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M2 > Resp. path > Flashcards

Resp. path Flashcards

0
Q

What is the main enzyme implicated in emphysema?

A

Neutrophilic Elastase

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1
Q

Define emphysema

A

COPD w/ permanently enlarged air sacs distal to terminal bronchioles w/ destruction of their walls and w/o obvious fibrosis

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2
Q

5 morphological subtypes of emphysema

A
  1. centrilobular - esp. w/ cigarettes
  2. panlobular / panacinar - a1-antitrypsin and end-stage centrilobular
  3. paraseptal - assoc. w/ pulmonary fibrosis. may -> spontaneous pneumothorax
  4. irregular - associated w/ pulmonary scars
  5. interstitial - subcutaneous. due to trauma or elevated intraalveolar pressure
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3
Q

What type of emphysema is cigarette smoking usually associated with?

A

Centrilobular

Anthracosis often present

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4
Q

What part of respiratory tree is involved in centrilobular emphysema?

A

Primarily respiratory bronchioles due to high conc. of inhaled irritants
More prominant in upper lung fields

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5
Q

Chronic Bronchitis Definition

A

Productive cough w/o discernible cause for at least 3 months in 2 consecutive years

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6
Q

Reid index

A

Ratio of thickness of mucous glands to total thickness of airway wall.

Elevated in chronic bronchitis

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7
Q

status asthmaticus

A

most severe subtype of asthma - prolonged interval of continual symptoms, unresponsive to treatment

May be life-threatening

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8
Q

Common effector pathway of asthma

A

Stimulus in susceptible host -> release of inflammatory mediators -> increased vascular permeability, edema, neural and cytokine mediated bronchoconstriction, mucus hypersecretion, chemotaxis of additional inflamm. cells -> amplification

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9
Q

Major chemical mediators of acute phase of asthma

A 
Histamine
LTC4, D4, E4
PGD2 - mucus prod
PAF
Parasympathetic neural reflexes
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10
Q

What happens in late phase of asthma?

A

Infiltration of white cells (esp. eosinophils) in response to locally released chemotactic factors
LTB4, eotactin
Prolongation and augmentation of disease process

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11
Q

2 common drugs that can contribute to asthma

A

aspirin: decreased prostaglandin production and relative increase in leukotriene

B-antagonists: may precipitate bronchospasm

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12
Q

What respiratory disease is assoc. w/ mucus plugs?

A

asthma

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13
Q

Curschmann Spirals and Charcot-Leyden Crystals - what are they and what are they associated with?

A

Curschmann Spirals: mucoid swirls of epithelial cells

Charcot-Leyden Crystals: extruded eosinophil granules - needle-like crystals

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14
Q

What is bronchiectasis

A

Permanent airway dilation due to recurrent infections w/ necrosis

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15
Q

Atelactasis neonatorum

A

Incomplete expansion of lungs at birth

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16
Q

What happens to the mediastinum in obstructive atelactasis?

A

Mediastinal shift toward atelactic lung

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17
Q

What happens to the mediastinum in compression atelactasis?

A

Mediastinal shift away from atelactic lung

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18
Q

Effects of alpha, B1, and B2 agonists

A

alpha: vasoconstriction and vasopressor -> decongestion
B1: increased myocardial conductivity, increased HR and contractile force
B2: relax bronchial sm. muscle, inhibit inflamm. mediator release, stimulate mucocilliary clearance

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19
Q

What receptors do epinepherine, ephederine, and isoproterenol work at?

A

epinepherine: B1, B2, alpha
ephedrine: B1, B2, alpha
isoproterenol: B1, B2

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20
Q

How do selective B2 agonists work?

A

increase AC -> increased cAMP -> sm. muscle relaxation

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21
Q

3 short acting B2 agonists

A

Albuterol
Levalbuterol
Pirbuterol

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22
Q

What is the difference between albuterol and levalbuterol?

A

Albuterol is a racemix mix of R and S enantiomers
Levalbuterol is only R (active)
considered equal, but levalbuterol is expensive.

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23
Q

What is the difference between salmeterol and formoterol?

A

Both last 12+ hrs
Formoterol is a full B2 agonist and has faster onset
Salmeterol is a partial B2 agonist

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24
Q

2 long acting B2 agonists available in 1x daily dosing?

A

Indacaterol
Vilanterol

Both available as DPI

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25
Q

What genetic factor has been associated with increased susceptibility to B2 agonist tolerance?

A

Gly16 polymorphism of B2 receptor.

-> reduced responsiveness to agonists

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26
Q

What is the recommendation regarding use of long acting B2 agonists in treating asthma?

A

Black box warning: should not be used as monotherapy. increased risk of death

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27
Q

What is the primary mechanism of action of anticholinergics in treatment of obstructive respiratory disease?

A

Reduction of intrinsic vagal tone

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28
Q

In what patient population is ipratropium contraindicated?

A

Those w/ soy lecithin or peanut allergy.

Propellant contains lecithin

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29
Q

2 long acting anticholinergic drugs for control of COPD and sites of action.

A

Tiotropium blocks M1-M3 receptors, but dissociates from M2 quickly. M1 and 3: long duration of action
Aclidinium blocks M1-M5. pharmacological action at M3

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30
Q

Zileuton

A

Blocks 5-LOX preventing leukotriene production.

Used in chronic maintenance of asthma

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31
Q

Montelukast and Zafirlukast

A

Long acting controlers of COPD

Selective and competitive inhibition of Cys LT1 receptor -> prevention of production of LTD4 and E4

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32
Q

What would be a good medication for chronic management of asthma for a child under 5?

A

Montelukast
No drug interactions
Chewable tablet / granule form
Indicated for children >1

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33
Q

What is lipocortin?

A

Induced by corticosteroids

Inhibits PLP A2 -> decreased production of prostaglandins and leukotrienes

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34
Q

What is the time of onset for inhaled corticosteroids?

A

From days up to 2 weeks

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35
Q

Adverse reactions to inhaled corticosteroids?

A 
Cough, dysphonia
Oral Thrush (rinse mouth after using inhaler)
Adrenal suppression, osteoporosis, skin thinning (high doses)
Decreased growth velocity in children at low doses - may be transient.
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36
Q

What is the mechanism of methylxanthines?

A

Nonselective inhibition of phosphodiesterase
Increased cAMP -> smooth muscle relaxation
Effects intercellular Calcium
Mild anti-inflammatory

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37
Q

2 methylxanthine drugs

A

Theophilline
Aminophilline

Narrow therapeutic window!

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38
Q

What is the main concern w/ theophilline use and what factors must be considered?

A

Narrow therapeutic window (3rd line agent)
Must consider: caffeine use - additive effect
cigarettes - inhibition of cyp -> increased toxicity

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39
Q

Target concentration of theophylline and toxic concentration

A

5-15 mcg/ml

>20 mcg/ml -> toxicity: tachycardia, restlessness, agitation, emesis, seizure

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40
Q

Roflumilast

A

PDE-4 inhibitor
-> accumulation of cAMP -> smooth muscle relaxation
P450 metabolism

Bronchodilation and anti-inflammatory effect - treatment for COPD

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41
Q

Cromolyn - mechanism and time to onset of activity.

A

Mast cell stabilizer - takes 1week for full effect

Does not have bronchodilatory, anti-histaminic, or corticosteroid effects.

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42
Q

Omalizumab - what it is and how administered

A

humanized monoclonal antibody to IgE
Good for pts. w/ comorbid allergies
Subcutaneous injection - expensive

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43
Q

Combivent

A

Combination MDI

Ipratropium / Albuterol combo - COPD quick relief

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44
Q

Advair

A

Salmeterol / Fluticasone - DPI, MDI

COPD and Asthma controller

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45
Q

Symbicort

A

Formoterol + Budesonide
DPI for asthma and COPD
Controller

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46
Q

Dulera

A

Mometasone + Formoterol

MDI asthma controller

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47
Q

Breo Ellipta

A

Fluticasone + Vilanterol
DPI
COPD controller

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48
Q

What racial / ethnic groups have the highest incidence of TB infection?

A
  1. Asian
  2. Hispanic
  3. African American
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49
Q

What toxins are produced by TB?

A

None

But it does produce niacin - old ID Method

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50
Q

What is the most common mycobacterial infection in AIDS?

A

MAC: mycobacterium avium complex
consists of M. intracellulare and M. avium
risk of infection when CD4 is <50
Disseminated infection

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51
Q

What are some Non-Tuburculous Mycobacteria species and associated diseases?

A

M. scrofulaceum - Lymphadenitis
M. marinum and M. ulcerans - cutaneous disease
MAC - disseminated disease in HIV pts.

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52
Q

What NTM pathogen causes pulmonary disease in CF?

A

M. abscessus

person to person spread in CF centers

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53
Q

What NTM is most similar to TB?

A

M. kansasii

not treated with PZA

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54
Q

What is the source of NTM spread?

A

Water and soil source - no person to person

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55
Q

TB infection depends on what 3 factors?

A

Number of droplet nuclei exposed to
Number of TB organisms in droplet nuclei
Duration of exposure

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56
Q

5 measures for preventing TB infection

A

Ventilation (neg. pressure isolation) >20 air volume changes per hour
UV light
Chemotherapy: 1-2 weeks of therapy prevents infectivity
Covering infected person’s mouth
Masks

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57
Q

What % of people w/ TB exposure become infected? What % of those develop TB?

A

1/3 become infected (pos skin test or IGRA)
Of those: 10-15% develop TB
Of those: 50% develop early (w/in 2 years), 50% late

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58
Q

How long does it take to develop a positive skin test after TB exposure?

A

3-8 weeks

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59
Q

Describe the course of infection of TB from exposure to disease manifestation

A

Inhalation -> lung -> lymph -> blood and spread
Macrophage endocytosis -> multiplication, inhibition of phagolysosome formation -> macrophage death and realease
3 weeks: Th1 response: IFN-gamma-> macrophage activation and phagolysosome formation - mycobacteria destruction
Macs release TFN-a: increases monocyte response
relative immunity

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60
Q

Describe TB skin testing

A

Mantoux Method:
Intracutaneous injection of 5 Tuberculin Units (TU) of PPD (Purified Protein Derivative)
Induration measured after 48-72 hours

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61
Q

What is a positive TB skin test?

A

5,10, and 15 mm induration depending on risk

High risk: 5mm (close contact of infected, HIV, immune suppressed, etc)

Low-moderate risk: 10mm (health care workers, skin test conversion, recent immigrants from endemic areas, children <4yrs)

Low risk: 15mm: no risk factors - targeted skin testing not recommended.

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62
Q

What should be done if TB is suspected?

A

3 sputum sample collections at least 8 hrs apart w/ one first morning sample
Order: AFB test and culture for mycobacteria

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63
Q

What are the fastest turn-around tests for TB?

A

AFB: Acid fast bacillus stain can be completed in 24-48 hrs

Direct Nucleic Amplification Test on sputum sample: 24-48 hrs

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64
Q

What are the shortcomings of AFB staining?

A

Low sensitivity and Low specificity: produces both false + and -

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65
Q

What is the definitive diagnostic test for TB and how long does it take to complete?

A

Culture and sensitivity

Very slow: 1-2 weeks. maybe up to 6-8 weeks

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66
Q

4 major TB drugs

A

Isoniazid (INH)
Rifampin (RIF)
Pyrazinamide (PZA)
Ethambutol (EMB)

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67
Q

What is multi-drug resistant TB?

A

Resistant to AT LEAST Rifampin and Isoniazid

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68
Q

What is XDR-TB?

A

Extremely Drug Resistant TB
MDR-TB (resistant to RIF and INH) resistant to any fluoroquinalone
Plus any one of the following injectibles:
Amikacin, Capreomycin, Kanamycin

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69
Q

What is the duration of treatment for TB?

A

Depends on drugs used, presence of resistance, presence of + cultures after initiation phase, and cavitary or HIV add 3 mos.
If RIF and PZA - treat 6 mos

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70
Q

What is initial phase and continuation phase treatment of TB?

A

Initial: standard 4 drug regimen: INH, RIF PZA, EMB for 2 mos
Continuation: additional 4 months (of RIF / INH) or more if pos culture after initial phase (drugs may differ based on susceptibility)

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71
Q

What is the definition of latent TB?

A

TB infection w/ no indication of disease
Pos skin test or IGRA
Lifelong risk of TB - assumed persistence of organisms somewhere in body

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72
Q

What is treatment for latent TB?

A
  1. 9 mos of Isoniazid @ 300mg / day or 900mg 2/wk
    or
  2. 4 mos of Rifampin @ 600 mg / day

watch for Hepatitis

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73
Q

What are risks for disease development in cases of TB infection?

A

Immune suppression: HIV, transplants, Prednisone (15mg/day for 1month or more, TNF-a agonists (infliximab, etanercept, adalimumab)
Stable x-ray consistent with old healed TB
Children < 4yrs
Silicosis, Diabetes, ESRD, underweight, low dose corticosteroids, cancer of head and neck

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74
Q

What is BCG?

A

Bacillus Calmette and Guerin - TB vaccine of M.bovis
varies in efficacy
does not prevent infection, but prevents dissemination

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75
Q

What is IGRA and what tests are used?

A

IFN-gamma release assay
1. QuantiFERON Gold: ELISA to determine IFN-g production in blood sample when Ag added (Ag: ESAT-6, CFP-10, TB7.7)
+: >/= 0.35 IU/mL
-: < 0.35 IU/mL

  1. T-Spot TB: incubation of peripheral blood monocytes with 2 separate mixtures of peptides (ESAT-6 and CFP-10).
    ELISpot detects # of IFN-g secreting cells
    +: +/= 8 spots
    -: <7 spots
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76
Q

define pneumonia

A

Inflammation of gas exchanging areas of lung / lower respiratory tract

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77
Q

What is the #1 cause of death from infectious disease?

A

pneumonia

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78
Q

What is rust colored sputum suggestive of?

A

Pneumococcal pneumonia

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79
Q

What is “currant jelly” sputum suggestive of?

A

Klebsiella pneumoniae pneumonia

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80
Q

What is creamy yellow sputum suggestive of?

A

Staphylococcus pneumonia

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81
Q

What is very foul smelling sputum suggestive of?

A

Aspiration pneumonia - oral anaerobes

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82
Q

What pneumonia causing organsisms are not seen in sputum?

A

Mycoplasma, Legionella, TB, viruses

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83
Q

What is treatment for Pneumococcal pneumonia?

A

Macrolide (azithromycin) or doxycycline

Plus 3rd gen cephalosporin (Cefotaxime, cephtriaxone, cephixime, cefpodoxime

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84
Q

What is type 3 serotype S.pneumo?

A

Highly virulent strain. Poorer prognosis.

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85
Q

4 groups of community acquired pneumonia

A
  1. Outpatient w/o comorbidity 60 yoa. (s.pneumo, mycoplasma)
  2. Outpatient w/ comorbidity or >60yoa (s.pneumo, virus, h.influ)
  3. Hospitalized w/ CAP 5-25% mortality
    (S.pneumo, H. influenzae, poly (inc. anaerobe), gram -, legionella)
  4. Severe hospitalized - ICU. Up to 50% mortality
    (S. pneump, legionella, gram -, resp. viruses)
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86
Q

What does Mycoplasma pneumonia cause?

A

Atypical or “walking” pneumonia in young otherwise healthy people.

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87
Q

What are clinical symptoms of Mycoplasma pneumonia?

A

insidious onset
non-productive cough
fever, headache, chills
No leukocytosis
Blistering of eardrum (Bullous Myringitis)
Rare signs of consolidation - usually patchy rales and crackles

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88
Q

How is mycoplasma treated?

A

Macrolide (azithro, clarithro, erythromycin)

or Tetracycline

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89
Q

What are indicators of Legionella infection?

A

Fever over 102 w/ relative bradycardia, GI involvement w/ diarrhea, hyponatremia, hypophosphatemia

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90
Q

How is legionella pneumonia treated?

A

Macrolides- rifampin

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91
Q

What populations are associated with H.influenzae pneumonia?

A

alcoholics, COPD, healthy adults, sickle cell pts.

Lots of sputum

treat w/ cephalosporin, sulfa

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92
Q

What populations are associated with Klebsiella pneumonia?

A

Diabetics, alcoholics, debilitated

bulging fissure on cxr

treat w/ cephalosporin or aminoglycoside

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93
Q

In aspiration pneumonia how long does it take following aspiration for tissue necrosis / liquefaction?

A

~12 days

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94
Q

3 tests for Cocciodiomycosis

A

Skin test: Positive bet. 3 days and 3 weeks after onset.

  • *- change to +: new infection
  • *+ change to -: severe infection or dissemination

IgM titer: latex agglutination: + w/in 2-4 weeks of infection

IgG titer: complement fixation: + w/in 8 weeks after infection
diagnostic and prognostic. high titer - high prob. of disseminated disease

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95
Q

2 forms of cocciodiomycosis

A

arthrospore- in soil, infectious

spherule - tissue form - contains endospores

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96
Q

2 forms of histoplasmosis

A

microconidia: infective form in soil. assoc. w/ bird and bat droppings

narrow-necked budding yeast: tissue form

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97
Q

What are 2 forms of blastomycosis?

A

dumbell shaped yeast

broad based budding yeast (tissue)

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98
Q

How is blastomycosis diagnosed?

A

Serologic testing: not useful - high titer may inappropriately indicate disease
Skin testing: not useful - frequently indicates histoplasmosis
Culture: definitive. fast growing and easy to culture

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99
Q

How is blastomycosis treated?

A

Usually no antifungal needed.

Only in disseminated disease - IV anti-fungal

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100
Q

How is aspergillus diagnosed?

A

Skin testing for acute infection

Serology: IgE in acute and fungus balls. IgG also possible

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101
Q

4 types of aspergillus infection and treatments

A
  1. Hypersensitive pneumonitis / Extrinsic Allergic Alveolitis - cough, fever, dyspnea, chills w/in 4-6 hrs of exposure
    - treat w/ steroids
  2. Allergic Bronchopulmonary Aspergillosis (ABPA) - pts. w/ long standing asthma. + skin, + serology, migratory CXR infiltrates. Cough up brown plugs. Treat w/ steroids
  3. Aspergilloma - fungus ball. bleeding due to erosion. Surgical removal
  4. Invasive aspergillosis - only in immunocompromised. Culture for Dx. multiple IV antifungals. High mortality.
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102
Q

What organisms are associated w/ nosocomial pneumonia?

A

60% enteric gram (E. coli, Klebsiella, enterobacter, pseudomonas, Serratia, Proteus)
10% S. aureus
Legionalla and other

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103
Q

What is the most common viral infection seen in AIDS pts?

A

CMV

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104
Q

In what patients is P.carinii seen?

A

HIV: slowly progressive, fever, cough, dyspnea, CXR infiltrate
Children w/ leukemia: fulminant downhill course

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105
Q

What is treatment for P.carinii?

A

TMP/SMX

Pentamidine IV or aerosol for those who can’t tolerate.

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106
Q

How is INH activated, how does it work, how metabolized?

A

Activated by mycobacterium
mycobacterial catalase-peroxidase (KatG)
Action: interferes w/ mycolic acid synthesis (bactericidal against actively growing organisms, bacteriostatic against non-replicating)
Metabolism: N-acetyltransferase

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107
Q

What is Rifampin’s MOA?

A

binds B-subunit of bacterial DNA dependent RNA-pol

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108
Q

What lab values are elevated in Rifampin toxicity? What about Isozianid?

A

Rifampin: elevated bilirubin and alkaline phosphatase
Isoniazid: aminotransferase elevated

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109
Q

What options are available if there are concerns about Rifampin and DDI?

A

Rifapentene and Rifabutin - less likely to cause interactions
Rifabutin is usually used.

Rifampin > Rifapentene > Rifabutin

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110
Q

What are some examples of drugs that Rifampin interferes with?

A

Rifampin induces many CYP450 enzymes
Decreases concentrations of: warfarin, cyclosporine, HIV meds (esp. protease inhibitors), anticonvulsants, oral contraceptives.

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111
Q

What is Pyrazinamide’s MOA?

A

Unknown. Prodrug activated by mycobacterial pyrizinamidase -> active pyrazinoic acid.
High activity at acidic pH in lysosomes

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112
Q

What is the MOA of Ethambutol?

A

Inhibits arabinosyl transferases - needed for cell wall components.

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113
Q

What was the first drug useful against TB, what class, what MOA?

A

Streptomycin (Aminoglycoside) binds 30s subunit of bacterial ribosome - oxygen dependent

ototoxicity

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114
Q

What limits streptomycin use in TB infections?

A

Rapid development of resistance - 80% of RIF / INH resistant strains are streptomycin resistant.
Does not work intracellularly

Vestibular toxicity - watch for gait abnormalities

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115
Q

What are the differences between Rifampin, Rifabutin and Rifapentene?

A

Rifabutin: more potent than Rifampin, 50% less CYP450 induction

Rifapentene: long half-life: 1x /week option for HIV - patients. Between Rifabutin and Rifampin in CYP450 induction

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116
Q

4 major cell types associated w/ asthma

A

Mast cells - histamine, LT, PG, PAF
Eosinophils - MBP, eosinophil cationic protein
Macrophage - cytokines, ROS, PAF, act as APC
TH2: IL 4, 5, GM-CSF

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117
Q

What systems innervate airway sm. muscle?

A

Parasympathetic: maintains tone. PS constricts airways.
Sympathetic: relaxes airways. Small role in humans.
Nonadrenergic Noncholinergic Neural pathways: mediate tone
-NO and VIP are inhibitory
- Substance P and neurokinins A and B are excitatory
–nerve injury secondary to inflamm -> increased excitatory input, bronchoconstriction and vascular permeability

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118
Q

How long does the early asthmatic response last?

A

resolves by 2 hours

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119
Q

How often does the late phase asthmatic response occur and how long does it last?

A

Occurs in 50% of asthmatics

Occurs w/in 6-8 hrs and may last up to 24 hours

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120
Q

3 causes of airway obstruction in asthma

A
  1. bronchospasm
  2. vascular congestion and bronchial edema
  3. accumulation of airway secretions, mucus casts, and cellular debris
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121
Q

What happens to PFTs during an asthma attack?

A

Reduced FEV1 and FVC
Reduced FEV1/FVC
Lung volume increase, esp RV and FRC

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122
Q

How does the work of breathing change in asthma?

A

Increases

  1. Flattened diaphragm w/ hyperinflation - no longer optimal length/tension relationship
  2. Hyperinflated lungs shift on compliance curve -> require more pressure for change in volume
  3. V/Q mismatch -> hypoxemia and dead space
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123
Q

What is criteria for intermittent asthma?

A

Rule of 2:
symptoms < / = 2x /week
night time awakenings </= 2 days per week

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124
Q

What are the 3 levels of persistent asthma?

A

Mild: symptoms >2x week, not daily, awakening 3-4/mo, B2 ag >2x/ week, not more than 1x/ day
Moderate: symptoms daily, awakening >1x/week, b2 daily
Severe: symptoms throughout day, awakening daily, b2 multiple/ day

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125
Q

What is the goal of asthma therapy and what are its components?

A

Goal: control

  1. Impairment: prevent symptoms, minimize use (<2/week) of SA B2 agonists
  2. Risk: minimize hospital visits and pulmonary function decline, minimize adverse medical effects
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126
Q

What is the only major disease in US w/ an increasing death rate?

A

COPD

4th most common cause of death

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127
Q

What % of chronic heavy smokers develop COPD?

A

10-15%

Genetic component

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128
Q

What chromosome is implied in families w/ COPD?

What other polymorphisms have been identified?

A

2q

IL1, TGF-B (both increasing and decreasing risk), GSTM-1

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129
Q

Where is a1-antitrypsin gene found? Is deficiency AD or AR?

A

on chromosome 14

AR

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130
Q

What other organ system is affected in persons w/ a1-antitrypsin deficiency emphysema?

A

Hepatic cirrhosis is seen in 1-3% of emphysema pts.

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131
Q

What is the role of oxidative stress in COPD?

A
  1. activates NFk-B -> transcription of inflammatory proteins (TNF-a)
  2. inactivation of anti-proteases
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132
Q

What is the role of amplification in COPD?

A

COPD patients have amplified inflammatory response compared to normal.

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133
Q

3 key symptoms for COPD diagnosis

A
  1. chronic cough
  2. chronic sputum production
  3. dyspnea: starts insidiously and escalates - persistent
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134
Q

What is the most common cause of COPD exacerbation?

A

bacterial or viral infection of airways

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135
Q

What is the most common genotype of a1-antitrypsin deficiency? What is normal?

A

PiZZ (homozygous, disease is AR): in 90-95% of cases

PiMM is normal

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136
Q

What chromosome houses the genes associated with a1-antitrypsin deficiency?

A

14

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137
Q

What inflammatory cells are associated with COPD?

A

Macrophage (critical)
CD8 Lymphocyte
Neutrophil

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138
Q

What changes in V/Q are seen in COPD?

A

Both high and low
High: increased dead space (V/Q -> infinity)
Low: hypoxemia, shunt (V/Q -> 0)

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139
Q

What are major considerations for COPD diagnosis?

A 
Chronic cough
Sputum
Recurrent bronchitis
Dyspnea - persistent, progressive, worse w/ exertion
Exposures - smoking
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140
Q

When should ABG be checked in COPD evaluation?

A

FEV1 <40%
signs of Cor Pulmonale / Right sided HF
During exacerbations

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141
Q

What is a chronic CO2 retainer?

A

COPD patient with elevated PCO2 between exacerbations

Blood gas reflects compensated respiratory acidosis (normal pH, high HCO3-

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142
Q

Why do people lose weight in COPD?

A

Loss of skeletal muscle, particularly in limbs

  • increased TNF-a, increased metabolism
  • seen in 50% w/ severe disease, 10-15% in mild-moderate
  • inverse relationship w/ survival
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143
Q

5 etiologies of bronchiectasis

A
  1. infection: Pertussis, necrotizing pneumonia, viral pneumonia (measles, influenza), TB
  2. Immotile cilia syndrome / Kartagener’s
  3. Hypogammaglobulinemia
  4. Cystic Fibrosis (frequent infections w/ S.aureus and PSA)
  5. Allergic bronchopulmonary aspergillosis
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144
Q

How is bronchiectesis detected?

A

CT scan reveals dilated bronchi that do not taper toward periphery.

CXR is not reliable, though increased bronchovascular markings and cystic air spaces are suggestive.

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145
Q

Treatment for bronchiectasis?

A
  1. Treat underlying problem
  2. Improve clearance of secretions: chest physiotherapy
  3. Control infections: vaccinations, daily abx (CF - macrolide 3x/wk)
  4. Bronchodilators
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146
Q

From what tissue do lungs develop?

A

Foregut endoderm

buds at ~4weeks

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147
Q

3 stages of lung development

A

Pseudoglandular 5-16 wks
Canalicular 16-26 wks
Alveolar / Viable 26- birth

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148
Q

What test is used to asses lung maturity prenataly?

A

Lecithin: sphingomyelin

Lecithin increases w/ maturation, sphingomyelin stays stable

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149
Q

What substances accelerate fetal lung maturation?

A

cortisone, stress, thyroxine, prolactin, theophylline, sympathomimetics

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150
Q

3 factors that decrease rate of fetal lung maturation

A

Insulin
Metapyrone
Barbiturates

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151
Q

At what age are all alveoli formed?

A

~10
few alveoli at birth
8-10 yrs - intense alveolar prolif
10-20 increase in size

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152
Q

What is a tracheal-esophageal fistula and when is it formed?

A

Failure of separation of esophageal and lung buds from foregut. Abnormal connection between trachea and esophagus.

Insult at ~4th week

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153
Q

When would failure of a lung or lobe to develop occur and what are the ramifications?

A

Insult ~4-8 weeks gestation

Generally asymptomatic (60% reserve at max exercise in normal)
but reduced reserve - sx, trauma, infection
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154
Q

What are cysts in terms of lung development? Blood supply? What do they cause?

A

Abnormal detachment of lung tiss from primitive airway buds. Connected to bronchial tree by defective airway - blood from pulmonary circulation
Insult ~4-12 wks of preg.
Poor mucus clearance -> infections.
May need to be removed - easy due to low pressure circ.

155
Q

What are sequestrations in terms of lung development?

A

Insult in 1st trimester -> ectopic lung tissue w/ systemic blood supply (high pressure)
Non functional
Clinically similar to cysts, but difficult to remove.

156
Q

What population is at high risk for infant RDS?

A

High: Born 26-30 wks, Low birth weight

more frequent: diabetic mothers, asphyxia to infant, mother w/ bleeding

157
Q

What occurs in RDS?

A

Infant born w/ insufficient surfactant. Fibrinogen containing materials deposit on alveolar walls -> fibrosis
Low compliance, atelectasis, increased WOB
Hypoxemia
Respiratory acidosis
Pulmonary HTN
Capillary endothelial damage - leak
Epithelial necrosis

158
Q

3 complications of RDS

A
  1. Oxidative damage: a) lung injury due to high FIO2 b) retrolental fibroplasia (blindness - prevent w/ vit E)
  2. Barotrauma
  3. Chronic lung disease (fibrosis, pulmonary HTN)
159
Q

What is retrolental fibroplasias? How is it prevented?

A

Seen in infants w/ RDS who are treated w/ oxygen.
Oxidative damage to developing vasculature of retina can -> blindness

Vitamin E prevents.

160
Q

How is RDS prevented?

A
  1. Prenatal care

2. Corticosteroids at least 24 hrs before delivery accelerates lung maturation

161
Q

What is seen on autopsy of SIDS infant?

A

signs of chronic asphyxia

subtle brain stem lesions

162
Q

3 SIDS theories

A
  1. poorly developed / abnormal brainstem respiratory controls -> decreased chemoreceptor response to CO2
  2. poor control and decreased receptor input from upper airway leads to apnea
  3. problems w/ sleep arousal
163
Q

Genetic factors in SIDS

A

Not strongly familial

Type B blood

164
Q

Peak age for SIDS?

A

2-4 mos

rare after 6 mos

165
Q

3 immotile cilia syndromes

A

Type I: Kartagener’s - lack of dynein arms
Type II: defect in radial spokes
Type III: transposition of A and B outer tubules

166
Q

Clinical manifestations of Immotile Cilia Syndromes

A
  • Recurrent infections of upper and lower airways.
  • -sinusitis, nasal polyps, otitis media, bronchitis, bronchiectasis, pneumonia
  • Kartageners: situs inversus and dextrocardia
  • Immotile sperm
167
Q

What organs are affected by Cystic Fibrosis?

A

Primary: lungs, sinuses, pancreas
Other: Sweat glands, intestines, liver, male GU tract

168
Q

What pattern of inheritance is cystic fibrosis?

A

Autosomal Recessive

169
Q

What chromosome carries CF gene?

A

7

170
Q

What is the main mutation seen in CF?

A

delta F508
Loss of 3 nucleotides and a phenylalanine

1800 others!

171
Q

What is the relative incidence of CF by race?

A

White > Hispanic > Native Am > AA > Asian

172
Q

What is estimated median survival in CF (2010)

A

38.3 yrs

173
Q

What is CFTR?

A

cAMP dependent Cl- channel found in epithelial tissue of lung, pancreas, gall bladder, salivary and sweat glands, epididymis, etc.

174
Q

What abnormalities can result from CFTR mutation?

A 
Quantity
Processing
Trafficking
Function
Rate of Turnover
175
Q

Class I CFTR mutation

A

CFTR is not produced due to a DNA defect- premature stop codon

176
Q

Class II CFTR mutation

A

Defective processing and trafficking
seen w/ delta-F508
mutation -> improper folding -> abnormal interaction w/ chaperone proteins -> degradation in ER

177
Q

Class III CFTR mutation

A

Defective cAMP Regulation -> defective Cl- transport

178
Q

Class IV CFTR mutation

A

defective conductive pathway of CFTR

179
Q

Class V mutation of CFTR

A

Abnormally spliced CFTR -> partial or complete reduction

180
Q

Class VI CFTR mutation

A

Accelerated turnover at apical membrane

181
Q

3 transport systems in apical airway epithelium

A

ENAC - controls transepithelial Na and volume absorption
CFTR - tonic Cl- conductance regulates other channels
CaCC - Ca++ activated Cl- channel responds to acute stimuli

182
Q

What is the lumen potential in CF?

A

More negative due to impermeability of epithelium to Cl- and excessive Na+ transport

basis of nasal potential difference test (diagnostic)

183
Q

What genotype of CF is associated with mild lung disease?

A

A455E

184
Q

What antibiotics are used prophylactically for CF?

A

TOBRI, colistin, aztreonam

185
Q

What drugs are used in CF patients to help with mucus?

A

Dornase Alpha
Hypertonic Saline

change viscosity of mucus

186
Q

What is azythromycin used for in CF?

A

Improves lung functions and decreases exacerbations. Not used as antibiotic in usual sense.
Anti-inflammatory?
PSA biofilm?

187
Q

What is the peak age range for nasal polyposis in CF?

A

5-19 w/ high recurrence rate after surgery (58-89%)

188
Q

What process leads to diabetes in CF?

A

Pancreatic duct occlusion -> self-digestion of pancreas and destruction of endocrine pancreatic cells -> diabetes

189
Q

What GI complaints typically accompany CF?

A
  1. Meconium ileus in newborns
  2. Stool fat loss (>7%)
  3. Steatorrhea
  4. Gastritis, Esophagitis, reflux (low bicarb)
  5. Malabsorption of fat sol. vitamins (A,D,E, K)
190
Q

What are 3 therapies for CF related GI disease?

A 
Pancreatic enzyme replacement therapy (Lipase 500-2500 w/ meals, 1/2 dose w/ snacks)
Gastric acid suppression (helps w/ enzyme function)
Osmotic agents (for DIOS (Distal Intestinal Obstruction Syndrome)
191
Q

What is the application of Ursodeoxycholic acid in CF?

A

Treatment of billiary cirrhosis - destruction of small bile ducts of liver -> cholestasis

192
Q

What is the incidence of Diabetes in CF?

A

24% at 20 yoa

76% at 30 yoa

193
Q

What is the sweat test in CF?

A

Pilocarpine ionophoresis - tests salt content of sweat
>= 60mmol/L is abnormal
Infants 6mos: 40-59 intermediate <40 normal

194
Q

Criteria for CF diagnosis:

A

2 known mutations OR

1) 2 sweat Cl- tests >60 and one of: a) fam. hx b) +newborn scrn c) typical symptoms/findings
2) intermediate sweat Cl- due to CF, non-classic CF, CF related disorder - nasal potential dif. may help

195
Q

What is cigarette “tar” and what does it contain?

A 
Residue of cigarette smoke minus nicotine and water
Contains many carcinogens:
-aromatic hydrocarbons
-radioactive elements (nickel)
-free radicals
196
Q

In addition to lung cancer, what others are smoking associated?

A 
laryngeal
oral
esophageal
pancreas
bladder 
cervical
197
Q

How does radon cause cancer?

A

radioactivity: alpha particles

198
Q

What are the 2 leading causes of lung cancer?

A

smoking

radon

199
Q

Where does small cell lung cancer originate?

A

Centrally

200
Q

What is the doubling time for small cell lung cancer?

A

Fast! 30 days

201
Q

Where does small cell lung cancer spread?

A

Bone Brain Liver

202
Q

How does small cell lung cancer react to therapy?

A

Very good initial response, but doesn’t last

High rate of recurrence

203
Q

What % of lung cancers does small cell comprise?

A

20%

204
Q

What is the origin of squamous cell lung cancer? where is it found?

A

From endobronchial tissue

Central tissue - large

205
Q

What lung cancer is least likely to metastasize?

A

Squamous

206
Q

What is the growth rate of squamous cell lung cancer?

A

Medium

Doubling rate: 100days

207
Q

What lung cancers have a tendency to cavitate?

A

Squamous cell

208
Q

Where does squamous lung cancer generally metastasize?

A

Hilum

Least distant spread

209
Q

How does squamous lung cancer respond to therapy?

A

Poorly

210
Q

Where is adenocarcinoma located in the lung?

A

Peripherally

211
Q

What is the growth rate of adenocarcinoma of the lung?

A

Medium - slow

Doubling rate 100-180 days

212
Q

Where does adenocarcinoma of the lung tend to metastasize?

A

Pleura
Chest wall
distant

Squamous <small

213
Q

In what population is bronchioalveolar cancer usually found?

A

Elderly

Can occur in non-smokers

214
Q

What is a common misdiagnosis of BACA?

A

Pneumonia

Failure of infiltrate to resolve w/ chemo may be clue to diagnosis

215
Q

What is the appearance of Large Cell Lung Cancer?

A

Large, highly undifferentiated cells.

Large mass w/ necrosis and hemmorhage

216
Q

Which of the non-small cell lung cancers has the worst prognosis?

A

Large cell

217
Q

How must a suspected large cell tumor be biopsied?

A

Several samples from different locations taken - look for more differentiated cells
Diagnosis of exclusion

218
Q

What is a concern with a COPD patient who experiences sudden weight loss?

A

Cancer

219
Q

How might a tumor cause elevation of the diaphragm?

A

Impingement on phrenic nerve

220
Q

What is Pancoast Syndrome?

A

Apical lung tumor grows, invades chest wall, destroys bone.
Involves C8, T1, T2 of brachial plexus and cervical sympathetic plexus-> shoulder and back pain, weakness and atrophy of arm, ipsilateral horner syndrome

221
Q

What is superior vena cava syndrome?

A

Tumor compresses/ invades SVC -> obstruction
Edema and venous dilation of face, neck, arms
Headache and dizziness
-Medical emergency. Radiation to shrink tumor.

222
Q

What lung cancer cells are most associated w/ endocrinopathies?What are examples?

A 
Small cell (Oat cell)
ACTH, MSH, ADH
insulin, gonadotropins
223
Q

What cancer type is know for producing PTH?

A

Squamous cell carcinoma

-> hypercalcemia

224
Q

What tumor type is most associated with neuromuscular paraneoplastic issues?

A

Oat cell

225
Q

What is Myasthenic syndrome and what is it associated with?

A

Lambert-Eaton
Associated w/ small cell lung cancer
Autoantibodies (elicited by tumor ion channels) directed toward neuronal Ca++ channel
Proximal muscle weakness - no improvement w/ anticholinesterase - enhanced transmission w/ frequent stim (opposite myasthenia gravis)

226
Q

What is hypertrophic pulmonary osteoarthropathy?

A

connective tissue disease seen w/ some lung cancers
-> clubbing of fingers
Smoker w/ finger clubbing - look for tumor

227
Q

How is lung cancer diagnosed?

A

Sputum cytology - usually only squamous (difficult to collect, false + and -)
Bronchoscopy or transthoracic needle aspiration (ct guided), depending on tumor location
Thoracotomy
Pleural tap and biopsy
Tissue or fluid from metastatic site

228
Q

Is radiation therapy curative?

A

No
Local control - external beam or endobronchial
Palliation

229
Q

Is chemotherapy curative?

A

Only in small cell, otherwise no

Controls distant disease

230
Q

What is major criteria in evaluating operability of lung cancer?

A

Will patient tolerate resection and have adequate pulmonary function post-op?
PFT’s, ABG, V/Q testing

231
Q

At diagnosis of lung cancer, what % is considered resectable?

A

30%

232
Q

What is overal 5 year survival for lung cancer and w/ surgery?

A

Overall 5-year survival: 13%

W/ surgery 30%

233
Q

What is the most common histotype of lung cancer?

A

Adenocarcinoma (32-37%)

followed by Squamous (28-30%)

234
Q

What lung cancer is most likely to occur in a non-smoker?

A

Adenocarcinoma

followed by Large Cell

235
Q

What two cancers are most closely associated with smoking?

A

Squamous and Small cell

Risk persists after cessation

236
Q

Small cell and Squamous cell lung cancers arise from what cell types?

A

Respiratory mucosa of main or lobar bronchi (bronchial stem cells)

237
Q

Adenocarcinoma most often arises from what cell types?

A

bronchioles and terminal alveolar units - Clara cells and type II alveolar cells

238
Q

What is BACA?

A

Bronchioalveolar lung cancer

Slow growing adenocarcinoma

239
Q

What mutations are frequently associated with Small Cell lung Cancer?

A

increased p53, Cyclin D1 and E, EGFR, telomerase activation
Chromosomal losses at 3p, 9q, 5q w/ loss of CDKi p15 and p16

Increasing genetic abnormalities parallel morphological change

240
Q

What is the pathogenesis of Adenocarcinoma?

A

Normal terminal bronchioles / alveoli -> atypical adenomatous hyperplasia -> adenocarcinoma CIS -> invasive adenocarcinoma

241
Q

What occurs in atypical adenomatous hyperplasia?

A

An increase in number and grade (N/C ratio, hyperchromasia) of alveolar lining pneumocytes
Parallel thickening of alveolar septa due to fibrosis

242
Q

What are the size definitions of AAH, AIS, and Aca?

A

AAH: < or = 5mm
AIS: 5mm-3 cm
Aca: 3cm - becomes more aggressive w/ size increases

243
Q

What mutations are seen in Aca in smokers and non-smokers

A

smokers: K-Ras

non-smokers: EGFR

244
Q

What cancer type is most likely to have EGFR mutations, what is the frequency of mutation and what happens with the mutation?

A

Adenocarcinoma, esp. non-smokers
20% of all Aca
Mutation in TK domain -> increased activity, increased cell proliferation and increased sensitivity to TK inhibitors

245
Q

In what type of pattern does squamous cell lung cancer grow?

A

Nests w/ undifferentiated basal cells at the periphery w/ cells becoming more differentiated toward the center.
Center of accumulating squames mixed w/ apoptotic cells and necrotic debris.
Most likely to cavitate.

246
Q

What secretory products are often made by Aca cells?

A

Mucins

products normally made by Type II or Clara cells

247
Q

Describe the typical appearance of LC carcinoma cells

A

Large, undifferentiated, non-squamous, non-glandular
Cells have large nuclei, prominent nucleoli, moderate cytoplasm.
Grow in solid discohesive sheets w/ prominent cell borders.

248
Q

How is large cell lung cancer diagnosed?

A

Diagnosis of exclusion

Thorough sampling - multiple samples from tumor to look for differentiation.

249
Q

What are the major lung cancer types showing neuroendocrine differentiation?

A

Large Cell Neuroendocrine Carcinoma
Small Cell
Typical Carcinoid
Atypical Carcinoid

250
Q

What is crush artifact?

A

Seen in small cell lung cancer

Artifact of preparation - long smears of DNA

251
Q

Describe a Typical Carcinoid tumor

A

Nested pattern, no necrosis, at least 0.5 cm
Neuroendocrine features
Low proliferative rate (<2 mitoses / 2mm^2)

Cells: low N/C ratio, salt and pepper chromatin, absent or small nucleoli

252
Q

Are carcinoid tumors assoc. w/ smoking?

A

No association w/ smoking

253
Q

What is the prognosis of typical carcinoid lung cancer?

A

Excellent - 95% survival at 5 years.

254
Q

What syndrome may carcinoid lung cancer appear with?

A

Multiple Endocrine Neoplasia 1 (MEN1)

255
Q

What are Synaptophysis and Chromogranin?

A

neuroendocrine markers that may be used to ID neuroendocrine tumors via immunochemistry.

256
Q

What is atypical carcinoid?

A

Carcinoid tumor exhibiting either elevated mitotic rate or necrosis

More aggressive, lymph node metastases common, worse prognosis (60-70% at 5 yrs, 35-59% at 10 yrs)

257
Q

What is a suspected atypical carcinoid tumor exhibiting >10 mitoses / 10 hpf (2mm^2)?

A

Considered Small Cell carcinoma at that point.

258
Q

What mechanisms prevent fluid accumulation in the pleural space?

A

1) starling forces favor resorption
2) active solute coupled fluid pumps in mesothelium
3) lymphatic drainage has large reserve

259
Q

What is the normal volume of pleural fluid?

A

0.2-0.2 ml/kg

260
Q

Indications for pleural biopsy and 2 types.

A

Exudate effusion of unknown etiology or suspected TB or malignancy.

1) Closed: by pulmonologists. Rarely done. Useful for TB
2) Open: by thoracic surgeion. Definitive diagnosis. Malignancy.

261
Q

Criteria for transudative vs. exudative effusion

A

Exudate:
Pleural fluid protein : Serum protein >0.5
or
Pleural fluid LDH : Serum LDH >0.6
or
Pleural fluid LDH > 2/3 upper limit for normal for serum

All others are Transudate

262
Q

Major causes of transudative effusion

A

CHF
Nephrosis
Cirrhosis
Peritoneal dialysis

(systemic factors)

263
Q

3 homeostatic sleep mechanisms

A

a) sleep need accumulates w/ wakefulness
b) sleep need can only be met by sleeping
c) more sleep = less need to sleep

264
Q

3 Stages of sleep

A

N1: perceive that you are still awake. Transition from wake - sleep
N2: true sleep. thoughts are short, fragmented.
N3: slow wave sleep - little or no mentation.

265
Q

3 categories of insomnia

A

Transient: adjustment sleep disorder. <1wk. precipitated by anxiety/ emotion
Short-Term: up to several weeks. temporary stressful events or inability to adjust sleep-wake cycle to new needs
Chronic: months - years. many causes.

266
Q

4 causes of chronic insomnia

A
  1. Sleep related disorders: sleep hygiene, disruptive or irregular sleep-wake cycle, obstructive sleep apnea, RLS
  2. Medication / drug related: extended use of sleep meds or others that interfere w/ sleep. ETOH and drugs of abuse.
  3. Medical disorders: chronic pain, GERD, asthma
  4. Psych: esp. mood and anxiety
267
Q

2 categories of symptoms of insomnia

A

Night-time complaints

Day-time complaints (required for insomnia to be a disorder rather than a complaint)

268
Q

What is the hyperarousal theory of insomnia?

A

Insomniacs have generalized hyperarousability.

  • higher rates of depression and anxiety than gen. pop.
  • score higher on scales of arousal
  • more night-night variability in sleep
  • more beta EEG (memory processing - task performance) at sleep onset
269
Q

What is cognitive theory of insomnia?

A

Patients prone to rumination
increased problem solving -> insomnia
w/ chronic insomnia, worry about sleep all day

270
Q

What is the behavioral theory of insomnia?

A

Stimulus control model: normal cues assoc w/ sleep become assoc w/ wakefulness
Predisposing factors for chronic insomnia
Insomnia begins w/ precipitating factor
Chronicity w/ onset of perpetuating factors and conditioned arousals. TARGET OF BEHAVIORAL THERAPY

271
Q

What is psychophysiologic insomnia?

A

Most common primary insomnia
Disorder of somatized tension and learned sleep preventing associations
-sleepy until bedtime routine
-racing thoughts
-tries to force self to sleep
-sleeps better on couch or away from home

272
Q

What is the difference between physiologic sleep tendency and manifest sleep tendency?

A

Physiologic: tendency toward sleep in absence of alerting factors
Manifest: changes moment to moment depending on host factors - light, noise, motivation, recumbency.
–reduction in impinging stimuli unmasks physiological sleep tendency, not cause it

273
Q

What are 2 tests used for diagnosis of excessive daytime sleepiness?

A
  1. Multiple Sleep Latency Test: Objective. measures tendency to fall asleep at 4 times throughout the day. Normal sleep latency is >15min in adults.
  2. Epworth Sleepiness Scale: questionairre - Subjective. Asks about liklihood to fall asleep in 8 situations
    Score < or = 10 is normal
274
Q

What is the apneic threshold?

A

pCO2 below which a subject becomes apneic during NREM sleep
apnea: higher threshold
Men higher than women

275
Q

What happens to the normal ventilatory pattern during sleep?

A

N1: can be irregular, periodic
N2 and 3: regular
R: irreg. w/ REM
Overall: decrease in TV and minute ventilation. No change in freq. decreased metabolism. increased PaCO2

276
Q

What is the difference between apnea and hypopnea?

A

Apnea: complete cessation of airflow for 10 sec.
Hypopnea: 20-50% reduction in airflow assoc. w/ arousal or 2-4% decrease in O2 sat.

277
Q

Apnea-hypopnea index

A

(# of apneas + hypopneas)/ total sleep time = AHI

30: severe

278
Q

What is OSAS?

A

Obstructive sleep apnea syndrome

Obstructive sleep apnea with daytime sequelae

2% of women and 4% men age 30-60

279
Q

what cardiovascular risks is OSA associated with?

A

Hypertension
Heart disease (LVH and diastolic dysfunction)
Metabolic syndrome (esp. insulin resistance)
Cerebrovascular disease

Pulmonary HTN and Right-sided HF uncommon w/o lung disease and/or daytime hypoxia

280
Q

What polymorphisms is narcolepsy associated with?

A

HLA-DQB1*0602

loss of hypocretin neurons in hypothalamus - control/coordinate other wake centers

281
Q

How are the symptoms of narcolepsy treated?

A

EDS: stimulants
cataplexy: TCAs or SSRIs
Behavioral: avoidance of triggers, short scheduled naps, maximize sleep hygiene

282
Q

What is pharmacologic management of Restless Leg Syndrome?

A

Dopamine Agonists: ropirinole, pramipexole, levodopa
Opiates: oxycodone, propoxyphene
Anticonvulsants: gabapentin, enacarbil

283
Q

How is nicotine metabolized?

A

10-20% unchanged in urine
70-80% metabolized to cotine (inactive)
10% to other metabilites

284
Q

What are the half-lives of nicotine and cotine?

A

Nicotine: 2 hrs
Cotine: 16 hrs

285
Q

How is nicotine/cotine excreted?

A

Mostly renally

Also in breast milk

286
Q

What are the effects of nicotine?

A

Stimulatory: CNS, CV, appetite suppression, increased metabolic rate.

Stim DA reward pathway

287
Q

What is the timeline of nicotine withdrawal?

A

Onset of withdrawal symptoms: 1-2 days
Peak: 1st week
Subside: 2-4 weeks

288
Q

5 A’s of smoking intervention

A 
Ask about use
Advise to quit
Assess readiness to quit
Assist w/ quit attempt
Arrange follow-up care
289
Q

5 stages of readiness to quit smoking

A
  1. precontemplation: not ready to quit in next 6 mos
  2. contemplation: considering quitting in next 6 mos, but not next 30 days (5 Rs: Relavence, Risk, Reward, Roadblocks, Repetition)
  3. preparation: considering quitting in the next 30 days
  4. action: have quit w/in last 6 mos. Goal: 6 mos smoke-free
  5. maintenance: quit > 6 mos. ago. still vulnerable to relapse. Goal: smoke-free for life
290
Q

Points to discuss in preparation stage of smoking cessation

A

Praise decision to quit
Use history and previous quit attempts
Reasons, Confidence in ability to quit, Triggers
Concerns: weight gain, withdrawal

291
Q

2 coping strategies to employ in smoking cessation

A

Cognitive: retrain way of thought
Behavioral: involve specific actions to reduce relapse risk

292
Q

When should a physician follow up with a patient who has decided to quit smoking?

A

1: after first week
2: after first month
3: as needed afterward

293
Q

non pharmacologic methods to assist w/ smoking cessation

A 
cold-turkey
fading:  reduced nicotine cigs, tapered use, special filters / holders
quit key
formal programs
accupuncture, hypno, massage
294
Q

Who should not use nicotine replacement therapy?

A

Underlying CV disease (arrhythmia, recent MI, severe/worsening angina) or pregnant/lactating
TMJ: shouldn’t use gum

295
Q

Dosing for NRT gum and lozenges

A

2mg: if you smoke 1st cig more than 30 mins after waking
4mg: if you smoke 1st cig w/in 30 mins of waking
Week 1-6: 1 piece q1-2h
Week 7-9: 1 piece q2-4h
Week 10-12: 1 piece q4-8h

Max: 24/day (gum) 20/day (lozenge)

296
Q

What strength Nic patches are available?

A

7,14,21 mg

297
Q

How are patches dosed for heavy smokers (generic vs. nicoderm)?

A

Generic step 1: 21mg / day X 4 wks

Nicoderm step 1: 21mg / day X 6 wks

298
Q

What is the standard nic patch dose schedule?

A

Step 1 (heavy smokers) 21 mg x 4-6 wks
Step 2 light smoker: 14mg x 6 wks
heavy smoker: 14mg x 2wks
Step 3: 7mg x 2 weeks

299
Q

When using a nic patch, how long should pass between reapplying a patch to a given location?

A

1 week

300
Q

What is the recommendation for nic patch users in the case of vivid dreams?

A

try 16 hour application rather than 24

301
Q

What is dosing for nicotine nasal spray?

A

0.5mg nicotine / 50mcL spray ( 1 dose = 2 sprays)

start: 1-2 dose/ hr, increase prn to max 5doses / hr.
1st 6-8 weeks: recommend at least 8 doses / day
Gradually taper over next 4-6 weeks

302
Q

What is dosing for a nicotine inhaler?

A

4mg nicotine vapor / cartridge
Start: 6 cartridges/day, increase prn to max of 16/day
Gradual dosage reduction over 3-12 weeks. Extend if needed.

303
Q

What antidepressant may be used as adjunct therapy in smoking cessation?

A

Bupropion SR
DA/NE reuptake inhibitor
Decreases nic craving / withdrawal symptoms

304
Q

Bupropion dosing for smoking cessation

A

Start 1-2 weeks prior to quit date

150 mg qAM / 3days then 150 bid for 7-12 weeks

305
Q

What is varenicline?

A

Partial nicotinic receptor agonist (low-level activity) - competitively inhibits binding of nicotine.

  • reduces withdrawal symptoms
  • blocks DA stim. responsible for reinforcement / reward
306
Q

How is Varenicline dosed?

A

start 1 week prior to quit date
day 1-3: 0.5mg qd
day 4-7: 0.5mg bid
weeks 2-12: 1mg bid

307
Q

what are the 2 most effective smoking cessation aids?

A

Nicotine inhaler

Varenicline

308
Q

Can Varenicline be used w/ a NRT or bupropion?

A

Safety not established

309
Q

For maximum success, what should smoking intervention consist of?

A

Counseling + one or more meds

310
Q

Cues to expect ILD

A

Pt. w/ cough, dyspnea
Abn CXR - diffuse, not necessarily uniform, changes
Crackles on PE - cellophane or velcro

311
Q

What exposures can result in ILD?

A

Pneumoconiosis: inorganic - silicosis, asbestosis
Toxins - oxides of nitrogen
Drugs - Amiodarone, bleomycin
Radiation
Oxygen
Hypersensitivity (farmer’s lung) - organic

312
Q

What ILDs are attributed to unknown causes?

A

make up 2/3 cases
Idiopathic Interstitial Pneumonias / Idiopathic Pulmonary Fibrosis
Sarcoidosis

313
Q

What is Idiopathic Interstitial Pneumonia? What is the most important diagnosis tool?

A

Includes: Interstitial Pulmonary Fibrosis (IPF) and Nonspecific Interstitial Pneumonia (NSIP)
Radiologic criteria most important for diagnosis
Consists of 7 entities differentiated by clinical, radiologic, and pathologic criteria

314
Q

7 classifications of IIP

A

UIP: usual interstitial pneumonia
DIP: desquamative interstitial pneumonia
RB: respiratory bronchiolitis
DAD: diffuse alveolar damage
OP: organizing pneumonia
NSIP: non-specific interstitial pneumonia (cellular and fibrotic)
LIP: lymphoid interstitial pneumonia (smoking related, corticosteroid responsive)

315
Q

What is the most common IIP?

A

Idiopathic Pulmonary Fibrosis (IPF) - 60% of IIP cases
Chronic, Progressive, Fatal
corresponds to UIP histologic pattern

316
Q

What is the usual age of onset of IPF?

A

40-70 years w/ 2/3 >60

male > female

317
Q

Risk factors for IIP

A

Familial
Smoking
possibly: exposure (wood/metal dust), GERD, infection

318
Q

Is familial IPF AR or AD? What gene(s) are involved?

A

AD
variable penetrance
ELMOD2 on 4q31

319
Q

What mutations have been identified in IPF?

A

seen in 10% of cases
pulmonary surfactant protein C
TERT -telomerase reverse transcriptase
TERC -telomerase RNA component

320
Q

What are IPFs clinical features?

A

progressive dyspnea w/ exertion, tachypnea
paroxysmal cough
clubbing (25-50%)
fine bibasilar crackles
abnormal CXR or HRCT
**restrictive pulmonary physiology, reduced DLCO, wide A-a O2

321
Q

Diagnostic criteria for IPF

A

Variation w/in lung - “temporal heterogeneity”
Subpleural distribution
Fibrosis
Honeycombing
Fibroblastic foci
absence of features of alternative diagnosis

322
Q

How does NSIP differ from IPF?

A

More uniform distribution
“ground glass” opacities
cellular and fibrotic types
better prognosis (cellular > fibrotic) - more responsive to corticosteroids

323
Q

What is the treatment for IPF?

A

None.

Cortiticosteroids - don’t work - evidence against underlying inflammatory cause

324
Q

What is the survival rate for patients w/ IPF?

A

Median survival: 3 yrs from diagnosis
5 yr survival: 20-40%

Poor prognosis

325
Q

In what populations is sarcoidosis most frequent?

A

Swedes, Danes, Blacks

326
Q

Pathophys of sarcoidosis

A

Stimulus in susceptible host
Accumulation of CD4 cells and macrophages at site of ongoing inflammation
IFN-g, IL-2, other cytokines

327
Q

Is sarcoidosis restrictive or obstructive?

A

Restrictive +/- obstructive component

328
Q

What are sites of disease in sarcoidosis?

A

Lung: restrictive +/- obstructive, abnormal diffusion,
Lymph nodes: enlarged (hilar, mediastinal, peripheral)
Skin: papules, macules, pigment change
Heart: conduction defect, sudden death
GI: liver very common, spleen
Eyes: common - uveitis can -> glaucoma / blindness
Nervous system - base of skull, facial palsies, pituitary lesions, space occupying masses

329
Q

What is the prognosis of sarcoidosis?

A

spontaneous remission in 60%
chronic/ progressive 10-30%
death in 1-5% - respiratory failure

330
Q

Treatment for sarcoidosis?

A

corticosteroids

331
Q

In what ILD are bronchoscopic biopsies most useful?

A

sarcoidosis

332
Q

Desquamated Interstitial Pneumonitis

A

Rare
strong link to smoking
good prognosis: 90-100% survival - responds to steroids
Lots of alveolar macrophages, lymphocytes, mild fibrosis

333
Q

What is BOOP?

A

Bronchiolitis Obliterans-Organizing Pneumonia
Associated w/ Hypersensitivity Pneumonitis
Granulation tissue plugs in bronchi and/or alveoli

334
Q

What type of hypersensitivity is involved in Hypersensitivity Pneumonitis?

A

Combination of type III and IV

335
Q

What is Histiocytosis X?

A

Involves proliferation and tissue infiltration by Langerhaan’s cells

336
Q

Types of Histiocytosis X

A

Unifocal - lung or bone

  • Eosinophilic granuloma of lung (most common 60-80%)
  • -children and young adults
  • -lung only
  • -best prognosis

Multifocal

  • Hand-Schuller-Christian disease
  • -1-3 yoa: lung, bone - may be systemic
  • Letterer-Siwe
  • -0-1: worst prognosis (70% mortality)
337
Q

What is Virchow’s Triad?

A

Risk factors for DVT
Stasis
Endothelial Injury
Hyper-coagulable state

338
Q

Initial patient evaluation for suspected PE

A

CXR: rule out pneumothorax, pneumonia, other
ECG: rule out acute MI or pericardial effusion
ABG: non-specific, but often present w/ PaO2 <80
-absence of hypoxia strike against PE

339
Q

How is d-dimer useful in evaluation for possible PE?

A

Product of fibrinolysis - always present when there is a clot.
Not diagnostic
Neg test - PE highly unlikely.
Pos test - further testing

340
Q

What is the current tool of choice for diagnosis of PE?

A

Spiral CT angiography
High specificity (72%) and sensitivity (95%)
Positive: treat
poor for sub-segmental emboli
requires cooperation and 15-25 sec breath hold
more radiation than V/Q scan
requires IV contrast

341
Q

3 types of heparin

A

Unfractionated (UFH)
Low Molecular Weight
Fondaparinux

342
Q

Where does heparin work?

A

Factors IXa, Xa, IIa (thrombin) via antithrombin III

343
Q

What did PIOPED I suggest as the first diagnostic test for suspected PE?

A

ventilation - perfusion lung scan

344
Q

What is the gold standard for PE diagnosis?

A

Pulmonary angiogram - will shoe intravascular filling defect in area of clot
Risks - hypotension, arrhythmia, arterial rupture, dye reaction

345
Q

How is a V/Q scan performed?

A

Nuclear markers introduced to chest and scans done for perfusion and ventilation
Negative: virtually excludes PE
High Probabillity: V/Q mismatch - PE very likely
Most results are indeterminate

346
Q

How does heparin induced thrombocytopenia occur?

A

Heparin binds PF-4. Complex recognized by Ab -> platelet activation and thrombosis

347
Q

How is HIT managed?

A

Immediate stop of heparin
Anticoagulation: direct thrombin inhibitors: Agatroban
Fondaparinux: heparin like activity - binds AT-III

348
Q

What coagulation factors are affected by Vitamin K antagonists?

A

Coumadin, Warfarin work at factors II, VII, IX and X

349
Q

3 characteristics of normal pulmonary circulation

A

Low pressure
Low resistance
High capacitance

350
Q

Physical exam findings in case of pulmonary HTN

A 
Loud S2 (P2) heart sound 
With worsening disease:  edema of lower extremities, ascites, hepatomegaly, pulsating liver, JVD, right ventricular heave
351
Q

5 groupings of pulmonary HTN

A

I: PAH: vasculopathy of PA - treat w/ dilators
II: PVH - pulmonary venous hypertension - due to L. heart disease
III: Hypoxemia related
IV: Chronic thromboembolic disease
V: Miscellaneous

352
Q

What mediators are imbalanced in type I pulmonary hypertension?

A

Type I: PAH
Increased: Thromboxin A2 (vasoconstrictor, mitogen) and Endothelin (vasoconstrictor and mitogen)
Decreased: Prostacyclin (vasodilator, antiproliferative, anti-platelet activation) and NO synth (vasodilator, antiproliferative)

353
Q

What is the theme of therapy for type I pulmonary hypertension?

A

Inhibit endothelin, promote NO synthesis, replace prostacyclin

354
Q

What test is needed for a diagnosis of pulmonary hypertension? Diagnostic findings?

A

Right heart cath- gold standard for diagnosis
PH: mean PA pressure: >=25mmHg, w/ exercise: >=30 mmHg, systolic: >=40 mmHg
PAH: mean PA pressure: >=25 ,30 w/ exercise, PCWP =3mmHgxmin/L

355
Q

Once diagnosed w/ group I pulmonary hypertension, what needs to be ruled out?

A

autoimmune, CT, collagen vascular disease, ILD, HIV, portal HTN, OSA, R->L shunt due to ASD or VSD.

356
Q

Therapeutic approach to pulmonary hypertension

A

Treat underlying condition
general treatment beneficial to most:
supplemental O2 (keep O2 sat >90), diuretic, inotropic therapy (digoxin)

357
Q

4 therapies for group I pulmonary HTN

A

Calcium channel blockers - must pass vasodilator test (only ~5%)
Endothelin agonistss: Bosentan, Ambrisentan: Functional class II and III - vasodilator, antiproliferative
PDE5 inhibitor: Sildenafil, Tadalafil: Functional class II and III - increase duration of cGMP -> increased NO production
Prostacyclin derivatives: Epoprostenol, Treprostinil, Iloprost: pulmonary vasodilator, anti-proliferative - class III and IV
NO (acute)
Anticoag -

358
Q

How are class II, III, and IV symptomologies of pulmonary HTN treated?

A

II: CaCB - if no help add PDE5i or ERA(oral)
III: ERA and/or PDE5i + sq or inhaled prostacyclin analog
IV: IV or sq prostacyclin analog. If needed add ERA / PDE5i - if not already using

359
Q

What anticoagulant is monitored w/ PTT?

A

Unfractionated Heparin

360
Q

How are UFH and LMWH excreted?

A

Renally
LMWH much moreso than UFH
LMWH must be adjusted for renal function

361
Q

Can warfarin be used during pregnancy?

A

No - vit K
-> bone growth issues
Use LMWH instead for anticoag

362
Q

What is the most common clinical presentation of patients w/ HIT?

A

thrombocytopenia

363
Q

Mortality rate of HIT

A

5-10%

364
Q

Treatment principles when HIT is suspected

A
  1. stop heparin
  2. give non-heparin alternative
  3. postpone warfarin pending platelet count (give vit K if warfarin already being taken)
  4. test for HIT Ab
  5. investigate for LL DVT
  6. avoid prophylactic platelet infusion
365
Q

What is the target of warfarin? Effect?

A

Vitamin K Epoxide Reductase (VKOR)
Prevention of reduction of Vitamin K epoxide -> no gamma carboxylation of factors II, VII, IX, X

Also inhibits carboxylation of C and S -> procoagulant activity

366
Q

How long does it take for warfarin to have therapeutic effect?

A

~5 days needed for depletion of clotting factors

367
Q

What polymorphisms affect warfarin activity?

A

polymorphisms of CYP2C9
CYP2C92 and CYP2C93 -> decreased metabolism -> increased S warfarin half life

VKOR polymorphisms -> usually increased sensitivity

368
Q

What is is the target INR value for warfarin pts?

A

usually 2-3

w/ mechanical mitral valve replacement - 2.5 - 3.5

369
Q

Options for immediate warfarin reversal

A

fresh frozen plasma (must be thawed, heated)

prothrombin complex concentrate - ready to go

370
Q

What is Rivaroxaban?

A

Direct factor Xa inhibitor for reduction of stroke risk and systemic embolism in pts with nonvalvular Afib, treatment of DVT or PE, and VTE prophylaxis (pre-procedural)

371
Q

Silicoproteinosis

A

Acute massive exposure to silica
Progressive and often fatal - rare w/ protective
Lung rxn is outpouring of proteinaceous material
hypoxia, resp. failure, pulm. edema
“ground glass” CXR - esp. upper lung

372
Q

Chronic “simple” silicosis

A

silicotic nodules <1-1.5cm
egg-shell calcifications of hilar lymph nodes
few symptoms, minimal to no changes in PFTs

373
Q

Complicated silicosis

A

Progressive
Simple nodules coalesce -> large densities
restrictive and obstructive characteristics
autoimmune markers may be present

374
Q

Caplan’s syndrome

A

complex silicosis + RA

large nodules, but more benign than typical complex silicosis

375
Q

Effect of silicosis on TB

A

silica poisons macrophages -> 4-6x increased risk

silicotuberculosis: TB in person w/ silicosis

376
Q

2 diseases caused by asbestos exposure

A
  1. asbestos pleural disease: thickening of pleura -> exudative, bloody pleural effusion
  2. asbestosis: interstitial disease - lung bases, “shaggy heart” on cxr. dry cough and crackles. restrictive. -> clubbing, cor pulmonale, respiratory failure
377
Q

Malignant mesothelioma

A

malignant tumor of pleural mesothelial cells
very poor prognosis
usually non-resectable, not very responsive to chemo or radiation

378
Q

When do farmer’s lung symptoms occur related to exposure?

A

4-8 mos later

379
Q

Course of farmer’s lung

A

usually spontaneously resolves w/in 24 hours. Repeat exposures may -> restrictive disease

380
Q

symptoms of farmer’s lung

A

fever, chills, sweating, cough dyspnea ( mirrors acute pneumonia)

crackles on exam
CXR: bilateral reticulonodular infiltrates

381
Q

How can occupational asthma be diagnosed?

A

spirometery before and after work

382
Q

Treatment for occupational asthma?

A

bronchodilators help

removal from exposure is key. Continued exposure may -> COPD

383
Q

Silo Filler’s disease

A

Oxides of nitrogen form over freshly cut hay -> toxic lung injury
Immediate effects or gradually over 18-24 hours depending on exposure.
ARDS type clinical picture / DADS / Bronchial Obliterans
Treat - O2, respiratory support, corticosteroids

384
Q

2 categories of respiratory failure

A

hypoxia w/ hypercarbia: caused by inadequate ventilation (high PaCO2) and oxygenation.
problems: CNS, chest wall, airway
hypoxia predominating: low PaO2, CO2 normal until the end. inability to get O2 through pulmonary system -> tissues
Problems: circulatory, hemoglobin, intrinsic lung disease, ARDS

M2 (19 decks)

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