a TON of energy & accessory muscles to try to get more air out & to breathe air in = pink puffer - dyspnea & cachexia

Destruction of wall = decreased ventilation b/c of loss of elastic recoil

Destruction of wall and capillary beds = decreased perfusion

Emphysema = matched V/Q deficit - have dec O2 and inc CO2 in blood - same hypoxemia & hypercapnea that occurs in chronic bronchitis but not as severe

Pathologic description: abnormal permanent enlargement of terminal airspaces

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11
Q

Definition of chronic bronchitis

A

Productive cough x3 months for two consecutive years

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12
Q

Why are patients with chronic bronchitis from COPD prone to microbial infections?

A

Because mucus plugging & mucociliary escalator destruction = body can’t get bugs out & perfect environment for bac to grow :(

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13
Q

What is the most common symptom of emphysema?

A

Dyspnea

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14
Q

Describe a patient with severe emphysema?

A

PINK PUFFER

DYSPNEIC

Accessory muscle use, tachypnea, prolonged expiration, cachectic, pursed-lip breathing

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15
Q

Describe a patient with chronic bronchitis?

A

BLUE BLOATER

Chronic productive cough = HALLMARK SYMPTOM

Obese & cyanotic

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16
Q

PE of chronic bronchitis vs emphysema

A 
Emphysema: 
Hyper-resonance to percussion
Decreased breath sounds
Decreased tactile fremitus
Barrel chested (inc AP diameter) 
Pursed lip breathig

Chronic bronchitis:
Rales (crackles), wheezing that changes in location w/ cough, signs of cor pulmonale (peripheral edema, cyanosis)

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17
Q

V/Q mismatch in emphysema vs chronic bronchitis

A

Emphysema: Matched V/Q defects, mild hypoxemia

Chronic bronchitis: Severe V/Q mismatch = severe hypoxemia, hypercapnia

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18
Q

ABG/Labs in chronic bronchitis vs emphysema

A

Chronic bronchitis: Respiratory acidosis - retention of CO2 and increased Hct/RBC count (polycythemia) 2/2 chronic hypoxia that stimulates EPO)

Emphysema - either

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19
Q

What is the gold standard for diagnosis of COPD?

A

PFTs/Spirometry

FEV1 < 1 L = inc mortality

FEV1/FVC < 0.7 = obstructive lung dz

More emphysema =
Decreased DLCO

Hyperinflation = increased lung volumes - TLC, RV etc

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20
Q

CXR findings in emphysema

A 
Emphysema: 
Hyperinflation 
Flat diaphragm
Inc AP diameter
Dec vascular markings
\+/- bullae/blebs

Chronic bronchitis:
Inc vascular markings
Enlarged right heart border

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21
Q

EKG findings chronic bronchitis

A

Remember chronic bronchitis = cor pulmonale eventually b/c chronic local hypoxemia = vasoconstriction = pulm HTN = RAE/RVH = R-HF = cor pulmonale

ON EKG:
RAE = p wave amplitude > 2.5 mm)
RVH = RAD, poor r wave progression

Signs R-heart strain etc (s wave in 1, Q in 3, T in 3)

Atrial enlargement = afib/flutter, or multifocal atrial tachycardia

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22
Q

Triggers for COPD exacerbation

A

Pollutants, beta blockers (non-selective = bronchoconstriction), infections (viral bronchitis, bacterial pna (HCAP)

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23
Q

What is the most important step in the management of COPD?

A

Smoking cessation

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24
Q

What is the mainstay of COPD treatment?

A

Besides smoking cessation (= most important management tool), anti-muscarinics to initiate bronchodilation - prevents broncho-constriction - opens up airways, gets more air in

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25
Q

Management of exacerbation of COPD

A

Keep SaO2 > 90%

Nebulizer (albuterol (SABA or duoneb w/anti-muscarinic)

Add oral or IV corticosteroids

Consider abx therapy

Consider ABG to check for acidosis (CO2 retention) in hospitalized/sick pt

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26
Q

Role of spirometry in COPD

A

Initial assessment -
diagnosis and prognosis

Follow up assessment -
Rapidly declining lung fxn

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27
Q

Definition of COPD exacerbation

A

An acute worsening of respiratory sx that results in additional therapy

Mild - SABA/SAMA only
Moderate - SABA, steroids, +/- ABX
Severe - hospitalized

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28
Q

Name the two SABA used in acute COPD exacerbations

A

Albuterol

Levalbuterol ($$$)

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29
Q

Name the only SAMA

A

Ipratropium

Comes before T (tiotropium) in the alphabet, acts shorter

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30
Q

Name the only SAMA

A

Ipratropium

Comes before T (tiotropium) and U (umedlidinium) in the alphabet, acts shorter

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31
Q

Name the 4 LAMA’s used in COPD maintenance

A

Tiotriopium
Umeclidinium
Aclidinium
Glycopyrrolate

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32
Q

Name the some LABA’s used in COPD maintenance

A

Anything that ends in “ol” that is not albuterol/levalbuterol (SABS’s)

Salmeterol
Formoterol
Olodaterol

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33
Q

Does regular use of a SABA or SAMA in COPD improve FEV1 and symptoms?

A

YES

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34
Q

Is combination therapy, or a LABA or LAMA alone superior in improving COPD symptoms and decreasing exacerbation rates?

A

COMBINATION TREATMENT is superior!!!

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35
Q

Do LAMA’s or LABAs have greater effect on exacerbation reduction?

A

LAMA’s have greater effect on exacerbation reduction !!!

This is why group C patients (exacerbations prominent w/ less symptoms) a LAMA Is preferred initial treatment, with second treatment being a combo LAMA/LABA if that doesn’t work

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36
Q

Are SAMA’s or SABA’s preferred monotherapy in preventing acute mild exacerbations with moderate/severe COPD?

A

SAMA’s

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37
Q

Are short-acting or long-acting preparations preferred in COPD maintenance?

A

Long-acting - for both anti-muscarinics and beta2-agonists

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38
Q

What is the only treatment shown to slow the progression of COPD?

A

STOP SMOKING

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39
Q

What is the only treatment that reduces mortality in COPD?

A

OXYGEN

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40
Q

Red flags of COPD management

A

ICS alone….?! Can increase infections in severe COPD and doesn’t help the airflow obstruction, especially if they have predominantly emphysema-type - need a BRONCHODILATOR = mainstay of COPD therapy

Therapeutic duplicaiton - 2 LABA’s or 2 LAMA’s etc

OTC cough medicine

Poor or erratic adherence

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41
Q

Prevention of exacerbations

A

Pneumococcal vaccine

Flu vaccine every year

Pulmonary rehab - improves QOL, subjective DOE & exercise tolerance

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42
Q

Indications for abx in COPD exacerbation

A

Used only for acute bacterial exacerbations of chornic bronchitis IF….

Increased sputum
Change in sputum quality
And/or CXR evidence of infection

Remember azithromycin has anti-inflammatory properties in the lung!

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43
Q

Mild (stage I) COPD definition

A

Fev1/FEV < 70%

And FEV1 >80%

Therapy: SABA, SAMA
Vaccinations

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44
Q

Moderate (stage II) COPD definition

A

FEV1/FEV < 70%

And FEV1 50-79%

Therapy:
If FEV1 is not >80%, need a long acting bronchodilator, short not good enough anymore:

LAMA/LABA

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45
Q

Severe (Stage III) COPD definition

A

FEV1/FEV < 70%

And FEV1 30-50%

Therapy:
Stage II recs: LAMA/LABA

PLUS: Pulmonary rehab & steroids if increased exacerbations

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46
Q

Very severe COPD (Stage IV)

A

FEV1/FEV < 70%

FEV1 < 30%
Cor pulmonale
Respiratory failure

Stage III recs: LAMA/LABA, pulmonary rehab & steroids if increased exacerbations

PLUS

O2 therapy

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47
Q

What is the signet ring sign? what disease is it seen in?

A

Signet ring sign is a pulmonary artery coupled with a dilated bronchus seen in bronchiectasis

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48
Q

What are the MC CXR findings in bronchiectasis?

On CT?

A

“tram-track” markings
Irregular opacities
Crowded bronchial markings

Proximal airway dilation w/ thick walls & lack of airway tapering giving “tram-track appearance

Anything that talks about PROXIMAL (larger airways) that are dilated with thick walls…think bronchiectasis

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49
Q

Pathophys of bronchiectasis?

A

Permanent abnormal dilation & destruction of BRONCHIAL walls = LARGE airway disease

CF causes >50% of all cases - B. thought to be caused by recurrent inflammation or infection (Rb, fungal, lung abscess, PNA - MYCO!, alpha-1 anti-trypsin def) - lung develops an abnormal defense mechanism that leads to localized airway obstruction = OBSTRUCTIVE physiology

Since infection is the trigger, antibiotics are ALWAYS part of the treatment

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50
Q

Sign & sx of bronchiectasis

A

VISCID THICK sputum
Chronic daily cough
Rhinosinusitis
Recurrent pleurisy (2/2 lung lining inflam)

Chronic pulmonary crackles
Wheezing

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51
Q

Dx bronchectasis

A

High resolution CT scan

Will show airway dilation
Lack of tapering of bronchi (BRONCHIAL DILATION!!!)

“Tram-track” (WALL THICKENING)

Mucopurulent plugs consolidations

“Signet ring” sign (= pulmonary artery coupled with a dilated bronchus)

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52
Q

PFTs bronchiectasis

A

Will show obstructive pattern

Dec FEV1, Dec FVC
FEV1/FVC < 70%

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53
Q

MC pathogen if bronchiectasis is caused by CF

A

PSEUDOMONAS

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54
Q

3 problematic pathogens a/w bronchiectasis

A

Pseudomonas (CF)

Mycobacterium avium complex (MAC) - clarithromycin & ethambutol

Aspergillus - thick brown sputum - corticosteroids & itraconazole

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55
Q

Cornerstone of bronchiectasis tx

A

ANTIBIOTICS

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56
Q

Thick brown sputum

A

Aspergillus bronchopneumonia

Tx: Itraconazole, corticosteroids

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57
Q

CF etiology, epidemiology

A

Autosomal recessive mutation in cystic fibrosis transmembrane receptor (CFTR) - defect prevent chloride transport (water movement out of cell) = build up of thick, viscous, mucus in the lungs, pancreas, liver, intestines & reproductive tracts = obstructive lung disease & exocrine gland dysfunction (pancreatic insufficiency)

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58
Q

Indications for bronchoscopy in bronchiectasis?

A

If have hemoptysis & you’re worried about a tumor

If a therapeutic intervention & you want to removed retained secretions

If you’re worried about obstructive airway lesions (foreign body)

BUT dx = HIGH RES CT!

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59
Q

Someone with recurrent respiratory infections and chronic sinusitis….you’re thinking what?

A

Cystic fibrosis!!!

Sign is recurrent URI - esp pseud & staph - productive cough, chronic cough, sinusitis

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60
Q

Three most common clinical manifestations of CF

A
  1. GI:
    - Meconium ileus at birth (DO CF TEST!)
    - Pancreatic insufficiency (dec ab fat-soluble vitamins ADEK & steatorrhea, pale stools, weight loss - FTT in kids)
  2. Pulmonary:
    - Recurrent URI, chronic sinusitis
  3. Infertility (95%)
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61
Q

What do you do if a full term infant presents with meconium ileus?

A

DO A CF TEST!!!

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62
Q

Dx of CF

A

Sweat chloride test

People with CF will have increased chloride levels in their sweat

< 29

30-59 = may have it, additional testing needed

> 60 mmol/L on two occasions after administration of pilocarpine (cholinergic drugs that induces sweating)

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63
Q

Management CF

A
  1. Airway clearance tx: bronchodilators, mucolytics, abx, degongestants
  2. Pancreatic enzyme replacement, supplement fat-soluble vitamins
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64
Q

CXR of CF

A

Will show bronchiectasis:

Nonspecific findings, tram-track, irregular opacities, crowded bronchial markings (peribronchal fibrosis), signet ring sign etc

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65
Q

Name 4 lung diseases with obstructive physiology & name what their PFTs would likely show

A

Asthma
COPD
CF
Bronchiectasis

PFTs: 
FEV1/FVC < .7
Dec FEV1
Dec FVC
TLC INCREASED
RV increased
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66
Q

What is the definitive test for CF? What is the gold standard test?

A

Definitive:
DNA analysis

Initial & GOLD standard:
Sweat chloride test

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67
Q

4 restrictive lung diseases and their expected PFTs

A 
Sarcoidosis
Pneumoconiosis
Idiopathic pulm fibrosis
MG (dec effort to expand)
Mesothelioma
Scoliosis, kyphosis

PFTS:
DECREASED lung volumes
Normal or inc FEV1/FVC
Dec TLC, RV, etc

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68
Q

WHEEZING more indicative of COPD or asthma

A

Think more asthma in general

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69
Q

Predominant cell in pathophysiology of asthma

A

Eosinophil - airway hypersensitivity and hyper-reactiveness - to ALLERGENS = mast cell degranulation = histamine, leukotriene, IgE, cytokine release =

Early response: Bronchospasm, edema, airflow obstruction (reversible)

AND

Late response:
Airway inflammation
Airway hyper-responsiveness

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70
Q

Child with recurrent episodes of chest tightness, wheezing and SOB..what to do?

A

Refer for spirometry

Measure baseline FEV1
Give bronchodilator
FEV1 inc >12% & or FEV1 inc >200 ml = ASTHMA =

REVERSIBLE airway obstruction!!!

If spirometry comes back normal, can order methacholine challenge = cholinergic that asthmatic pt will have an exaggerated response to (>20% decline in FEV1 is diagnostic)

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71
Q

Initial evaluation of asthma

A

Spirometry w/ bronchodilator test

HX - exzema, allergic rhinitis,

Refer for allergy testing (decreasing triggers = dec need for meds!!! Control sneeze = control the wheeze)

Stage the asthma severity - based on functional impairment (symptom burden) and risk of exacerbations

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72
Q

What is a part of every asthma action plan?

A
  1. Daily management - controller medication & environmental control measures (avoid triggers)
  2. How to manage worsening asthma - how to adjust meds, when to seek medical care
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73
Q

What is the easiest way to assess asthma control?

A

Peak flow

Make sure pt has personal best peak flow recorded when healthy

Then if they’re at 80-100% of that = green zone = continue w/ regular activities

50-80% = yellow zone - may require med adjustment/intervention - contact health care provider

<50% = emergency - dial 911

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74
Q

Risk factors for death in asthma (4)

A

Prior severe exacerbation (intubation/ICU)

2+ hospitalizations or 3+ ED visits in the past year

> 2 canisters of SABA per month (call pharm to see)

Poor perceiver of sx, LSES, illicit drug use, psychiatric disease, severe comorbidities

REFER TO PULMONOLOGIST IF PT HAS THESE!!!

Consider pulmonologist if hospitalized, difficulty achieving control & on Step 4 adults or step 3 kids, if immunotherapy is under consideration or if > 2 oral steroid bursts in past year

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75
Q

What is the preferred treatment for long term management of asthma?

A

INHALED CORTICOSTEROIDS

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76
Q

What monotherapy is contraindicated in asthma?

A

LABA

NEVER USED ALONE IN ASTHMA MAINTENANCE

CAUSES INCREASED NUMBER OF DEATHS IN TRIAL!!!

YOU MUS HAVE AN ANTI-INFLAMMATORY CONTORLLER AGENT

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77
Q

Why are ICS the TOC for maintenance therapy for asthma?

A

Because the main pathophys involves inflammation and immune system/ bronchial hypersensitivity to allergens/irritants

To prevent this immune response and resultant inflammation we need an inhaled corticosteroid on board

Bronchodilators can only open up airway so they help but aren’t directed right at main pathophys of diseae

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78
Q

Asthma treatment

A

CONTROLLER: ICS =
Fluticasone, flunisolide, beclomethasone, mometasone, budesonide etc

RESCUE: SABA =
Albuterol

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79
Q

Stepwise approach to asthma tx

A

Start on SABA if step 1 (exercise-induced, intermittent - SABA<2x/week, awake < 2/mo, 0-1 exac/year)

Otherwise all need a controller - start w/ low dose ICS, then add LABA (-ol) or increase to med dose ICS If not controlled

5 YO + can try LTRA (zafirlukas, montelukast, zilueton - MONTE = preferred) if > or equal to step 3 as well but not the preferred regimen

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80
Q

When would you consider biologics in asthma management?

A

LAS LINE therapy - for pt who are step 5/6 who have ALLERGIC asthma with HIGH IgE ab counts who are very poorly controlled on high dose ICS & flaring frequently

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81
Q

Formulations of biologics for asthma

A

Xolair (omalizumab)
Cinqair (reslizumab)
Nucala (mepoluzumab)

Must have eosinophilic type asthma not controlled on ICS + skin testing for allergies

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82
Q

When do you give oral steroids in asthma?

A

May be needed to re-establish asthma control if:

Failure of SABA to produce sustained response

Given promptly if pt is deteriorating, if have already tried rescue inhaler before presenting

Continue OCS for 5 days

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83
Q

ACUTE ASTHMA ATTACK managment

A
  1. Stacked albuterol nebs

2.

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84
Q

Classic triad asthma sx

A
  1. Wheezing
  2. SOB
  3. Cough (**esp at night)

Also chest tightness, “lungs feel tight” etc

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85
Q

PE asthma

A 
Prolonged expiration 
Expiratory wheezing
Decreased breath sounds
Tachycardia
Tachypnea
Use of accessory muscles
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86
Q

What is the best & most objective way to assess asthma exacerbation severity & responses to a treatment in the ED?

A

Peak expiratory flow rate

PEFR> 15% initial value = response to treatment

Normal = 400-600

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87
Q

Admission criteria vs discharge criteria acute asthma attack

A

Admit: PEFR <50% (red zone), prior ER visit w/in 3 days this exacerbation, status asthmaticus, post-treatment failure, AMS

Discharge:

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88
Q

Admission criteria vs discharge criteria acute asthma attack

A

Admit: PEFR <50% (red zone), prior ER visit w/in 3 days this exacerbation, status asthmaticus, post-treatment failure, AMS, no air movement (garden hose closed)

Discharge: PEFR > 70%, clear lungs w/ good air movement, adequate follow up w/in 24-72 hrs, response sustained >1 hr post-treatment

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89
Q

What is sarcoidosis?

A

Chronic, MULTI-systemic, inflammatory, granulomatous d/o or unknown etiolgy

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90
Q

What is sarcoidosis? Pathophys?

A

Chronic, MULTI-systemic, inflammatory, granulomatous d/o or unknown etiology

Patho: Exaggerated T-cell response to variety of antigens or self-antigens = granuloma formation (mass of immune cells that’s walled off) –> the granulomas (non-caseating) –> the granulomas disrupt normal structure and or function of tissues they form in, resulting in clinical manifestations seen (pulm, LAD< skin, eyes, heart, rheum, neurologic) etc

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91
Q

Typical pt w/ sarcoidosis

A

20-40 YO AFRICAN AMERICAN or northern european FEMALE

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92
Q

Two most common organ systems involved in sarcoidosis

A

Lungs - dry nonproductive cough, chest pain, dyspnea

Skin - erythema nodosum, lupus pernio = PATHOGnomonic!!!

Although Eyes = 2nd MC system causing complications - anterior uveitis (blurred vision)

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93
Q

Clinical manifestations of sarcoidosis

A

SARCO-Not Me!

Skin - erythema nodosum, lupus pernio

Anterior uveitis (inflam of iris/ciliary body = blurred vision, ciliary flush etc - optho exams yearly!)

Rheum - arthralgia, fever, malaise

Cough - dry, nonproductive cough & CP (90%)

O - think of O as a large lymph node - B/L hilar and RIGHT peritracheal LAD = V COMMON but not specific

Not - neurologic - CN VII palsy, DI, pituitary lesions - SARCO-NM = 7, = CN 7 palsy!!

Me - myocardial - infiltrative restrictive cardiomyopathy, arrhythmias!!

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94
Q

Def of interstitial lung disease

Signs of ILD on a CXR

Examples of interstitial lung dz

A

Definition:
Interstitial lung dz = diseases of lung parenchyma (happening w/in pulm interstitium) = inflam/scarring of the lung tissue = leads to restrictive lung disease

Signs on CXR:
Reticular opacities, +/- fine ground glass appearance

Examples:

  • Idiopathic fibrosing interstitial PNA
  • Pneumoconiosis (any occupational lung dz inc coal worker’s lung, silicosis, asbestosis etc)
  • Sarcoidosis
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95
Q

Stage I sarcoidosis on CXR

A

Bilateral hilar lymphadenopathy (no sx or mild pulm sx)

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96
Q

Stage II sarcoidosis on CXR

A

Bilateral hilar LAD & moderate pulm sx

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97
Q

Stage III sarcoidosis on CXR

A

Interstitial lung disease on CXR

Reticular opacities, +/- fine ground glass appearance

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98
Q

Stage IV sarcoidosis on CXR

A

Fibrosis (volume loss and full on restrictive lung disease)

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99
Q

What is the most common finding on PFTs in sarcoidosis?

A

Isolated decreased DLCO (diffusing capacity of CO2 the lung) 2/2 firbrosis

Can also see restrictive patterns w/ advanced dz (dec TLC, RV, normal FEV1FVC etc)

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100
Q

Diagnosis of sarcoidosis

A
  1. Compatible clinical and radiologic findings
  2. Noncaseating granulomas
  3. Exclusion of other diseases
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101
Q

Lab studies supporting dx of sarcoidosis (3 specific ones related to granulomas/immune rxn)

A
  1. 40-80% have increased ACE bc granulomas secrete it
  2. Hypercalciuria/hypercalcemia - 2/2 granuloma = ince activated vit D prod
  3. Cutaneous anergy (70%) - aka no skin response to skin allergens b/c peripheral immune system depressed b/c central immune system activated

Also: Inc IgG, eosinophilia, leukopenia, Inc ESR

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102
Q

When would you use a broncheolar lavage in relation to sarcoidosis and what would it show if it was sarcoidosis?

A

Broncheolar lavage is used to r/o other infectious causes of granulomas

It would show inc CD4 in relation to CD8 if sarcoid (sarcoidosis = 4 syllables = more CD4)

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103
Q

Management of sarcoid

A
  1. Observation- most have spontaneous remission w/in 2 years (fibrosis = poor prognosis, but good prognosis overall)
  2. Oral corticosteroids - TOC when treatment is needed - reduces granuloma formation & fibrosis - ACE levels usu fall after clinical improvement after OCS
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104
Q

Indications for oral corticosteroids in sarcoid

A

Worsening sx
Deteriorating lung fxn
Progressive radiologic decline

**MUST rule out Tb & infectious etiologies before initiating OCS

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105
Q

When is hydroxychloroquine used in sarcoid?

A

For chronic disfiguring skin lesions/granulomas

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106
Q

Which two factors are a/w poorer prognosis in sarcoid?

A
  1. ILD
    (stage III CXR w/ Reticular opacities, +/- fine ground glass appearance, PFTs of restrictive pattern etc)
  2. Lupus pernio
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107
Q

Lupus pernio is pathognomonic for which disease? Describe

A

for sarcoid

Looks like frost bite - violaceous raised discoloration of nose, ear, cheek & chin

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108
Q

What is the classic sarcoid presentation in clinical practice?

A

Young female w/ respiratory sx (dry nonproductive cough) & systemic sx (malaise, fever, arthralgias) ….sounds like a bronchitis or PNA maybe BUT will also have BLURRED VISION….weird & doesn’t fit PNA….AND likely have skin involvement (painful nodules)….also weird if just PNA…..

Must recognize this pattern!
Cough + 
Blurred vision + 
Painful skin nodules = 
Sarcoidosis
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109
Q

What do sarcoidosis granulomas consist of?

A

Langerhan’s giant cells w/ star-shaped areas or Schuamann bodies

Epitheloid macrophages

Asteroid bodies

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110
Q

What is the most common interstitial lung disease?

A

Idiopathic fibrosing interstitial PNA (aka pulmonary fibrosis)

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111
Q

What is chronic progressive interstitial fibrosis caused by?

A

Persistent inflammation (chronic alveolitis) –> loss of pulmonary function with restrictive component

Etiology unknown

Survival < 10 years at time of diagnosis aka POOR prognosis

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112
Q

What would the typical Idiopathic fibrosing interstitial PNA (aka pulmonary fibrosis) patient look like?

A

40-50 YO MALE SMOKER

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113
Q

Dx Idiopathic fibrosing interstitial PNA (aka pulmonary fibrosis)

A

ILD CXR patterns - AKA reticular markings (MC finding), fine ground glass opacities

Specific to pulm fibrosis = HONEYCOMBING, more diffuse patchy FIBROSIS (sarco can have but only in advanced)

“tell your honey to stop smoking b/c he will get pulmonary fibrosis w/ honeycombing”

Also - Persistent inflammation (chronic alveolitis) –> fibrosis is the pathophys - if think of what hardened alvioli would look like, it’s honeycomb

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114
Q

CXR finding descriptions specific to Idiopathic fibrosing interstitial PNA (aka pulmonary fibrosis)

A

HONEYCOMBING

BX also shows HONEYCOMBING!!!

“tell your honey to stop smoking b/c he will get pulmonary fibrosis w/ honeycombing”

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115
Q

Clinical manifestations and PE pulm fibrosis

A

CP: Similar to other restrictive lung disease - gradual onset dry non-productive cough, DOE, fatigue, tachypnea

PE: Clubbing, inspiratory rales

What sets it apart is patient population it occurs in - OLD MEN w/ exposure risk (smoke, occupational exposures)

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116
Q

Dx of pulm fibrosis

A

CT Scan w/ characteristic findings (diffuse reticular opacities = synonym for honeycombing) & matching clinical presentation

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117
Q

Tx pulm fibrosis

A

No effective tx
Stop smoking
Oxygen
Corticosteroid in exac

118
Q

What is the only cure for pulm fibrosis?

A

Lung transplant (poor prognosis w/o transplant)

119
Q

What is pneumoconiosis? Examples?

A

Environmental or occupational lung dz - chornic fibrotic lung dz 2/2 inhalation of mineral dust = inflam rxn = parenchymal fibrosis = restrictive lung dz & decreased lung compliance

Silicosis
Asbestosis
Coal-worker's pneumoconiosis
Berylliosis
Byssinosis
120
Q

CXR findings coal workers pneumoconiosis

A

Small, rounded, nodules w/ preference for UPPER lobes

Think of it looking like two little round lumps of coal in upper lung lobes

Later - progressive massive fibrosis

121
Q

Management Silicosis, asbestosis, coal workers’s pneumoconiosis

A

No proven treatment! :(

Supportive: bronchodilators, O2, vaccinations (flu, pneumococcal), +/- corticosteroids, rehabilitation

122
Q

CP pneumoconiosis

A

All have similar CP - non-productive cough - gradually worsens, DOE, can be ASX, fatigue etc - think about lungs not working (not able to expand and not able to exchange gasses - which sx would you have?)

123
Q

History of working in manufacturing, working with fluorescent light bulbs …what is the patient at risk for?

A

May have been exposed to beryllium which can cause berylliosis, a form of pneumoconiosis (group of occupational lung disease causing restrictive ILD)

124
Q

What are similarities between beryllosis and sarcoidoss, differences?

A

Both can cause hilar LAD & non-caseating granulomas on CXR, both have CP dry nonproductive cough & other common sx restrictive ILD

Berylliosis wil have exposure hx to beryllium & positive beryllium lymphocyte proliferation test

125
Q

Tx berylliosis

A

No treatment - give steroids, O2 + methotrex if steroid unsuccessful

126
Q

Cotton exposure = risk for ? ILD

A

Byssinosis - type of pneumoconiosis (occupational restrictive ILD)

AKA “Brown lung disease” or “Monday fever”

Sx worse at beg of week = “monday fever”

127
Q

Man who worked in ship building, been retire 17 years presents w/ DOE, nonproductive cough

A

ASBESTOSIS - form of occupational lung dz (pneumoconiosis) 2/2 inhalation of asbestosis - found in ship building, pipe fitters, insulation, destruction & renovation of old buildings

Occurs 15-20 years after exposure

Presents w/ DOE, fatigue dry nonproductive chronic cough etc (all non-specific restrictive ILD sx)

128
Q

CXR asbestosis

A

Plaques in LOWER lobes

Think of asbestosis dust settling down & forming a plaque

129
Q

Asbestosis increases your risk of which cancers?

A

Bronchogenic carcinoma (MC)!!!

Mesothelioma (RARE but specific)

130
Q

Silicosis CXR

A

Small nodular opacities in pper lobes

Nodular densities progress from periphery to hilum

+ EGG SHELL CALCIFICATIONS of hilar & mediastinal nodes

Don’t want sand on your eggs = gross - sand (silicosis) = EGG SHELL calcifications

Think of little eggs in upper lobes of lungs - round small nodules in upper lobes w/ egg shell classifications of hilar nodes- whereas asbestosis dust settles to lower lobes & = plaques

131
Q

Etiology psitacosis, CP, TX

A

AKA Parrot fever - think PSIT = PARROS

Etio = chlamydophilia psittaci from infected birds (parrots, ducks)

CP: Atypical PNA - dry cough, FEVER, myalgias, headache

Tx: Tetracyclines FIRST LINE

132
Q

What is the DLCO? When is it low?

A

The diffusing capacity of CO

Low in restrictive lung dz, emphysema

133
Q

What is a pleural effusion?

A

Abnormally large accumulation of fluid in the pleural cavity - indicator of an underlying pathologic process or underlying illness…

134
Q

MCC transient pleural effusion

A

CHF (fluid backup into pulm vasc = inc hydrostatic pressure = fluid leakage)

135
Q

Dx pleural effusion

A

CXR - can see effusions >150 ml as blunting of costophrenic angles

Seen in posterior sulcus first (look at lateral film) then lateral sulci

136
Q

PE pleural effusion

Percussion
Tactile fremitus
Breath sounds
Egophony

A

Dullness to percussion
Dec tactile fremitus
Inaudible breath sounds
+ Egophony (E–>A)

137
Q

Light’s criteria (3)

A

Fluid is EXUDATIVE if >1 criteria are met:

Ratio of pleural fluid LDH : serum LDH > 0.6

Pleural fluid LDH >2/3 ULN reference range of serum LDH

Ratio of pleural fluid protein : serum protein >0.5

Note: Infection = inflammation = inc capillary permeability

138
Q

When is thoracentesis indicated for pleural effusion?

A

Done with ALL effusions of unknown causes

C/I systemic anti-coagulation or infected area on skin

139
Q

MCC exudative effusion

A

Malignancy

140
Q

Causes of exudative effusions

A

Malignancy, inflammation (SLE, RA, granulamatous d/o - sarcoid), or infection

141
Q

Causes of transudative effusions

A

Cardiovascular - fluid overload/heart failure

Hypoalbuminemia - liver failure, nephrotic syndrome

Hypothyroidism

142
Q

Indications for chest tube (indwelling pleural catheters)

A

RAPIDLY re-accumulating pleural effusions

Failure of lung expansion after thoracentesis

143
Q

What is a PTX?

A

Communication through the lung parenchyma into the plural cavity

144
Q

MCC primary spontaneous PTX

A

Rupture congenital pulmonary blebs

145
Q

Typical pt w/ spontaneous primary PTX

A

YOUNG MALE

14-18YO

SKINNY

TALL

146
Q

MCC secondary spontaneous PTX

A

COPD (emphysema)

147
Q

PTX PE

A

Decreased breath sounds
Dec tactile fremitus
Hyper-resonant percussion
(air = hyper-resonant)

148
Q

Gold standard of pleural effusion treatment

A

Thoracentesis

149
Q

Treatment for malignant or chronic effusions

A

Pleurodesis

Talc MCly used

150
Q

Tx pleural effusion

A

Tx underlying dx

Gold standard = thoracentesis

151
Q

Tension PTX

A

WORST kind - progressive build up of air pushes mediastinum to opposite hemithorax & obstructs venous return to the heart causing cardiac arrest!!!

MC with trauma or iatrogenic cause

152
Q

CP tension PTX

A

JVP, pulsus paradoxus, hypotension (b/c no blood getting back to right atria)

Diaphoretic, cyanotic, tachy (HR >135), CP

153
Q

Treatment tension PTX

A

Needle decompression - 2nd intercostal space, mid-clavicular line

154
Q

Foreign body aspiration CP

A

Sudden onset wheezing,

Stridor, hoarseness, dyspnea,

Severe respiratory distress

80% in children < 3 YO

Marbles = most fatal
Nuts (food)= MC in younger, non-food items in older

60% in right main bronchus

155
Q

Tx FBA

A

Rigid/flexible bronchoscopy

156
Q

Chest pain characteristics if 2/2 PTX

A

PLEURITIC

UNILATERAL

NON-EXERTIONAL

SUDDEN ONSET

157
Q

Tx PTX

A

Chest tube (thoracostomy) placement if large or symptomatic

Observation if small (<15-20%) of diameter of hte hemithorax - O2 increases air resoprtion

158
Q

Etiology pulmonary nodules

A

Granulomas - Tb, histo, coccidio

Tumors - benign or malignant

Inflammation - Sarco, RA, wegener’s

Mediastinal tumor - thymoma = MC mediastinal tumor

159
Q

Characteristics of benign pulmonary nodule

A 
Round
Smooth
Slow growth 
\+ Calcifications
Cavitary (without thickened walls - thickened walls = malignant)
160
Q

Characteristics of malignant pulmonary nodule

A

Irregular border
Speculated
Rapid growth
Cavitary WITH thickened walls

161
Q

Management of pulmonary nodule

A

Observation/surveillance if low malignant probability (<50 YO, never smoker, small size, smooth, round, not changing in size)

Often tend to be a Tb granuloma if above is true

Thoracic needle aspiration or bronchoscopy if intermediate probability of malignancy

Resection with biopsy if high probability of malignancy

162
Q

Bronchial carcinoid tumor

MC site
Clinical manifestations

A

MC site is GI tract
2nd MC site is lung

Usually well-differentiated, low grade malignancy - rare neuroendocrine tumor from enterochromaffin cell, low risk of mets

163
Q

Dx bronchial carcinoid tumor

A

Bronchoscopy

164
Q

Pathologic description of bronchial carcinoid tumor

A

Pink to purple well vascularized central tumor

165
Q

DIARRHEA, FLUSHING & WHEEZING = ?

A

Bronchial carcinoid tumor secreting serotonin & causing increase in bradykinin & histamine = flushing, wheezing etc

166
Q

Management bronchial carcinoid tumor

A

Surgical excision

Often resistant to chemo/radiation

Ocreotide to decrease secretion of active hormones from tumor

167
Q

Management bronchial carcinoid tumor

A

Surgical excision

Often resistant to chemo/radiation

Ocreotide to decrease secretion of active hormones from tumor

168
Q

Lung cancer (bronchogenic carcinoma)

MC form
Most deadly form
Least deadly form

A

1 cause death

MC form is non-small cell - adenocarcinoma

Most deadly is small cell carcinoma

Least deadly is subtype of Non-small cell adenocarcinoma called broncioalveolar

169
Q

Squamous cell carcinoma - characteristics?

A

SQCC = CCCC

Centrally located
Cavitary lesions (central necrosis)
Calcium - high
Coast - Pancoast tumors

170
Q

Non-small cell carcinomas

A

Adenocarcinoma

Squamous cell carcinoma

171
Q

Clinical syndromes caused by small cell lung cancer (para-neoplastic syndromes)

A

** All can cause it but most common with small cell =

SVC syndrome
SIADH/hypoonatremia
Cushings
Lambert-Eaton syndrome - ab against NMJ - similar to MG but weakness IMPROVES with continued use

172
Q

Which lung cancer causes gynecomastia?

A

Adenocarcinoma

173
Q

Which lung cancer causes cushings syndrome by secreting ACTH?

A

Small cell

174
Q

Which type of lung cancer most frequently causes pancoast tumor & which syndrome does a pancoast tumor cause?

A

Squamous cell carcinoma

Causes pancoast syndrome = tumor at superior sulcus = shoulder pain, horner’s syndrome (miosis, ptosis, anhydrosis), due to cervical cranial sympathetic nerve compression, & atrophy of hand/arm muscles

175
Q

Pancoast syndrome causes which other syndrome?

A

Pancoast syndrome = 2/2 tumor at superior sulcus that presses on cervical nerve - compression = HORNER’s syndrome! (miosis, ptosis, anhydrosis)

Pancoast also = shoulder pain, arm/hand atrophy

176
Q

Characteristics of small cell carcinoma

A

Mets early - usu found on presentation

Centrally located

Surgery usually NOT treatment b/c already mets on presentation, can’t just resect it

177
Q

Characteristics of adenocarcinoma of the lung

A

MC lung cancer - in women, smokers & non-smokers

PERIPHERAL - arises from mucus glands - think of the pleura on periphery as mucousy

178
Q

Dx of lung cancer

A

Bronchoscopy used for central lesions (squamous, small cell) or mediastinoscopy used

Transthoracic needle biopsy for peripheral lesions (adenocarcinoma)

Pleural fluid analysis

CT scan used for staging

179
Q

Non-small cell management

A

Central lesion so surgical resection preferred

180
Q

Small cell lung cancer

A

Chemo = TOC b/c already mets on time of presentation

Done with or without radiation

181
Q

MC symptom PE

A

SOB

182
Q

MC sign PE

A

tachycardia

183
Q

PE pulmonary embolism

A

Often normal

184
Q

CP PE

A

Dyspnea
Pleuritic CP
Hemoptysis

Post-op patient w/ sudden tachypnea

Hypoxia

185
Q

Massive PE CP

A

Syncope
Hypotension
PEA

186
Q

Dx PE - gold standard

A

Pulmonary angiography

Ordered if v high suspicion and CT scan neg

187
Q

Dx PE - best initial test

A

Helical CT scan (CT-PA)

188
Q

CXR signs of PE

A

Hamptom’s hump - wedge-shaped infiltrate

Westermark’s sign - avascular markings distal to thrombus

189
Q

ABG of PE

A

Respiratory alkalosis initially 2/2 hyperventilation

*respiratory acidosis may occur with time

Increased A-a gradient

190
Q

When to order D-dimer if suspecting PE

A

Order if LOW suspicion for PE –> only helpful if negative

191
Q

When to use alteplase (thrombolysis) in PE

A

MASSIVE hemodynamically unstable PE

Usually preferred over embolectomy

192
Q

Standard treatment PE

A

LMWH (not in Cr>2.0) or UFH to prevent potentiation of the clot & as a bridge to therapeutic levels of warfarin - compliant pt may be discahrged on LMWH injections. UFH is an IV drip, must be hospitalized for it

Then need to be on anticoagulant (Warfarin or NOAC) for 3 months - NOAC remember not in CKD

193
Q

Who gets PE prophylaxis & what do they get?

A

Low risk clot (<40 YO, minor procedure) - early ambulation

Moderate risk - stockings & pneumatic compression devices

High risk - LMWH - in pt undergoing orthopedic or neurosurgery, trauma patients

194
Q

PERC PE criteria - what used for? Components?

A

PERC = PE rule out criteria

Age < 50 YO
Pulse < 100
O2 sat > 95%
No prior PE

No recent trauma/surgery
No hemoptysis
No use of exogenous estrogen
No unilateral leg swelling

195
Q

MC EKG finding PE

A

Tachycardia w/ NSSTTWC

196
Q

Cor Pulmonale 2/2 PE on EKG =

A

S1Q3T3

197
Q

Definition of pulmonary HTN

A

Mean p. aa. pressure > 25 mmHg at rest or > 30 mmHg during exercise

Pathophys - inc p.a. pressure = inc pulm vasc resistance = RVH = R-HF

198
Q

Describe likely patient w/ primary pulmonary HTN

A

MC in middle-aged women

  • mean age of dx 50 YO
  • Idiopathic or BMPR2 gene defect - usually prevents pulm vessel sm muscle growth & vasoconstriction
199
Q

MCC secondary pulm HTN

A

COPD - Pulm HTN 2/2 chronic lung dz or hypoxemia is class III

200
Q

EKG findings pulm HTN

A

Think = RVH = RAD & poor R -wave progression

Cor pulmonale

201
Q

Class I pulm HTN

A

primary pulm HTN

202
Q

Class II pulm HTN

A

secondary - pulm HTN 2/2 left heart dz

203
Q

Class III pulm HTN

A

secondary pum HTN 2/2 chronic hypoxemia/lung dz (COPD)

204
Q

Class IV pulm HTN

A

secondary pulm HTN due to chronic thormoboembolic disease (PE)

205
Q

PE for pulm HTN

A

Signs of R sided heart failure (inc JVP, peripheral edema, ascites)

Accentuated S2 (due to prominent P2) first or if worse….a widened or split S2 if worse

Note: Any condition that causes a non-fixed delay in the closure of the pulmonic valve, or early closure of the aortic valve, will result in a wide split S2. Therefore, a persistent split S2 would occur in the setting of a right bundle branch block, pulmonary hypertension or pulmonic stenosis (delayed P2) or severe mitral regurgitation/ventricular septal defect (early A2 closure).

206
Q

CXR pulm edema

A

Enlarged pulm arteries

SIgns of heart failure

207
Q

Cor pulmonale

A

abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels

208
Q

Causes of cor pulmonale

A

Pulm HTN
PE
Restrictive ILD
COPD

209
Q

Gold standard pulm HTN dx

A

Right-sided heart catheterization

210
Q

CBC pulm HTN

A

Polycytemia w/ increased Hct

211
Q

Management primary pulm HTN

A

Do vasoreactivity trial - if vasoreactive then tx w/ CCB

If not reactive or need additional thearpy, tx w/ prostacyclins - epoprostenol, iloprost, PDE-5 inhib (sildenafil, tadalafil)

Oxygen therapy
Long term anticoagulation

212
Q

Management Type II pulm HTN

A

Type II is 2/2 left heart disease - treat the underlying disease

213
Q

Management type III pulm HTN

A

Type III is 2/2 chronic hypoxiemia or lung dz

Treat underlying cause - OXYGEN decreases mortality

214
Q

Type IV pulm HTN

A

TYpe IV is due to chronic thromboembolic dz

Treat w/ long term anticoagulation

215
Q

Health care-associated or hospital-acquired PNA etiology

A 
S. pneumo
MSSA
GNR
Pseudomonas
MRSA
216
Q

Tx HCAP

A

COVER FOR MRSA - Vanco IV

PLUS GNR coverage & pseudomonas coverage - cefepime, ceftazadime, carbepenem, zosyn or levo IV

217
Q

CAP etiology & tx

A

S pneumo
M pna
C pna
H flu

Tx: healthy - Azithro x 5 d or doxy x 5 d

Looks good but immunosuppressed (DM, ETOH, CA, asplenia) - give them PO respiratory fluoroquinolone

Looks sick - admit - IV fluoroquinolone or IV betalactam (ceftriaxone) + atypical coverage (doxy, macrolide etc)

218
Q

MCC PNA in kids

A

VIRAL - RSV, adenovirus

219
Q

Who does fungal PNA occur in? Examples

A

IMMUNOCOMPROMISED PT

Histoplasmosis
Cryptococcus
Aspergillus
Pneumocystis jirovecci (PCP)

220
Q

Which population does mycoplasma pna occur more in?

A

College students, school-aged, military recruits

Mycoplasma = Myringitis (bullous), URI sx, pharyngitis

221
Q

CXR atypical PNA

A

“patchy” infiltrates

222
Q

Aspiration PNA etiology

A

AAA
Aspiration = anaerobes = abscess

Also staph & strep

223
Q

When is staph PNA often seen?

A

Occurs most frequently after the flu or another viral illness

Usually bilateral w/ multilobar infiltrates or abscesses

224
Q

Chemical pneumonitis caused by?

A

Aspiration of gastric acid contents

225
Q

PCP sx

A

Pneumocystis jirovecii =

IMMUNOCOMPROMISED HOST

Dry cough
Fatigue
DOE

CLUE ON TEST = DEC O2 SAT ON AMBULATION

226
Q

MC viral cause of viral pna in adults

A

Influenza

227
Q

Histoplasma etiology

A

MI & OH river valley - from soil contaminated with bat/bird droppings

228
Q

Klebsiella PNA a/w what kind of infiltrates?

A

CAVITARY lesions

causes severe illness in ETOH, debilitated, chornic illness

229
Q

CXR description & PE atypical PNA

A

Diffuse, patchy, interstitial or reticulonodular infiltrates

Kind of sounds like interstitial lung disease description more than a PNA descrpition - but word PATCHY = key for PNA

PE often normal w/ si consolidation (tactile fremitus, etophony etc) absent

230
Q

CXR & PE typical PNA

A

Lobar pna on cxr

PE - signs of a consolidation - local dullness to percussion, bronchial breath sounds, INCREASED tactile fremitus + egophony (E–>A), inspiratory crackles

231
Q

CP atypical PNA

A

More of dry cough
Low grade fever
Extrapulmonary sx - myalgias, malaise, sore throat, headache, n/v/d

232
Q

CP typical PNA

A

Sudden onset fever
Productive cough - purulent
RIGORS (esp s. pna)
Tachycardia, tachypnea

233
Q

Rusty sputum - pathogen?

A

Strep- PNA

234
Q

Currant jelly sputum

A

Klebsiella

235
Q

Green sputum

A

H. flu, pseudomonas

236
Q

Foul-smelling sputum

A

Anaerobes - aspiration

“fetid breath”

237
Q

Lung disease in which tactile fremitus is increased?

A

PNA

Decreased in pleural effusion, PTX

238
Q

Lung disease where breath sounds are bronchial and you have + egophony

A

PNA

Decreased in pleural effusion, PTX - because more space between the lung tissue and rib cage = decreased sounds

239
Q

When to give PCV13 vaccine

A

Given to kids in 4 doses - 2, 4, 6, and 15 months of age

High risk children > 2 should also receive single dose of PPSV23 8 weeks after completed immunization series of PCV13

240
Q

When to give PPSV23?

A

Given to all adults > 65

If they’ve received PPSV23 before, wait until they’re > 65 and it’s been > 5 years since they’ve received PPSV23

Age > 2-64 if chornic disease - cardiac, pulmonary, diabetes, ETOH, liver, chronic care facility, immunocompromised (HIV, malignancy, chronic renal disease, chemotherapy, asplenia, sickle cell)

241
Q

A PNA in which lobe would obscure the R heart border

A

Right MIDDLE lobe

242
Q

Which PNA obscures the left heart border

A

A left LINGULAR PNA would obscure the left heart border

243
Q

RIGHT UPPER LOBE PNA W/ bulging fissure, CAVITATIONS = ?

A

Klebsiella PNA

244
Q

When do pt w/ Tb become PPD positive?

A

2-4 weeks after infection

245
Q

Are patients with latent TB infection contagious?

A

No

246
Q

Describe location and characteristics of a Tb granuloma - in primary, latent and in secondary reactivation

A

Primary: Lower lobe consolidation

Latent: Caseating w/ central necrosis

Reactivation: Cavitations in APICES of lungs (Tb likes the apices b/c there’s more O2 concentration up there)

247
Q

Positive PPD for HIV + OR immunosuppressed (15 mg prednisone/day for example or biologics) person

A

INDURATION > 5 mm

248
Q

Positive PPD for person in close contact w/ Tb

A

INDURATION > 5 mm

249
Q

Positive PPD for person w/ CXR consistent w/ old/healed Tb (calcified granuloma)

A

INDURATION > 5 mm

250
Q

CP Tb

A

Chronic, productive cough
Pleuritic CP, hemoptysis

Night sweats, fever, chills, fatigue, weight loss, anorexia

251
Q

High risk populations/ high prefalence population considered + PPD if what size?

A

> 10 mm

Health care workers, immigrants form high-prevalence areas, homeless

252
Q

False negative PPD

A

Cutaneous anergy (sarco, HIV), faulty application (SQ instead of TD)

253
Q

False positive PPD

A

Improper reading (erythema is NOT considered positive)

BCG vaccination 2-10 years ago (although usu < 10 mm)

254
Q

Test used for Tb screening

A

PPD

255
Q

Dx studies in suspected cases of active Tb

A

Acid-fast smear & sputum cultures x 3 days

CXR - indicated to exclude active Tb (ex in newly positive PPD), as yearly screening in pt w/ known positive PPD

Interferon gamma release assay - quantiferon gold - prior BCG vaccination doesn’t affect this!

256
Q

Tx regimen active Tb

A

4-drug regimen for SIX months –mnemonic: RIPS, RIPE

Rifampin - orange secretions
Isoniazid - hepatitis, peripheral neuropathy - prevented w/ vit B6 (pyridoxine) 
Pyrazinamide- hepatitis, inc Ca
Ethambutol - optic neuritis
Streptomycin - oto/nephrotox

**Pt no longer considered infectious after 2 weeks of treatment

Treatment can be stopped 3 mo after negative sputum culture. PZA stopped after 2 months regardless. Can stop ETH, STM if culture comes back as sensitive to INH and RIF.

257
Q

Treatment latent Tb

A

Isoniazid & pyridoxine (B6) for NINE months (if INH-sensitive)

Alterative: Rifampin x 4 mo

258
Q

Latent Tb dx

A
  1. Asx
  2. PPD +
  3. No evidence of active infection on CXR/CT

**Tx reduces risk of reactivation Tb in the future

259
Q

MCC acute bronchitis in adults

A

VIRUSES - adenovirus

260
Q

Definition of acute bronchitis

A

Inflammation of the trachea or bronchi (conducting airways)

Often follows a URI

261
Q

Tx acute bronchitis

A

Symptomatic - fluids, rest, bronchodilators, antitussives (adults)

262
Q

CP Pertussis

A

3 stages jus tlike 3 sylab:

  1. Catarrheal - uri sx 1-2 wk - most contageous during this phase
  2. paroxysmal phase - severe parosysmal coughing fits w/ inspiratory whooping sound after coughing fit - +/- post-cough emesis
  3. Convalescent phase - resolution of the cough - may take weeks/months
263
Q

Gold standard dx pertussis

A

PCR nasopharyngeal swab = gold standard - performed in first 3 weeks of sx onset

Other dx - lymphocytosis (60-80% lymphocytes)

264
Q

Tx pertussis

A

Supportive tx = MAINSTAY

Abx - macrolide if present in first 7 days b/c shortens course & how contagious you are

265
Q

Complications of pertusis

A

PNA
Encephalopathy
otitis media
Sinusitis

Inc mortality in infants due to apnea & cerebral hypoxia a/w coughing fits

266
Q

Bronchiolitis - what is it? Etiology? Age?

A

Inflammation of the bronchioles (LRTI of small airways) = proliferation/necrosis of bronchilar epithelium = sloughing of epithelium & increased mucus plugging & edema = peripheral airway narrowing & airway obstruction

Etio: MC RSV, adeno

Age: Kids 2mo = 2 years

267
Q

RF bronchioligits

A

2 months old, no breast feeding, exposed to smoke, crowded conditions, premature baby (= lungs not fully developed)

268
Q

Most common acute complication of bronchiolitis

A

S. pneumonia PNA w/ otitis media

269
Q

Dx bronchiolitis

A

CXR - peribronchial cuffing

Nasal washings - Mab to RSV

PUls ox - single best predictor of disease in children (<96% = admit to hospital)

270
Q

Treatment bronchiolitis

A

Humidified O2, IV fluids, APAP/NSAID for fever

271
Q

Prevention of RSV?

A

HAND WASHING - transmitted via direct contact w/ secretions & self-innoculation w/ contaminated hands

Also palivizumab prophylaxis in high risk groups

272
Q

3 D’s of epiglotitis

A

Dysphagia, DROOLING, distress

Suspect in pt w/ rapidly progressing pharyngitis, muffled voice & otynophagis out of proportion to physical exam findings

273
Q

Epiglottitis definition

A

Inflammation of epiglottis that may interfere with breathing (medical emergency) - mortality 2/2 asphyxiation

274
Q

Xray sign for epiglottitis

A

Thumbprint sign - engorged epiglottis looks like thumbprint

275
Q

Definitive dx epiglottitis

A

Laryngoscopy - shows cherry red epiglottis w/ swelling

276
Q

Tx epiglottitis

A

Keep child calm - aka DO NOT attempt to visualize w/ tongue blade if high suspicion = UPSET

Maintain airway - dexamethasone to dec swelilng - intubation if severe

Ceftriaxone, cefoxatime

277
Q

Typical pt who would have epiglottitis?

A

Male child 3mo - 6 YO, hx DM, no vaccinations (MCC Hib but rates gone down 2/2 vaccination)

278
Q

Croup etiology

A

Parainfluenza

Croup = laryngotracheitis

Virus = inflammation of UPPER airway = subglottic larynx & tracheal swelling

279
Q

Typical child w/ cropu looks like what?

A

6mo - 6 years old
FALL/WINTER MONTHS
Common

280
Q

Cervical radiograph in cropu

A

Steeple sign (subglottic narrowing of trachea)

281
Q

Management of croup - mild vs moderate vs severe

A

Mild = no stridor, no resp distress = cool humidified air mist, hydration, dexamethasone, supplemental O2 if < 92%

Moderate - stridor at rest w/ mild retractions - Dexamethasone PO or IM & supportive treatment +/- nebulized epinephrine

Severe - stridor at rest w/ marked contractions - dexamethasone - nebulized epinephrine & hospitalization

282
Q

CP flu

A

Abrupt/SUDDEN ONSET!!! fever, chills, malaise, URI sx, pharyngitis, PNA,

Myalgias in legs & lumbosacral area

283
Q

When to give Tamiflu

A

IN pt w/ high risk of complications or if hospitalized - best if initiated win 48 hours of onset of sx

284
Q

ARDS definition, pathophys, who gets it?

A

Life-threatening acute hypoxemic respiratory failure

Patho: Inflammatory lung injury due to pro-inflam cytokines = diffuse alveolar damage = inc permieability of alveolar-capillyar barrier = pulmonary edema & alveolar fluid influx, loss of surfactant & vascular endothelial damage = decreased oxygen in blood

Critically ill pt get it - develop while in hospital for another reason - sepsis is MC - also severe trauma, aspiration of gastric contents etc

285
Q

CP ARDS

A

Acute dyspnea & hypoxemia

Multi-organ failure if severe

286
Q

Dx of ARDS

A

3 Components -
1. Severe refractory hypoxemia = HALLMARK

  1. B/l pulmonary infiltrates on CXR
  2. The absence of cardiogenic pulmonary edema/ CHF (PCWP< 18mHg) - ARDS spares the costophernic angles (non-cardiogenic pulmonary edema)
287
Q

Tx ARDS

A

Non-invasive or mechanical ventilation:
CPAP w/ full face mask
Attempt to keep O2 sat > 90%
PEEP

Treat underlying cause

288
Q

RF sleep apnea

A 
Obesity
Male
6th-7th decade
Large neck
Crowded oropharynx
Micrognathia
289
Q

Dx - sleep apnea

A

In -lab polysomnography
> 15 events/ hr = diagnostic - obstructive or mixed apneas, hypopneas, respiratory effort arousals etc

Labs - polycythemia 2/2 chronic hypoxia

290
Q

Tx sleep apnea

A

CPAP
Weight loss, exercise, no alcohol, changes in sleep positioning

Oral appliance if CPAP unsuccessful

*PANCE by subspecialty (22 decks)

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