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Pulm Flashcards

1
Q 
[Anatomy and Embryology]
1. Discuss stages of lung development 
2. Different pneumocyte types
A. Type I
B. Type II
C. Club cells
A

1A. 1st trimester (0-16 wks) - pseudoglandular - branching to terminal bronchioles
B. 2nd trimester (16-24 wks) - canalicular - terminal branch to respiratory brionchioles –> start of respiration
C. 3rd trimester (24-38 wks) - saccular - branching to alveolar sacs and devlpt of pneumocytes –> start of surfactant production
D. (36 wks - birth) - alveolar - septation of sacs and formation of alveoli (continues until age 10)

  1. Different pneumocyte types
    A. Type I - squamous/flat, 97% of alveolar surfaces - participate in gas exchange with capillaries
    B. Type II - secrete surfactant, stem cells for Type 1 pneumocytes
    C. Club cells - found in bronchioles only and secrete substances to protect the epithelium; equivalent to goblet cells in bronchi
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2
Q

[Anatomy and Embryology]

  1. Conducting vs respiratory zones
  2. Role of surfactant and relation to Laplace
A

1A. Conducting zone -
i. nose, pharynx, trachea, bronchi - pseudostratified ciliated columnar cells with smooth muscle and cartilage
ii. small airways (bronchioles, terminal bronchioles) - simple ciliated columnar with smooth muscle, no cartilage
B. Respiratory zone - gas exchange
- respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli - simple squamous (no smooth muscle)

  1. Surfactant - composed of phosphatidylcholine (lecithin); decreases surface tension by pushing water molecules on surface of alveoli apart –> reduces collapsing pressure –> prevents collapse of smaller alveoli with small radii –> increases lung compliance at low lung volumes
    Laplace: Collapsing pressure = 2(surface tension) / radius
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3
Q

[Anatomy and Embryology]
1. Most common sites for aspiration when
A. Upright
B. Supine

  1. Muscles of inspiration vs expiration
    A. Quiet breathing
    B. Exercise
A 
1A. Upright - Right lower lobe, posterior segment
B. Supine - R>L 
i. Right upper lobe, posterior segment
ii. Right lower lobe, apical segment
iii. Left lower lobe, apical segment
  1. A. Quiet breathing
    Inspiration - diaphragm
    Expiration - passive
    B. Exercise
    Inspiration - external intercostals, scalene muscles, sternocleidomastoids
    Expiration - rectus abdominis, internal and external obliques, internal intercostals
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4
Q 
[Anatomy and Embryology]
Diaphragm
1. Innervation 
2. Structures perforating
3. Bifurcations
A
  1. Innervation - C3, 4, 5 keeps the diaphragm alive (phrenic nerve) –> pain can be referred to shoulder
2. Structures perforating - 
I ate 10 eggs at 12
T8 - IVC
T10- esophagus
T12 - aorta
  1. Bifurcations - biFOURcations
    common carotid - C4
    trachea - T4
    abdominal aorta - L4
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5
Q

[Physiology]

Describe effects of alpha vs beta receptor activation

A

Epinephrine binds to Beta2 adrenergic receptor (arterioles and bronchi) –> Gs protein activation –> activates cAMP –> smooth muscle relaxation and vasodilation
cAMP has OPPOSITE effect in the heart - causes contraction (inotropy)

Epi or Norepi bind to alpha1 adrenergic receptor (Arterioles) and M3 cholinergic receptors (bronchi) –> Gq activation –> activates PLC –> IP3-DAG cascade –> increased Ca2+ –> smooth muscle contraction and vasoconstriction

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6
Q

[Physiology]
Describe the mechanics of breathing

What happens at functional residual capacity FRC?

A

PV = nRT

  1. Relative to outside - pressure in alveolus Palv = 0
  2. Inspiration: diaphragm expands –> volume in chest increases –> pressure goes down (Palv = -1 mmHg)
  3. Good air molecules come in from outside –> n and V increase
  4. Expiration: pressure increases –> volume decreases -> pushes bad air out of lung and reduces V and n

FRC - bottom of expiration (lung at rest)
balance between inward pull of lung (positive pressure) and outward pull of chest (negative pressure) –> Transmural pressure = 0, intrapleural pressure is negative

  • when you breathe in –> lung expands –> intrapleural pressure becomes more negative
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7
Q 
[Physiology]
Hemoglobin 
1. Review forms 
A. T vs R
B. fetal vs adult
C. effects of C02, temp, exercise
  1. Modifications
    A. Methemoglobin
    B. Carboxyhemoglobin
A

1A. Taut form in tissues (low 02 affinity), and Relaxed in Respiratory (high 02 affinity)
B. Fetal Hb has alpha and F subunits –> lower 2,3 BPG affinity (shifts curve to the LEFT) –> higher 02 affinity –> diffusion of 02 across placenta to fetus
C. exercise, C02, and temperature also shift curve RIGHT (higher p50) –> lower 02 affinity –> Hb release 02

  1. Modifications - Pa02 normal but Sa02 low
    A. Methemoglobin - oxidized Hb form with Fe3+ that does not bind 02 as readily and shifts dissociation curve LEFT –> appears blue bc not bound to 02
    B. Carboxyhemoglobin - CO binds to Hb with much higher affinity than 02 –> shifts curve LEFT –> decreased 02 binding and unloading –> appear pink bc Hb is fully saturated (just with C0 and not with 02)
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8
Q

[Physiology]
1. How is C02 transported from tissues to lungs

  1. Describe
    A. Bohr effect
    B. Haldane effect
A
  1. C02 transported from tissues into lung in 3 forms:
    A. Bicarbonate (90%) - in RBCs, C02 taken up and converted into H2C03 –> which is exchanged into plasma for Cl- –> chloride shift –> water moves into cell to maintain neutrality –> RBCs swell in venous blood en route to lungs for gas exchange
    B. CarbaminoHb (5%) - HbC02 where C02 is bound to N-terminus, not heme
    C. Dissolved C02 (5%)

2A. Bohr effect - in periphery (tissues) low pH (acidosis) –> H+ and C02 bind to Hb –> reduce affinity for 02 –> 02 dissociation curve shifts RIGHT (easier for Hb to release bound 02)
B. Haldane effect - in lungs, 02 binds to Hb –> decreases affinity for C02 by releasing H+ which combines with HC03- in RBC –> C02 is generated and released into the lung how we maximize C02 carrying in the blood

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9
Q

[Physiology]
1. Gas exchange in Health
A. Diffusion limited
B. Perfusion limited

  1. What factors increase or decrease diffusion?
  2. Gas exchange in disease
A
  1. Gas exchange in Health
    A. Diffusion limited - gas does not equilibrate by the time blood reaches the end of the capillary e.g. CO
    B. Perfusion limited - gas equilibrates early along length of capillary –> lack of driving pressure –> cannot get more into the blood e.g. 02, C02, N20
    - C02 has greater diffusion than 02 bc it is highly soluble

Diffusion = (area * diffusion constant * change in P) / thickness
2A. Increase - due to increase in pressure –> polycythemia (more RBCs), exercise and L–>R shunts (increased pulmonary blood flow / perfusion)
B. Decrease - lung fibrosis (increase thickness), emphysema (decrease area), PE or CHF (decreased blood flow), anemia (fewer RBCs)

  1. Gas exchange in disease - 02 perfusion-limited in lung at sea level BUT becomes diffusion-limited in strenuous exercise and fibrosis, emphysema, etc
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10
Q

[Physiology]
1. What is the A-a gradient? Equation

  1. Describe control of breathing
A
  1. PA02 (alveolar oxygen tension) = 100 mmHg = [(Patm-PH20)xFi02] - PC02/RQ = [(760-47)x0.21] - PC02/0.8
    = 150 - 1.25PC02
    *PaC02=PAC02 (C02 v soluble) ~ alveolar ventilation
    Pa02 (arterial oxygen tension) = 85-90 mmHg
    A-a gradient 20+ due to diffusion limitations (bc 02 is bound to Hb) and shunt blood (Eg bronchial circulation, coronary venous drainage)

2A. Brain: Central chemoreceptors are in the medulla, monitor PC02 (C02 crosses BBB); ↑ CO2 –> ↑ [H+] –> ↑ inspiration –> ventilation matches
- minute to minute control

B. Periphery: Peripheral chemoreceptors in carotid body, monitor severe changes to P02

  • if P02 > 60 mmHg - breathing rate constant
  • if P02 < 60 mmHg - breathing rapidly increases
  • control for extremes
  • Carotid sinus has baroreceptors to monitor P
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11
Q

[Physiology]
1. Response to high altitude
A. Acute
B. Chronic

  1. Response to exercise
A
  1. High altitude
    A. Acute - ↑ ventilation (hyperventilation) –> ↓ P02 (hypoxemia), ↓ PC02 –> Respiratory alkalosis (02 dissociation curve shifts left)
    B. Chronic - ↑ ventilation, ↓ P02, ↓ C02 +
    ↑ erythropoietin (↑ Hb)
    ↑ 2,3 BPG (Hb releases more 02)
    ↑ mitochondria
    ↑ renal excretion of bicarb (use acetazolamide) to compensate for respiratory alkalosis
    hypoxic pulmonary vasoconstriction –> RVH
  2. Response to exercise
    - ↑ C02 production
    - ↑ 02 consumption
    - however, NO change in P02 and PC02, only increase in venous C02 content and decrease in venous 02 content
    - ↑ ventilation to meet 02 demand
    - uniform V/Q ratio throughout the zones (more of lung working)
    - ↑ pulmonary blood flow
    - ↓ pH due to lactic acidosis
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12
Q 
[Pulmonary Disease Symptoms/Signs]
1. Define hypoxemia
A. Define Pa02
B. Sa02
C. Ca02 
D. Hypoxemia with normal vs increased A-a gradient
  1. Hypoxia
  2. Ischemia
A
  1. Hypoxemia - decreased Pa02 (causes decreased Sa02)
    A. Pa02 - partial pressure of 02 in arterial blood (normal= 80-100 mmHg)
    B. Sa02 - arterial 02 saturation –> tissue perfusion (normal = 95%+)
    C. 02 content - how much 02 is in the blood - Ca02 = (.003Pa02) + (1.36Hgb*Sa02)
    *Pa02 helps determine Sa02 (via 02 dissociation curve)
    D. hypoxemia with normal A-a gradient due to high altitude (lower Patm), hypoventilation e.g. opiates (higher PC02)
    - increased A-a due to diffusion limitation, R-L pulmonary or cardiac shunt, or V/Q mismatch
  2. Hypoxic - decreased 02 delivery to tissues
    - due to hypoxemia (↓ Pa02), anemia, CO poisoning, ↓ 02 content, inadequate oxygen delivery due to ↓ cardiac output
  3. Ischemia - loss of blood flow
    - due to impeded arterial flow, reduced venous drainage
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13
Q

[Pulmonary Disease Symptoms/Signs]

  1. Define cyanosis
  2. Peripheral cyanosis
A
  1. Cyanosis - increase in deoxygenated Hb level to above 3.5 g/dL in the capillaries
    - leads to bluish/purple tinge to skin and mucous membranes
    - patients with normal Hb get cyanosis at higher Sa02 (02 sat %) than patients with anemia–> hypoxemia (low Pa02) can occur in absence of cyanosis
    - central cyanosis (lips and tongue) is strong indicator of hypoxemia
  2. Peripheral cyanosis - decreased local circulation + increased 02 extraction in tissues
    - not a central or systemic problem
    - associated with peripheral vasoconstriction, blood stasis in extremities (due to circulatory shock, CHF, cold temp)
    - most intense in nail beds
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14
Q 
[Pulmonary Disease Symptoms/Signs]
Dyspnea 
1. Define
2. Differentiate from tachypnea 
3. Mechanism for perception of dyspnea 
4. Pathophys causes
A
  1. Dyspnea - patient’s perception that they are not getting enough air; subjective SOB
  2. Tachypnea - rapid respiratory rate, greater than 20, with the same tidal volume
    - could be breathing fast but not SOB eg respiratory compensation in acidosis
    - may not be breathing fast but feel dyspneic

3A. Ventilatory requirements processed centrally:
- cortex
- chemoreceptors (pC02) –> hypoxia, hypercapnia, acidosis (↓ CSF pH)
- carotid bodies (p02)
- mechanoreceptors in chest for mechanical load –> airflow obstruction, fibrosis
- vagal sensory fibers in chest for stretch
B. Ventilator command given
C. Corollary discharge - ascending copy of descending motor activity to ventilatory muscles is sent to sensory cortex –> “This is how hard I am breathing”
D. ventilatory muscles also send feedback to the sensory cortex –> “This is how good my breathing response is”
*- when ventilatory demand D exceeds supply/capacity C –> feeling of dyspnea

  1. Pathophys correlates
    A. structural interference due to obstruction to flow (asthma, emphysema)
    B. restriction to expansion
    i. intrinsic to lung (CHF)
    ii. extrinsic (obesity, ascites, pregnancy)
    C. dead space ventilation (emphsema, PE)
    D. increased respiratory drive (acidosis, exercise, hypoxemia)
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15
Q 
[Pulmonary Disease Symptoms/Signs]
Cough
1. Function
2. Phases of a cough 
3. Common causes of cough 
A. Acute
B. Chronic
A
  1. Cough - most common symptom of lung disease
    - normal defense mechanism of lungs - clears larynx, trachea, and large bronchi of mucus and foreign/infectious particles; protects airways
    - persistent cough (3+ weeks) needs to be looked into
  2. Phases: inspiration –> closure of glottis, diaphragm relaxes –> rapid contraction of expiratory muscles with rise in intra-abdominal and pleural pressures followed by opening of glottis
    - velocity is v high although amount of air expelled is smll

3A. Acute (under 3 wks) - most commonly viral; exacerbation of COPD or asthma, environmental exposure
B. Chronic (over 8 wks) - 90% due to upper airway cough syndrome (post nasal drip), asthma, or GERD
- also due to ACEIs, heart failure

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16
Q 
[Pulmonary Disease Symptoms/Signs]
Hemoptysis 
1. Define
2. ID common causes and source for hemoptysis
3. DD of hemoptysis in primary care setting
4. DD given following history findings: 
A. repeated small hemoptysis
B. fever, night sweats, weight loss
C. rust colored sputum 
D. massive bronchial hemorrhage
A
  1. Hemoptysis - coughing or spitting up of blood from lungs or bronchial tubes; secondary to pulmonary or bronchial hemorrhage
    - classified acc to volume
    - threatens gas exchange, risk of aspiration and hemodynamic collapse
  2. 90% bleeding comes from bronchial arteries
    10% from pulmonary circulation
  3. DD: 3B’s –> bronchitis (other infections include pneumonia and TB), bronchogenic carcinoma (lung cancer associated with airways), or bronchiectasis
  4. DD given following history findings:
    A. repeated small hemoptysis –> cancer
    B. fever, night sweats, weight loss –> TB
    C. rust colored sputum –> pneumococcus
    D. massive bronchial hemorrhage –> bronchiectasis (collapse of bronchi) or aspergillomas (type of fungal mycetoma)
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17
Q 
[Pulmonary Disease Symptoms/Signs]
Describe signs of impending respiratory failure
1. abnormal patterns of respiration 
A. Kussmaul
B. Cheyne-Stokes
2. Tripod position
3. Purse lip exhalation 
4. Barrel chest 
5. Clubbing
A

1A. Kussmaul - increased rate and depth (increased tidal volume) of respiration
- associated with compensation for metabolic acidosis
B. Cheyne-Stokes - constant rate but variable depth
- associated with neurologic disorder, CHF, and high altitude

  1. Tripod position - pec major fixes shoulder to make movement of accessory muscles (sternocleidomastoid, scalenes, trapezies) more effective
    - seen in COPD
  2. Purse lip exhalation - maintain positive pressure airway during expiration –> keeps airways open longer –> increase Pa02 and reduce PaC02
    - seen in emphysema
  3. Barrel chest - anteroposterior diameter increases
    - mechanically less efficient
    - seen in COPD
  4. Clubbing - angle between base of nail and nail bed itself (should be less than 160deg)
    - 80% acquired (bilateral), 20% inherited
    - associated with pulmonary diseases eg lung cancer, COPD, pulmonary fibrosis, abscess
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18
Q 
[Pulmonary Disease Symptoms/Signs]
Describe palpation findings and associated conditions 
1. Position of trachea 
2. Posterior chest expansion
3. Tactile fremitus
4. Percussion
A
  1. Position of trachea - mediastinal displacement
    - pulled due to fibrosis, parenchymal collapse
    - pushed away due to pneumothorax, pleural effusion
  2. Posterior chest expansion - asymmetric and reduced chest expansion (+ fever and cough) associated with pneumonia
  3. Tactile fremitus - only pathological when asymmetrical
    - decreased due to pleural effusion, bronchial obstruction, pneumothorax, obesity
    - increased due to consolidation eg pneumonia
  4. Percussion - compare sounds of resonance
    - hyper-resonance due to hyper-inflated lung, pneumothorax
    - dullness due to consolidation (pneumonia), atelactasis, and pleural effusion
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19
Q 
[Pulmonary Disease Symptoms/Signs]
Auscultation 
1. Describe normal breath sounds
A. Vesicular
B. Bronchial
2. Describe adventitious breath sounds and associated conditions
A. Stridor
B. Wheeze
C. Rhonchi
D. Crackles / Rales
A

1A. Vesicular - soft (alveoli are mufflers) and low-pitched, longer inspiration and soft expiration (2:1)
- most common abnormality is diminished sounds due to emphysema, asthma, etc
B. Bronchial - loud, high-pitched and darth-vader like, heard over trachea or right apex, pause between inspiration and longer expiration phase (1:1)
- not normal to hear this in periphery - will happen with consolidation i.e. pneumonia

2A. Stridor - high-pitched, musical sound, heard without stethoscope during inspiration eg in croup
- due to upper airway obstruction (laryngeal tumor, anaphylaxis, vocal cord dysfunction)
B. Wheeze - high-pitched continuous musical sound due to opposition of bronchus walls (airflow limitation)
- due to obstructive diseases - asthma, emphysema, bronchitis
- most often expiratory
C. Rhonchi - low-pitched version of wheeze that sounds like snoring, can clear with coughing
- associated with secretions
D. Crackles / Rales - discontinuous nonmusical sounds
i. fine - unaffected by cough but affected by body position; unrelated to secretions
- etiology - sudden opening of small airways closed during prev expiration; due to interstitial lung disease (pneumonia, CHF but not sarcoid
ii. coarse - affected by cough but not body position, related to secretions
- produced by gas passing through airways that open and close intermittently

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20
Q 
[Upper and Middle RTIs]
1. Rhinopharyngitis 
A. Transmission
B. Responsible agents
C. Pathophysiology 
D. Clinical features
E. Treatment
A
  1. Rhinopharyngitis = Common cold, affects nose + throat
    A. Transmission: communicable via contact with virus in secretions, enters through conjunctiva and nose
    B. Agents: due to rhinovirus mainly
    C pathophys: epithelial cells infected –> spreads to respiratory mucosa –> damaged due to direct infection and chemical mediators –> edema
    - host responds with local interferon production and secretory (IgA) Ab response
    D. clinical features: nasal discharge, obstruction, sore throat
    - variable incubation depending on viral load and cause
    E. Treatment: antihistamines (NSAIDs), symptomatic, Vit C
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21
Q 
[Upper and Middle RTIs]
2. Tonsillopharyngitis
A. Transmission
B. Responsible agents
C. Pathophysiology 
D. Clinical features
E. Treatment
A
  1. Tonsillopharyngitis (tonsillitis) - inflammatory illness of mucous throat membranes, no nasal involvement
    A. Transmission: disease of school-age children, humans are only hosts; transmitted via direct physical person-person contact

B. Agents:

i. bacterial - Group A beta-hemolytic streptococcus i.e. Strep pyogenes
ii. viral - EBV, influenza, adenovirus, etc

C. Pathophys: fimbriae attachment to respiratory epithelium –> toxins and enzymes released –> tissue damage –> rapid spread

  • produce toxins that can cause scarlet fever (sandpaper rash, strawberry tongue)
  • body makes Ab against M protein

D. Clinical features: fever, sore throat, headache, abdominal pain

  • pharyngeal inflammation with edema and tonsillar exudate (pus)
  • swollen, tender anterior cervical lymph nodes

E. Treatment: penicillin (10 days) or tonsillectomy

  • complications:
    i. suppurative (pus-forming) - otisis, sinusitis, peritonsillar abscesses
    ii. non-suppurative - acute rheumatic fever (cross-reactivity of anti-M protein antibodies with heart muscle, JONES criteria), APSGN (glomerulonephritis)
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22
Q 
[Upper and Middle RTIs]
3. Laryngotracheitis/laryngotracheobronchitis
A. Transmission
B. Responsible agents
C. Pathophysiology 
D. Clinical features
E. Treatment
A
  1. Laryngotracheitis/laryngotracheobronchitis i.e. Croup
    A. Transmission: personal contact, secretory droplets
    - most commonly in 6mos - 5yrs
    B. Responsible agents: most commonly parainfluenza 1 (viral)
    C. Pathophysiology: infection in nasopharynx and travels down –> tracheal inflammation with edema and epithelium destruction –> airway narrows –> obstruction of lumen and impairment of vocal chords
    D. Clinical features - hoarse voice, dry “barking” cough, inspiratory stridor –> respiratory distress due to upper airway obstruction
    - may or may not include lung
    E. Treatment: cold air to decrease edema, hydration, 02, steroid therapy
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23
Q 
[Upper and Middle RTIs]
3. Sinusitis
A. Transmission
B. Responsible agents
C. Pathophysiology 
D. Clinical features
E. Treatment
A
  1. Sinusitis - prurulent infection of sinus mucosal linings
    A. Transmission:
    B. Responsible agents: commonly bacteria; mixed infection (eg Haemophilus, pneumococcus)
    - usually post URI
    C. Pathophysiology: mucous discharge from sinus
    D. Clinical features: facial pain, headache, fever, cough, rhinorrhea
    - potts puffy tumor - pus under frontal bone –> Facial swelling
    E. Treatment: oral antimicrobial therapy; IV antibiotics if severe
    - complications
    i. intracranial - meningitis, brain abscess
    ii. orbital - cellulitis, abscess
    iii. respiratory
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24
Q 
[Upper and Middle RTIs]
4. Influenza - 
A. Transmission
B. Responsible agents
C. Pathophysiology 
D. Clinical features
E. Treatment
A
  1. Influenza i.e. flu- acute respiratory infection (lower RTI) which starts as URI; community-acquired viral pneumonia
    A. Transmission: droplet spread of airborne particles

B. Responsible agents: orthomyxoviruses (single stranded RNA virus)

  • Influenza A - humans and other mammals; avian flu
  • Influenza B - only humans
  • Influenza C - humans and swine
  • RNA genome surrounded by nucleocapsid and matrix protein with 2 glycoproteins (hemagglutinin HA for attachment and neuraminidase N for release of virus)
  • variations due to antigenic shift with new subtypes, responsible for pandemics (only A) and antigenic drift with only minor changes (A, B, C)
  • immunity is not long-lasting –> flu shot ever year

C. Pathophysiology: major infection site is ciliated columnar epithelial cell, which is damaged by host immune response –> necrosis, edema, infiltration –> infection of WBCs (lymphocytes, monocytes, PMNs i.e. neutrophils, eosinophils, basophils)

D. Clinical features: myalgia, chills, cough, headache, sore throat

  • children have more fever and GI symptoms
  • sickest with viral shedding peak

E. Treatment: supportive, avoid aspirin in children, one of few situations where antivirals lead to better outcomes (eg tamiflu - neuraminidase inhibitors)
- complications - bacterial secondary infection (pneumococcus, staph auereus) –> pneumonia *this is what causes mortality

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25
Q 
[Tuberculosis]
1. Epidemiology
2. Microbiology incl
A. Transmission
B. Distinguish between Myco and non-tuberculous bacteria
A
  1. Epidemiology - increase in incidence in 90s due to HIV, but overall decline in incidence among US-born people
    - most cases in US are reactivation esp in immigrants
    - primary is usually missed bc it is self-limiting through immune response
    - need to report primary/active (but not latent) to health dept
  2. Microbiology - caused by Mycobacterium tuberculosis
    - obligate aerobe, bacillus, non-spore forming, non-motile
    - cell wall of mycolic acid
    - 8 weeks to grow on Lowenstein Jensen agar
    A. Transmission - person to person via airbone particle (1-5 can cause infection); only those with active TB are infectious (NOT latent)
    B. Distinguishing bw non-TB bacteria - 100+ species but do not need to isolate (no person-person spread); presents in many ways incl pulmonary disease, skin infections
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26
Q

[Tuberculosis]

  1. Pathogenesis
  2. Medical conditions that increase risk of development of active TB
A
  1. Pathogenesis - inhalation –> phagocytosis by alveolar macrophages –> bacterial multiplication –> lymphatic spread to lymph nodes or via blood –> activates Th1 immune response –> macrophages secrete TNF and differentiate into epithelioid histiocytes –> granuloma formation (dormant mycobacteria in center and rim of lymphocytes, giant cells, and epithelioids) in lungs and hilar lymph nodes–> cell death in granuloma leads to caseous necrosis –> fibrous calcification = Ghon complex halts infection in healthy individuals
  2. Medical conditions that increase risk of development of active TB
    - HIV
    - silicosis (eg miners - silica deactivates macrophages )
    - chronic renal failure (not clear why)
    - diabetes (not clear why)
    - leukemias/lymphomas (immunosuppressive therapies)
    - weight loss (malnutrition)
    - gastrectomy/jejunoileal bypass (lack of gastric acid)
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27
Q 
[Tuberculosis]
Diagnosis modalities
1. Skin testing
2. BCG vaccine 
3. Interferon Gamma Release Assays (IGRAs)
A
  1. TB Skin testing - PPD - causes delayed type IV hypersensitivity reaction (CD4+ T cell response)
    - denotes TB infection but does does not distinguish between active and latent TB
    - threshold for immunosuppressed is 5mm, for hospital workers or recent immigrants is 10mm, low-risk is 15mm
  2. BCG vaccine - live attenuated strain from M. bovis
    - false positives for PPD –> ignore BCG history in interpreting PPD
  3. IGRAs - whole blood in vitro test –> lymphocytes release IFN gamma in presence of TB antigens
    - pros: no error in interpretation, not affected by BCG vaccine
    - cons: less reliable in immunocompromised or children, does not distinguish bw active and latent
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28
Q

[Tuberculosis]
1. Difference between latent and active infection
2. Symptoms/signs of TB
A. Miliary TB
3. Diagnose of active TB
A. CXR in primary, reactivated, and latent TB

A
  1. Latent TB will have positive PPD or IFN assay, but normal CXR and no symptoms or signs; active TB will have symptoms, signs, and abnormal CXR
  2. Symptoms/signs: fever, night sweats, cough, hemoptysis (coughing up blood), anorexia, weight loss, fatigue
    - commonly affects lung/pleura but other sites include lymph nodes, GU (Sterile pyuria - lot of WBCs but no organisms), CNS (meninges), abdomen, pericardium
    - Pott’s disease - demineralization –> anterior collapse of thoracic vertebrae

A. Miliary TB - TB infection with hematogenous dissemination –> leads to systemic disease –> multi-organ failure

  • can be primary infection or reactivation; in immunocompromised
  • millet seed type lesions in the lung or other organs
  1. Diagnose of active TB - sputum acid fast AFB stain and culture (for drug susceptibility), PCR, fluid aspiration or tissue biopsy (higher yield)
    A. CXR:
    i. primary - lower or middle lobe infiltrates
    ii. reactivated - apical upper infiltrates (poor lymphatic drainage and high 02 tension), cavitation
    ii. latent TB - usually normal, but some nodules or pleural thickening
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29
Q

[Tuberculosis]
1. Treatment
A. Active TB
B. latent TB

  1. How does TB differ in special pt populations
    A. HIV
    B. Children
    C. Pregnancy
  2. Role of isolation precautions in prevention of transmission of Tb
A
  1. Treatment
    A. Active TB - 2 months of RIPE (RIF INH PZA EMB), then 4 mos of INH and RIF - UNLESS patient is HIV+ or culture is positive, then give INH and RIF for 7 mos
    B. Latent TB - factors include old age, liver disease (drugs can lead to hepatitis)
    - INH daily for 6+ mos or RIF daily for 4 mos

2A. TB and HIV - can have false negatives
- extrapulmonary TB more common
- treat for latent TB if in contact with someone with active TB regardless of PPD
- same treatment regimens
B. TB in children - less likely to see anything in lung, sputum usually negative - need to do gastric aspirate
- under 5 at greater risk of dissemination
C. Pregnancy - breastfeeding not contraindicated
- treat active TB but defer latent TB until after delivery unless they have HIV (then give INH)

  1. Airborne isolation of patients with active pulmonary TB until clinical improvement and 3 negative acid fast smears
    - isolation not required for latent TB or extrapulmonary TB
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30
Q 
[Pneumonia]
1. Etiology of pneumonia 
A. Mechanical defense
B. Immunodysregulation
C. Immunocompromised
  1. How you get pneumonia?
  2. Clinical presentation
A

Pneumonia - infection of lung parenchyma (functional tissue - alveoli, alveolar ducts and respiratory bronchioles), leading cause of infectious death in the US; lower respiratory tract infection

  1. Etiology - host defense mechanisms impaired and systemic resistance lowered due to age, comorbidities, lifestyle
    A. Mechanical defense - loss of cough reflex, obstruction
    B. Immunodysregulation - induced immunosuppression eg alcoholism, cirrhosis, diabetes, cystic fibrosis
    C. Immunocompromised - problems with innate immunity (neutrophils, complement), humoral immunity (antibodies), cell-mediated immunity (due to aging, cancer, 3rd trimester pregnancy, steroids)

Leads to compromised defense mechanism –> injury to mucociliary apparatus (smoking, acute infection), alveolar macrophage dysfunction, pulmonary vascular congestion

  1. Sick contacts, travel/work, URTI that finds its way lower, hematogenous seeding from another site, nosocomial infections
  2. Clinical presentation - fever + abnormal breath sounds (3 days)
    - productive cough (2 wks), fatigue (2 wks), sputum, dyspnea, pleuritic chest pain
    - infiltrates on CXR (duration of 1 months)
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31
Q 
[Pneumonia]
 Describe the bacteria that can cause pneumonia
A. Streptococcus pneumoniae
B. Haemophilus influenzae
C. Moaxella catarrhalis
D. Staphylococcus aureus
E. Klebsiella pneumoniae 
F. Legionella pneumophila
G. Mycoplasma pneumoniae
A

A. Streptococcus pneumoniae = Pneumococcus - most common cause (MCC) of community-acquired pneumonia –> causes 90% of lobar pneumonias

  • Gram (+) lancet-shaped diplococci
  • normal flora in 20% adults

B. Haemophilus influenzae - Gram (-) with A-F serotypes; vaccine against capsulated B form (most virulent)

  • URI symptoms first (otitis media, sinusitis)
  • pediatric emergency, MCC of bacterial acute COPD exacerbation
  • more diffuse infiltrates than in CAP lobar pneumonia

C. Moaxella catarrhalis - more common in elderly, common cause of otitis media in children, colonize URT
- 2nd MCC of bacterial COPD exacerbation

D. Staphylococcus aureus - 2nd MCC of secondary bacterial pneumonia after virus or influenza (MCC is pneumococcus)

  • can get abscesses and empyema
  • seeds R side of heart via bacteremia in IV drug use

E. Klebsiella pneumoniae - MCC of Gram (-) bacterial pneumonia - lobar pneumonia

  • in malnourished alcoholics
  • produces thick “currant jelly” sputum tough to cough up –> can form abscess

F. Legionella pneumophila - Gram (-), flagellated

  • in artificial aquatic environment; causes GI symptoms
  • culture is gold standard, common in sicker people
  • atypical - give fluoroquinolone

G. Mycoplasma pneumoniae - walking pneumonia

  • atypical (interstitial) pneumonia–> treat with fluoroquinolone or macrolide (azithromycin) antibiotics
  • no cell wall - cannot gram stain; CXR patchy infiltrate
  • infects healthy people in close quarters (college kids, military recruits)
  • autoimmune hemolytic anemia (IgM cross reacts with RBC antigen and causes agglutination at cold temps)
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32
Q

[Pneumonia]
1. Describe chronic pneumonia
2. Describe endemic mycoses
A. Histoplasmosis

A
  1. Chronic pneumonia - 6 week + illness caused by less virulent pathogens, slower growing eg fungi, mycobacteria
    - recurrent aspect bc colonized by these microbes
    - can occur in immune competent patient –> granuloma formation (TB)
    - or patients with immune suppressive medications (TNFalpha inhibitors, methotrexate, rituximab, steroids)
  2. Endemic mycoses - fungi that live in soil, acquired by inhaling aerosolized spores –> cause non-specific pulmonary symptoms; unresponsive to antibiotics

A. Histoplasmosis - infectious spores from bird or bat droppings, Mississippi river area

  • clinical: coin lesions on CXR, fibrosis of mediastinum; similar to TB and sarcoidosis; usually self-limited symptoms
  • histo: tree bark appearance of calcification; thin budding yeasts
  • pts on TNF inhibitors at risk
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33
Q 
[Pneumonia]
Endemic mycoses 
B. Blastomycosis
C. Coccidiomycosis 
D. Aspergillus 
E. Cryptococcus
A

B. Blastomycosis dermatitidis - dimorphic fungus

  • central and southeastern US
  • resolves spontaneously
  • pulmonary but can become disseminated or cutaneous
  • histo: broad-based budding yeast

C. Coccidiomycosis - v pathogenic - inhalation leads to infection

  • Southwestern US
  • fungus blocks lysosome phagosome fusion
  • peripheral eosinophilia
  • delayed type hypersensitivity rxn (Type IV)
  • usually asymptomatic but patients can progress to lung lesions, cough, erythema nodosum

D. Aspergillus - opportunistic mycoses –> affects immunosuppressed

  • ubiquitous and unavoidable
  • can have asthma or chronic cavitary lesions or invasive pulmonary
  • prolonged neutropenia, 45 degree branching

E. Cryptococcus - budding encapsulated yeast associated with HIV; India ink stain

34
Q 
[Pneumonia]
Endemic mycoses 
F.  Mucormycosis 
G. Candida
H. Pneumocystis 
I. Cytomegalovirus
A

F. Mucormycosis - first infects sinuses, more nodular than aspergillus, 90 degree angles –> necrotic cavitation

G. Candida - normal flora in GI and GU tracts but can be invasive and cause pneumonia (RARE, from bacteremia)

H. Pneumocystis jirovecii - seen in HIV and immunosuppressed patients –> do prophylaxis

  • HIV is a subacute illness; HIV candidiasis can predispose
  • hypoxic on exertion, frothy intraalveolar susbtance on histology

I. Cytomegalovirus - immunosuppressed transplant patients
- get from CMV+ donors or blood products

35
Q

[Pneumonia]

Describe lung abscess and empyema including pathophys and causes

A
  1. Lung abscess - infection causes necrotic lung tissue to cavitate –> collection of pus in cavity
    - not always infectious
    - pathophys: small zones of necrosis in consolidated regions of pneumonia form abscesses that erode into bronchi –> fibrosis –> necrosis in middle
    - associated with Actinomyces (dental) and Nocardia (immunocompromised)
  2. Empyema - infection of pleural space
    - pus on fluid damage
    - starts with parapneumonic effusion –> lung expands –> surgery to peel way fibrous layer –> trapped lung that will not expand
    - causes: strep, anaerobes, MRSA; complication of pulmonary infection
36
Q

[Thorax Cancer]

  1. Mediastinal tumors
  2. Metastatic disease to lung
A

Thoracic cancer can be lung, esophageal, thymus, mesothelioma
1. Mediastinal tumors - 4 T’s:
Thymoma - tumor of epithelial cells in thymus
Teratoma - germ cell tumor that can involve anything eg hair, ectoderm remnants
Thyroid cancer - thoracic thyroid that starts at neck and descends into thorax
Terrible lymphoma - lot of lymph nodes in thorax

  1. Metastatic disease to lung - not v common. more common for lung cancer to metastasize to other organs
    A. Lymphangitic (has to be close to lung) - breast, stomach, pancreas, lung
    B. Hematogenous (usually farther, from vascular organs) - colon, thyroid, kidney
37
Q 
[Thorax Cancer]
Primary malignancy 
1. Categories
2. Epi
3. Risk factors
4. Clinical presentation 
     A. Local 
     B. Regional
     C. Metastatic
A 
Primary malignancy - lung cancer
1. Categories
A. Non-small cell (80%) - adenocarcinoma, squamous cell, large cell  
B. Small cell (15%)
C. Others (5%) - sarcoma
  1. Epi - less than 30% surgically resectable (bc cancers don’t have pain receptors - go asymptomatic for years); most deadly:
    Males: lung, colon, prostate
    Females: lung, breast, colon
  2. Risk factors: smoking, environmental factors (radon, asbestos, arsenic), F, black, genetics (family hx)
  3. Clinical presentation - most commonly asymptomatic
    A. Local effects - cough, weight loss, dyspnea, hemoptysis
    B. Regional - vocal cord paralysis, diaphragm paralysis, Pancoast’s syndrome (apical tumor), pleural effusion (stage IV)
    C. Metastatic effects - to lymph nodes, liver, brain, adrenals
    C. Paraneoplastic syndromes - can affect any organ eg Horner’s, clubbing (connective tissue growth in nail bed with hypoxia), hyper/hypoglycemia, dementia, DVT
38
Q 
[Thorax Cancer]
Primary malignancy 
5. Diagnosis 
6. Staging
7. Treatment
8. Prognosis
A
  1. Diagnosis - hx, physical exam, old imaging
    - low dose CT screening for smokers 40+ pack years
    - endobronchial ultrasound
    - percutaneous needle biopsy (more peripheral lesions) but high risk of pneumothorax
    - sputum cytology - for central lesions, squamous
  2. Staging
    A. Non small cell
    Ia-IIb are easier to operate/cure
    IIIa - transition zone, sometimes operable
    IIIb, IV - not operable
    B. Small cell - limited vs extensive disease (majority extensive); with diagnosis, presume there are metastases
  3. Treatment
    - operation contraindicated with poor cardiopulmonary status (recent MI, poor LV, low FEV1)
    A. Non small cell - Ib and II get adjuvant chemo with surgery; palliation - radiation, laser therapy
    B. Small cell - chemo, prophylactic whole brain irradiation, no surgery
  4. Prognosis - poor, depends on stage
    - small cell has poorer prognosis
    - 12% overall survival rate
39
Q

[Thorax Cancer]
Primary malignancy - Describe subtypes incl histology
A. Squamous cell
B. Adenocarcinoma
C. Adenocarcinoma in situ with lepidic growth
D. Large cell
E. Small cell

A

A. Squamous cell - centrally located, most common tumor in male smokers, ONLY type that cavitates

  • associated with Pancoast’s syndrome (apex of lung –> Horner’s syndrome, C8-T1 radiculopathy); histology - onion keratin pearls + intercellular bridges
  • paraneoplastic (altered immune system response)- produce PTHrP –> hypercalcemia

B. Adenocarcinoma (malignant tumor in glands of epithelium) - most common form, esp in dvlpd countries; more common in women and non-smokers, peripherally located (inside parenchyma); histology - glandular

C. Adenocarcinoma in situ with lepidic growth - prev called bronchioalveolar cell; subtype that grows only along alveolar spaces (thickens the alveoli); glandular with lot of secretions
- not associated with smoking; peripheral

D. Large cell - peripheral, early metastatic spread; poorly differentiated (so active they do not have time to differentiate) cells with lot of cytoplasm, paraneoplastic syndromes e.g. gynecomastia
- associated with smoking

E. Small cell - aka neuroendocrine tumor with grades, hilar mass on CXR

  • paraneoplastic syndromes - produce ACTH, ADH –> SIADH, Cushings, Eaton-Lambert syndrome
  • histo - poorly differentiated; appear like neutrophils with large nuclei, little cytoplasm
  • associated with smoking, v poor outcomes
40
Q

[Translational Science]
1. Describe ebola virus incl transmission, pathogenesis
2. Describe inhaled vaccines
3. Difference between lung and peripheral immune system
4. Stages of FDA drug approval
A. Animal Rule

NOT TESTED

A
  1. Ebola - filovirus - enveloped, (-) strand RNA virus
    A. transmission - through direct contact with blood or body fluids of symptomatic patients, corpse, or infected animal
    - viral load increases as pt becomes more ill; no transmission through aerosols (eg cough)
    B. Pathogenesis - virus directly infects tissue –> immune dysregulation –> vasodilatory (septic) shock and massive GI output (hemorrhagic fever) –> hypovolemia and vascular collapse –> multi-organ failure
    - disseminated intravascular coagulation - manifestation of low 02 delivery state
  2. Inhaled vaccines - could absorb large quantities of drug rapidly with high bioavailability bc of large surface area and thin vascularized alveolar epithelium
    - particles get stuck as airways narrow - removed by alveolar macrophages (1-5 micrometers reach alveoli)
    - lungs receive entire cardiac output - most richly perfused organ
  3. Mucosal respiratory dendritic cells (which present antigens to T cells) and lung resident T cells are phenotypically different from peripheral counterparts
    - bc lung is not sterile environment
    - CD4 T cells in lung tissue activate both mucosal and systemic Ab immune responses
  4. Pre-clinical - toxicological profile
    Phase 1 - prove safety in less than 100 healthy volunteers
    Phase 2 - prove efficacy in 100+ volunteers
    Phase 3 - test in 1000 patients; need at least 2 trials
    A. Animal rule - fast-track process with safety proven in humans and efficacy proven in animals
41
Q

[Asthma]
1. Define asthma
A. Epi

  1. Common symptoms
A

Asthma - type of obstructive lung disease along with COPD, bronchiectasis
1. Asthma - chronic airway inflammation with variable airway obstruction and symptoms that vary over time and in intensity
A. Epi - one of most common chronic conditions, increasing prevalence
- children: M>F, adults: F>M

  1. Common presenting symptoms - wheeze, SOB, chest tightness, cough, dyspnea, mucous
    - worsen at night
    - associated with hay fever, eczema, or family hx of asthma/atopy
    - pattern can be unpredictable or nocturnal, seasonal, associated with specific triggers
42
Q

[Asthma]

  1. Physical signs
  2. Triggers
A
  1. Physical signs - prolonged expiration, wheezing, symptoms vary could be normal
    - assess upper airway for signs of allergy and nasal polyps (due to aspirin intolerant asthma, chronic rhinitis, or cystic fibrosis)
    - less likely asthma if isolated cough, chronic sputum, SOB with dizziness (hypoventilation), chest pain (asthma should not cause pain)
    - wheezing may be absent during severe asthma (“silent chest”)
    - histology: Curschmann spiral mucus plugs and Charcot-leyden crystals of eosinophils in cough
  2. Triggers: allergy (pollen, cats, meds, house dust mites, cockroach feces), infection, cold air, GI reflux, emotion, exercise, aspirin (aspirin intolerant asthma leads to bronchospasms and nasal polyps), irritants (N02, ozone, aerosols, smoke)
43
Q

[Asthma]

  1. Pathophysiology
  2. Pathogenesis
A
  1. Pathophysiology - airway smooth muscle hypertrophy and bronchospasm –> airway obstruction –> acute sx
    - mucosal thickening from edema
    - basement membrane thickening
    - eosinophil inflammatory infiltrate (neutrophils in COPD)
    - increased goblet cells and glands
    - epithelial desquamation
    * NO destruction of alveoli or fibrosis
  2. Pathogenesis - allergens induce Th2 phenotype in CD4+ T cells of genetically susceptible individuals –> Th2 cells secrete IL-4 (mediate switch to IgE), IL-5 (attract eosinophils), and IL-10 (stimulate Th2, inhibit Th1) and IL-13 (boost IgE production)
    - reexposure to allergen - cross-link to surface IgE on mast cells –> activated mast cell release histamine granules and generate leukotrienes C4, D4, E4 –> vasodilation (arterioles) + increase vascular permeability
    A. early phase - bronchoconstriction, inflammation, edema
    B. Late phase - inflammation damages cells and perpetuates bronchoconstriction
44
Q

[Asthma]

  1. Testing
  2. Severity
  3. Treatment goals
A
  1. Testing
    - spirometry results are variable
    - increased exhaled NO - marker of Th2 eosinophil inflammation
    - hyperinflation on CXR, CT to rule out other diseases
    - decreased FEV1/FVC
    - provocative testing - decrease in FEV1 in response to methacholine, exercise (Delayed), cold air
  2. Severity assessed retrospectively based on level of treatment required to control symptoms
    - subjective and individual, severity may change
  3. Treatment goals: 12% increase in FVC or FEV1 AND absolute increase >200cc
45
Q

[Asthma]

  1. What happens during severe asthma?
  2. 5 physiologic causes of hypoxemia
  3. Managing asthma exacerbation
A
  1. Severe asthma -
    - gas exchange abnormalities - hypoxemia (V/Q mismatch), hypercapnea (decreased ventilation)
    - high lactate levels (respiratory muscle fatigue)
    - mental status changes
2. 5 Causes: 
A. R--> L shunt
B. V/Q mismatch *corrects with 02; asthma patient with normal pH 7.4 but in distress is in impending respiratory failure 
C. Hypoventilation 
D. Low Pi02 (high altitude) 
E. Diffusion abnormality
  1. Exacerbation mgmt - aggressive allergy control, add increased steroids or bronchodilators, systemic steroids
46
Q 
[Asthma Drugs]
Bronchodilators incl use, MOA, adverse effects
1. MOA 
2. B2-Selective agonists 
A. SABA
B. LABA
A
  1. Bronchodilators - Bronchodilation promoted by cAMP, which is increased by beta agonists and PDE inhibitors (theophylline)
    - bronchoconstriction inhibited by muscarinic antagonist and adenosine antagonist (eg theophylline)
  2. B2-Selective agonists - most widely used bronchodilators –> relax smooth muscle and inhibit release of bronchoconstricting substances from mast cells
    A. SABA (Short Acting) eg albuterol, terbutaline, metaproterenol, pirbuterol all equally effective
    - max effect in 15-30 min
    - Use: rescue therapy for relief of acute asthma symptoms and bronchospasm
    - inhalation (inhaler or nebulizer) preferred route
    B. LABA (Long acting) eg salmeterol, formoterol
    - potent B2 agonists with 12+ hour duration of action
    - no anti-inflammatory action - NOT rescue therapy as with SABAs
    - Use: with corticosteroids for chronic asthma control
47
Q 
[Asthma Drugs]
Bronchodilators incl use, MOA, adverse effects
3. Methylxanthine drugs 
4. Anticholinergic agents - SAMRAs 
A. Atropine
B. Ipratropium bromide
A
  1. Methylxanthine drugs eg theophylline, aminophylline
    A. MOA: adenosine receptor antagonist, PDE inhibitor
    - potent bronchodilators - relaxes airway smooth muscle, relieve airflow obstruction, improves contractility of skeletal muscle + reverses diaphragm fatigue
    - cannot be aerosolized –> take orally or parenterally –> systemic effects (gets in bloodstream)
    B. Adverse effects: limited TI –> toxicities when 20+ mg/L –> nausea, vomiting, headache, anxiety, seizures
  2. Short Acting Muscarinic Receptor Antagonists (SAMRAs)
    A. Atropine - low doses can cause dilation without increasing HR; duration of 5 hrs NOT first-line
    - Adverse effects: blind as a bat, mad as a hatter, dry as a bone, red as a beet, hot as a hare
    B. Ipratropium - quarternary ammonium derivative of atropine –> constitutively positive charge –> poorly absorbed –> does not enter CNS –> minimum negative effects
    - synergistic with albuterol
48
Q

[Asthma Drugs]
Anti-inflammatory agents incl use, MOA, adverse effects
1. Corticosteroids
2. Antileukotrienes

A
  1. Corticosteroids eg fluticasone, beclomethasone, budesonide, flunisolide *inhaled (ICS) - no bioavailability
    A. MOA: inhibit mucosal inflammation in asthmatic airways–> reduce frequency of asthma exacerbations
    B. Use: ICSs are first-line for treatment of chronic asthma pts of all ages and disease severity when when used with LABAs
    C. Adverse effects: severe if given chronically; reserve systemic corticosteroids eg oral prednisone for patients with acute severe asthma who do not respond to ICS
    - local - oropharyngeal candidiases (thrush - opportunistic infection) and dysphonia (vocal cord myopathy)
    - Inhalation ICS free of other adverse effects
  2. Antileukotrienes eg zileuton, zafirlukast, montelukast
    - leukotrienes are bronchoconstrictors –> mucus hypersecretion, mucosal edema
    A. MOA:
    i. inhibit 5-lipoxygenase to prevent leukotriene synthesis eg zileuton
    ii. LTRAs inhibit binding of leukotriene D4 (LTD4) to receptor e.g. zafirlukast, montelukast
    B. Use: not as good as ICS for improving symptoms, but equally effective in reducing exacerbation frequency
    - ORAL, idiosyncratic patient response
49
Q

[Asthma Drugs]
Anti-inflammatory agents incl use, MOA, adverse effects
3. Cromolyn and nedocromil
4. Anti-IgE therapy

A
  1. Cromolyn and nedocromil
    A. MOA: alter function of chloride channels –> inhibit activation of mast cells and eosinophils
    B. Use: equally effective as theophylline and antileukotrienes, less so than ICS
    - only inhalation - reduces bronchial reactivity and inhibits antigen and exercise induced asthma
    C. Adverse effects: minimal systemic toxicity (poor oral bioavailability)
  2. Anti-IgE therapy eg omalizumab
    A. MOA: monoclonal antibody that complexes with free IgE and inhibits IgE binding to mast cells and basophils
    B. Use: lessens frequency and severity of asthma attacks
    - only for refractory cases with frequent exacerbations bc v expensive
    C. Adverse effects: rare, incl injection site rxns and anaphylaxis
50
Q

[Asthma Drugs]
Describe preferred clinical pharmacologic approach for treatment of:
1. mild to moderate
2. refractory and severe asthma

  1. Step up therapy
A
  1. Mild to moderate asthma
    - start with inhaled SABA (albuterol) as needed
    - need addl treatment if using 2+/week, nocturnal sx 2+/month, and FEV1 less than 80% –>
    SABA + low-dose ICS (eg budesonide), or oral antileukotriene (eg montelukast) or cromolyn
    - theophylline + SABA for pts with poor response to other agents
  2. Refractory and severe asthma
    - ICS (eg fluticasone) + LABA (salmeterol or formoterol)
    - Combos - Advair (salmeterol + fluticasone) OR Symbicort (formoterol-budesonide) *black box warning bc of low risk of fatal attack
    - if that does not work, next step is anti-IgE omalizumab
  3. Step up therapy; step down if well controlled 3+ mos
    Step 1 - as needed inhaled short acting B2 agonist (SABA)
    Step 2 - SABA + low dose controller (ICS, LTRA, cromolyn, theophylline)
    Step 3 - medium dose ICS or low dose ICS + LABA
    Step 4 - medium dose ICS + LABA
    Step 5- high dose ICS + LABA and consider anti-IgE therapy
    Step 6 - high dose ICS + LABA + oral corticosteroid and consider anti-IgE therapy
51
Q 
[COPD]
Chronic bronchitis 
A. Etiology 
B. Pathophysiology
C. Clinical features
A

COPD - irreversible airflow obstruction and inflammation (asthma is reversible airflow obstruction)

Chronic bronchitis - clinically defined –> chronic, productive cough for 3+ mos/year for 2+ years

A. Etiology - smoking or other noxious stimuli –> ↑ neutrophils in airway lumen + ↑ CD8 lymphocytes in airway wall and parenchyma –> luminal inflammation

B. Pathophysiology- hypertrophy of bronchial mucinous glands (50%+ Reid index thickness of bronchial glands compared to overall wall) –> luminal occlusion + altered airway surface tension –> predisposition to expiratory collapse

  • diffuse disease process - affects all of lung
  • ↑ mucus production (viral/bacterial infection, inflammatory cells) and ↓ elimination (poor ciliary clearance, airway occlusion, respiratory muscle weakness)

C. Clinical features -

i. Cyanosis “blue bloaters” - mucus plugs trap C02 –> ↑ PAC02 –> ↓ PA02 –> ↓ Pa02
ii. infections common
iii. cor pulmonale (lung clamps down all hypoxic areas –> R heart overload and failure)

52
Q 
[COPD]
Emphysema 
A. Etiology 
B. Pathophysiology
C. Clinical features
A

Emphysema - destruction of alveolar air sacs –> abnormal permanent enlargement of air space distal to terminal bronchioles

A. Etiology - progression due to infections

i. Smoking - most common cause due to pollutants in smoke –> free radicals inactivate A1AT –> damage
ii. Alpha1-antitrypsin (A1AT) deficiency - A1AT neutralizes proteases released by neutrophils and macrophages when there is inflammation

B. Pathophysiology - air sacs (balloons) converted into blebs (shopping bags) due to destruction of elastin/hyperinflation –> loss of elastic recoil –> collapse of airways during exhalation –> air trapping –> increased positive pressure –> ↓ gas exchange, ↓ venous return, ↓ CO (and ↑ FVC ↑ TLC ↑ RV)

i. Smoking - centriacinar emphysema mostxevere in upper lobes
ii. A1AT deficiency - panacinar emphsema most severe in lower lobes

C. Clinical features -

  • dyspnea - “pink puffer” prolonged expiration with pursed lips
  • weight loss/emaciated bc breathing takes lot of work
  • cough with minimal sputum
  • “barrel chest” ↑ AP diameter of chest
  • late complications - cor pulmonale, hypoxemia
53
Q

[COPD]

  1. Why is hypoxemia early complication in chronic bronchitis and late in emphysema?
  2. Difference bw shunt and dead space
  3. Compare contrast chronic bronchitis and emphysema
  4. COPD treatment
A

1A. Chronic bronchitis is diffuse process –> generalized hypoxia –> lung constricts all arterioles –> early hypoxemia “blue boater”
B. Emphysema: lung constricts the bad lung units –> blood shunted to better ventilated alveoli –> over time, destruction of capillaries in alveolar sacs lead to late hypoxemia “pink puffer”

2A. Shunt - Perfusion to under-ventilated areas (low V/Q ratio) e.g. chronic bronchitis
- give 100% Fi02 but cannot improve their Pa02
B. Dead space - Ventilated alveoli are not being perfused (high V/Q ratio) e.g. emphysema

  1. CB vs E
    - dyspnea mild and late in CB, severe and early in E
    - cough early and productive in CB
    - cor pulmonale and infections common in CB, rare in E
    - airway resistance increased in CB, normal in E
    - elastic recoil normal in CB, low in E
    * maximum expiratory flow determined by airway R and elastic recoil pressure*
    - large heart in CB, small heart in E
  2. COPD treatment
    A. Acute - SABA (albuterol), SAMRA (ipratropium), or combo
    B. Chronic - LABA (arformoterol), LAMRA (tiotropium), or corticosteroid-LABA combo
54
Q 
[COPD]
Bronchiectasis 
A. Etiology 
B. Pathophysiology
C. Clinical features
A

Bronchiectasis - permanent dilatation of bronchi and bronchioles

A. Etiology

i. cystic fibrosis - secretions lead to mucous plugs; use inhaled antibiotics
ii. Kartagener syndrome - dynein defect –> ciliary dysfunction –> situs inversus, sinusitis, infertility, bronchiectasis
iii. tumor or foreign body - ↑ risk infection
iv. necrotizing infections
v. Allergic bronchopulmonary aspergillosis (ABPA)- hypersensitivity rxn to aspergillus in individuals with asthma or cystic fibrosis

B. Pathophysiology - necrotizing infections –> dilated airways –> cilia cannot function properly –> mucus pooling –> chronic airway infection and inflammation –> destruction of other airway walls and loss of airway tone –> air trapping

C. Clinical features - cough, dyspnea, foul-smelling sputum
- complications - hypoxemia with cor pulmonale, secondary (AA) amyloidosis

55
Q

[Restrictive DPLD]

  1. What are diffuse parenchymal (interstitial) lung diseases DPLD?
  2. Common characteristics of pts with DPLD
  3. Common clinical presentation
  4. Physical signs
A
  1. DPLD - heterogenous group of noninfectious, nonmalignant processes of lower respiratory tract
    - idiopathic interstitial pneumonias
    - occupational/environmental exposures
    - drug-induced lung injury
    - sarcoidosis
  2. Common characteristics - fibrosis of the lung interstitium (tissue between alveoli and bloodstream)–> impedes lung filling and gas exchange
    - restrictive ventilatory impairment (decreased lung compliance, ↑ FEV1/FVC but ↓ TLC, FRC, RV)
    - diffuse interstitial infiltrates on CXR
    - often progressive and fatal
  3. Common clinical presentation
    - most common DOE, cough, abnormal CXR, physiological impairment (eg low P02)
    - some will have normal CXR and PFTs but will have abnormal high res CAT or exercise test
  4. Physical signs - clubbing, crackles, skin changes, joint deformities
56
Q 
[Restrictive DPLD]
Sarcoidosis
1. Etiology
2. Pathophysiology
3. Clinical features
4. Diagnosis 
5. Treatment
6. Distinguish from berylliosis
A

Sarcoidosis -
1. Etiology - unknown, classically in black females

  1. Pathophysiology - noncaseating (no necrosis) granulomas in tissues of multiple organs, most commonly in lung and hilar lymph nodes (adenopathy)
    - “asteroid bodies” - stellate inclusions seen within the giant cells of the granulomas
  2. Clinical features - cough, dyspnea, pulmonary or constitutional symptoms
    - hypercalcemia (epithelioid histocytes in granulomas convert vitamin D to active form)
    - eye - ophthalmic granulomatosis –> blindness
    - skin - cutaneous rash, nodules, erythema nodosum
    - hepatitis
  3. Diagnosis - diagnosis of exclusion
  4. Treatment - usually resolves spontaneously without sequelae; could treat with steroids
  5. Berylliosis is similar to sarcoidosis in histology, CXR except seen more in nuclear and aerospace industries e.g. NASA
57
Q 
[Restrictive DPLD]
Hypersensitivity pneumonitis
1. Etiology
2. Pathophysiology
3. Clinical features
4. Diagnosis 
5. Treatment
A

Hypersensitivity pneumonitis = extrinsic allergic alveolitis

  1. Etiology - repeated inhalation of finely dispersed organic antigens
    - e.g. pigeon breeder’s lung, farmer’s lung
  2. Pathophysiology - associated with eosinophils; poorly formed granulomas in upper lobes of the lung
  3. Clinical features
    A. Acute - intense exposure with immediate symptoms - fever, chills, malaise; diffuse ground glass CXR appearance
    B. Subacute/chronic - continual, low level exposure - dyspnea and fatigue; reticular pattern on CXR
  4. Diagnosis - exposure to known offending antigen, don’t need to do lung biopsy
  5. Treatment - resolves with removal of antigen exposure
58
Q 
[Restrictive DPLD]
Silicosis
1. Etiology
2. Pathophysiology
3. Clinical features
4. Diagnosis 
5. Treatment
A

Silicosis - most common pneumoconiosis
1. Etiology - inhalation of silica eg sandblasters, miners, millers, quarry workers

  1. Pathophysiology - silica impairs formation of phagolysosome by macrophages
    - CXR shows fibrotic nodules in upper lobes of lungs
    - increases risk for TB
  2. Clinical features
    A. Simple silicosis - asymptomatic or chronic cough, normal PFTs
    B. Complicated silicosis - nodules coalesce and pull away from chest wall; PFTs progressively deteriorate
59
Q

[Restrictive DPLD]

What are drugs that can induce pulmonary fibrosis?

A

Chemotherapy - bleomycin, cyclophosphamide
Cardiovascular - amiodarone
Antimicrobial - niturforantoin

60
Q 
[Restrictive DPLD]
Asbestosis
1. Etiology
2. Pathophysiology
3. Clinical features
4. Diagnosis 
5. Treatment
A

Asbestosis - type of pneumoconiosis
1. Etiology - exposure to asbestos eg construction workers, plumbers, shipyard workers

  1. Pathophysiology - pulmonary parenchymal fibrosis
    - fibrotic thickening of lung and pleura and calcified pleural plaques –> increased risk for lung cancer (multiplicative in smokers), lower risk for mesolthelioma
    - asbestos bodies (brown fibers with beads of iron deposits) pathognomonic
    - starts in lower lobes
  2. Clinical features - DOE, basal velcro crackles, clubbing, restrictive PFTs
61
Q 
[Restrictive DPLD]
Idiopathic interstitial pneumonia 
1. Etiology
2. Pathophysiology
3. Clinical features
4. Diagnosis 
5. Treatment
A

Idiopathic interstitial pneumonia IIP- umbrella that includes idiopathic pulmonary fibrosis IPF (most common)

  1. Etiology - unknown, related to cycles of lung epithelial injury and abnormal repair
    - associated with smoking
  2. Pathophysiology - injured pneumocytes produce TGFbeta –> TGFbeta induces fibrosis
  3. Clinical features - progressive dyspnea and cough
    - exacerbation - deterioration in symptoms and gas exchange secondary to infection, PE, heart failure
    - fine velcro crackles at base of lung
  4. Diagnosis - fibrosis on lung CT –> initially subpleural patches –> diffuse fibrosis with “honeycomb” lung
    - temporal heterogeneity
  5. Treatment - IPF needs lung transplant, has high mortality rate; try increasing gastric pH or give pirfenidone (blocks TGFbeta) or nintedanib (R blocker) to slow disease progression
    - some other IIPs are responsive to steroids eg cryptogenic, lymphoid, nonspecific interstitial pneumonias
62
Q

[Exercise Science]

  1. Define normal cardiovascular responses to exercise in trained vs untrained people
  2. What happens to patients with cardiac disease?
A
  1. CO = SV x HR
    - during exercise, CO increases in proportion to severity of exercise from 5L/min at rest
    - SV increases to ~50% maximal 02 consumption V02max; after that, SV constant and HR increases to maintain CO increase

HR lower and SV higher in endurance athletes versus trained and untrained students for level of 02 uptake (L/min; ~CO)
- max HR is 180 regardless

  1. Cardiac disease - inability to raise SV (max 02 pulse) during exercise –> premature devlpt of lactate –> lower anaerobic threshold
63
Q

[Exercise Science]

  1. Define normal respiratory responses to exercise in trained vs untrained people
  2. What happens to patients with obstructive lung disease?
A
  1. Light to moderate exercise - minute ventilation increases linearly with 02 consumption (also C02 production, HR, CO)
    - large increase in pulmonary blood flow but only small increase in pulmonary artery pressure bc of dilation and recruitment of more pulmonary capillaries
    - pulmonary blood flow increases most in upper lung zones –> decreases physiological dead space from 30 to 15%
  • Trained individuals have lower minute ventilation (better 02 delivery to peripheral muscle) for level of 02 uptake
  • both trained and untrained stop exercising before they reach maximal voluntary ventilation MVV –> still some breathing reserve
  1. Obstructive lung disease (asthma, emphysema) - inability to increase minute ventilation and oxygen saturation
    - COPD patients reach MVV (which is much lower than normal) –> utilize all ventilatory capacity
64
Q

[Exercise Science]

  1. Describe acid-base change that occur during exercise and how they affect ventilation
  2. Explain anaerobic threshold
  3. How does lactate accumulate during exercise?
A

1A. Initial phase: ventilation increases linearly with metabolic rate (02 consumption, C02 production, HR, CO); no significant change in pH or ABG
B. Next phase anerobic threshold: ventilation driven both by metabolism AND excess C02 production
- when lactate production exceeds utilization –> blood lactate increases –> excess H+ ions buffered by bicarb –> forms C02 –> rise in ventilation
C. Last phase: lactate overwhelms bicarbonate buffering –> decrease in pH –> stimulation of chemoreceptors –> further increase in minute ventilation –> exercise ends due to sense of dyspnea

  1. Anaerobic threshold - point during exercise where aerobic mechanisms fail to meet energy demands (C02 production greater than 02 consumption)
  2. Lactate can be metabolized by liver and non-exercising muscle, only spills out in blood when production greater than metabolism
    - Trained people produce less lactate for given level of 02 uptake
65
Q

[Obstructive Sleep Apnea]

  1. Pathophysiology
  2. Epi / risk factors
  3. Clinical presentation
  4. Physical exam findings
A
  1. Obstructive sleep apnea - intermittent collapse of upper airway during sleep –> disrupts / blocks airflow

2A. Epi - more common in men (5%) vs women (3%), many cases undiagnosed
B. Risk factors: obesity!, increased neck size, increased age, male gender, race, anatomic factors (Recessed chin, oropharyngeal crowding, craniofacial abnormalities)

  1. Clinical presentation - loud snoring!, dry mouth in morning (more mouth breathing), morning headache (due to high C02), excessive daytime somnolence, witnessed apnea (stopping breathing during sleep)
4. Physical exam findings 
A. crowded upper airway - macroglossia (big tongue), narrowing of airway, high palate, tonsillar hypertrophy (common in children), retrognathia (Recessed chin) 
B. BMI > 30 
C. Increased neck size 
D. Sleepy
66
Q

[Obstructive Sleep Apnea]

  1. Diagnostic procedures
  2. Diagnostic criteria
  3. Difference obstructive vs central apnea
A
  1. Diagnosis - via sleep study (not clinical diagnosis)
    A. polysomnogram = sleep study = gold standard
    - overnight in sleep lab, respiration/movements/sleep staging
    B. Home sleep test - inexpensive but not as comprehensive
    C. Validated questionnaires
  2. Diagnosis via sleep study
    - apnea = cessation of air flow for 10+ seconds
    - hypopnea = decrease in flow by 30+% for 10+ seconds associated with 02 desaturation or electrophysiologic arousal on EEG
    - Apnea-hypopnea index: normal (under 5 events/hr), mild (5-14), moderate (15-29), severe (30+)

3A. obstructive apnea: presence of respiratory effort (air not coming in)
B. central apnea: absence of respiratory effort (not breathing)

67
Q

[Obstructive Sleep Apnea]

  1. Effects of sleep apnea
  2. Treatment
A
  1. Effects:
    A. oxygen desaturation - can go down into 70s
    B. sleep fragmentation - increase in stage I (transitional), decrease in slow wave and REM sleep
    - increase in number of electrophysiologic arousals
    C. poor quality sleep - sleep time may be similar but quality is much poorer
    D. increased sympathetic nerve activity during each obstructive event
  2. Treatment options
    A. weight loss - bariatric surgery
    B. positional therapy - sleep apnea worse on back
    C. mandibular advancement device - pulls jaw forward to increase airway
    D. oral pressure therapy WinX - negative pressure that pulls tongue forward to prevent it from falling back
    E. hypoglossal nerve stimulator Inspire - sensing lead on intercostal senses inspiratory effort –> generator causes stimulation lead to fire –> tongue protrusion
    F. continuous positive airway pressure CPAP - mask delivers positive pressure –> prevents airways from collapsing
    - gold standard but patient compliance is an issue
68
Q

[Obstructive Sleep Apnea]

Consequences of untreated OSA

A

Consequences of OSA:

  1. Symptomatic sleepiness
    - impaired attention, reaction time
  2. Adverse health effects
    - Diabetes
    - HTN
    - Afib - increases risk of recurrence
    These lead to:
    - Stroke - increases risk of incident stroke
    - Dementia / Mild cognitive impairment
    - Cardiovascular disease / heart failure
    These lead to:
    - increased mortality
69
Q

[ARDS]
Acute Respiratory Distress Syndrome
1. Define
2. Clinical features

A

ARDS

  1. Definition
    - Happens within 1 week of known clinical insult
    - CXR shows bilateral opacities (pulmonary infiltrates) not explained by effusions, lung collapse, or nodules - “white out”
    - respiratory failure not explained by cardiac failure or fluid overload (EKG to make sure heart is functioning normally, normal PCWP)
    - Pa02 / Fi02 ratio: 200-300 (mild), 100-200 (moderate), less than 100 (Severe)
  2. Clinical features
    - progressive arterial hypoxemia - decreased Pa02
    - increased work of breathing (much greater pressure to inflate the lungs bc of noncompliance) –> dyspnea and respiratory distress
    - pulmonary edema at low capillary pressures (capillary leak leading to fluid accumulation, NOT high venous pressures)
    - heterogenous process (compliant alveoli in apex but not in base of lung)
70
Q

[ARDS]

  1. Pathophysiology
  2. Difference between pathogenesis of ARDS and neonatal respiratory distress syndrome
A
  1. Pathophysiology
    Insult to body (eg sepsis, pneumonia, trauma, pancreatitis) –> activation of neutrophils –>
    inflammatory cascade with release of proteases and cytokines –> damage to Type I and II pneumocytes –> diffuse alveolar damage (damage to alveolar epithelium - capillary endothelium interface barrier) –>
    protein-rich edema fluid leaks from capillaries into alveolus –> formation of hyaline membrane –>
    (A) impairs ventilation and gas exchange, (B) inactivates surfactant and increases surface tension –>
    (A) V/Q mismatch shunt leading to hypoxemia, (B) atelectasis
  2. Pathology similar but pathogenesis sequence is different
    - End result is the same (diffuse alveolar damage) but no inflammatory cascade
    - Neonatal: primary insult is prematurity –> reduced surfactant –> atelectasis –> hypoxemia –> pulmonary vasoconstriction –> endothelial and epithelial damage (consequence, whereas it is primary process in ARDS)
71
Q 
[ARDS]
1. Describe stages of ARDS 
A. Early or exudative stage
B. Late or organizing stage
2. Possible ARDS outcomes
A
  1. Stages - not progressive, can stop any time
    A. Early or exudative stage (1 wk)
    - Type 1 pneumocyte necrosis and sloughing of epithelial basement membrane
    - congestion of alveolar capillaries, alveolar edema, intra-alveolar hemorrhage
    - formation of hyaline membrane pathognomonic
    - intracapillary neutrophil aggregates and inflammatory cells in alveolar space
    - interstitial thickening (fibrosis as part of healing)

B. Late or organizing stage (after 1 wk)

  • exudate in interstitium and alveolar space begins to organize and become fibrous
  • Type 2 pneumocytes proliferation along basement membrane
  • alveolar septal inflammation and fibrous proliferation
  • hyaline membranes become resorbed
  1. Outcomes:
    A. Resolution majority - regeneration of Type 2 pneumocytes –> restoration of normal gas exchange
    - exudate –> granulation tissue –> resorbed
    B. Stable fibrosis - extensive remodeling by dense fibrous tissue
    C. Progressive fibrosis - progresses to point of extensive reconstruction –> end-stage honey comb lung which can no longer ventilate
72
Q

[ARDS]

  1. Ventilator-induced lung injury and types of trauma that can result
  2. Mgmt of ARDS
A
  1. Ventilator-induced lung injury - have to be careful with treatment because you could accentuate acute lung injury due to heterogeneity of alveoli (posterior and base of lung have fluid-filled alveoli or collapsed alveoli; patent alveoli in other regions like the apex)
    - barotrauma - caused by applying lots of pressure –> alveoli rupture –> pneumothorax (air in chest), pneumomediastinum (regions between walls of alveoli rupture), subcutaneous emphysema (air under skin)
    - volutrauma - large amount of volume –> alveolar overdistension –> stretching and shear stretch injury
    - atelectrauma - alveolar close and open with tidal breath due to lack of surfactant
    - biotrauma - stretch injury –> release of pro-inflammatory cytokines in lung epithelial cells
  2. Mgmt - protective lung strategies
    - adequate end expiratory pressure to keep alveoli open through PEEP
    - gently ventilate to low tidal volume –> limit pressure and volume –> prevent volutrauma, barotrauma, atelectasis
    - patients become hypercapnic (permissive)
    - get patients off back where pathology is most severe - to improve V/Q matching
73
Q

[DVT]

  1. Differences in thrombi formed in arterial vs venous systems
  2. Pathogenesis of DVT
A

1A. Arterial - formed under high shear stress at sites of injury where endothelium is disrupted; platelet rich “white clots” treated with anti-platelets
B. Venous - formed under low shear stress, usually in lower extremities; fibrin rich “red clots” treated with anti-coagulants

  1. Virchow’s triad: (A) hypercoagulable state, (B) stasis –> disruption of blood flow –> hypoxia –> endothelial injury –> (C) endothelial cell activation –> produce tissue factor –> extrinsic coagulation pathway –> layers of fibrin build up –> platelets and red cells attach on top
    - thrombi form in valve pockets
74
Q

[DVT]
Risk factors for DVT based on Virchow’s triad:
1. Endothelial damage

2. Hypercoagulability
A. Hereditary
- Factor V Leiden, Prothrombin, Deficiencies
B. Acquired
- MOIST
C. Anatomic
  1. Stasis
A
  1. Endothelial damage
    A. Dysfunction - smoking, HTN
    B. Damage - surgery, PICC lines, trauma
  2. Hypercoagulability
    A. Hereditary - autosomal dominant mutations, heterozygotes most common
    - Factor V Leiden - most common; resistant to APC degradation –> enhanced clotting; RR ↑ with OCP use
    - Prothrombin gene mutation (in 3’ UTR)- increase in circulating prothrombin
    - Protein C deficiency - warfarin-induced skin necrosis, VTE at numerous venous sites
    - Protein S deficiency
    - Antithrombin deficiency - heparin insensitive
    B. Acquired - MOIST; M(malignancy, motherhood, myeloproliferative), O(OCPs, obesity, ortho), I(IBD, indwelling central line cause UE DVT, immobilization), S(Surgery, syndromes), T(trauma, tamoxifen, thrombosis)
    C. Anatomic - Paget-Schroetter syndrome (#1 cause spontaneous upper extremity DVT), May-Thurner syndrome (compression of left common iliac vein –> femoral vein DVT)
  3. Stasis - immobility, polycythemia (↑ RBC proportion)
75
Q 
[DVT]
Describe clinical presentations and treatment of: 
1. Superficial venous disease
2. DVT
A. Lower extremity
B. Upper extremity
3. Chronic venous disease
A
  1. Superficial venous disease
    A. superficial thrombophlebitis (in tributaries) - pain, erythema, induration, tenderness, fever, palpable no risk of embolizing varicose veins are risk factor
    B. superficial vein thrombosis SVT (in saphenous system) - can go into deep veins –> associated with thromboemboli
    - DVT risk increases when 60+, M, bilateral SVT, systemic infection, absence of varicose veins
  2. DVT
    A. Lower extremity - either proximal (femoral or popliteal veins) or distal vein (anterior tibial) thrombosis; most DVTs come from proximal veins
    - frequently no symptoms or leg pain, cramping, unilateral leg swelling
    - family hx and risk factor hx (MOIST)
    - physical exam findings non-specific –> use clinical prediction model for pre-test probability (Eg Wells score), and then do testing
    - treatment - prevent PE
    B. Upper extremity - rare, due to thoracic outlet problem or indwelling catheter
  3. Chronic venous disease - venous HTN due to varicose veins (bulging veins), chronic venous insufficiency (leg swelling, skin color and texture changes, venous ulcers)
    - #1 cause is valve incompetence due to DVT –> transmission of high pressure to superficial capillaries
76
Q 
[Pleural diseases]
Pleural effusion
1. Pathophysiology
2. Symptoms
3. Physical findings
4. Difference transudative vs exudative
A
  1. Pathophysiology - too much fluid in the pleural space
    Starling = Pc (capillary hydrostatic pressure) - Pi(interstitial hydrostatic pressure) + PI i (interstitial oncotic pressure) - PI c (capillary oncotic pressure)
    - eg elevation in Pc, decrease in PI i
  2. Symptoms - restrictive (reduced FVC, TLC)
    - flattening of diaphragm –> pushes chest wall out –> dyspnea
    - cough (productive cough suggests underlying pneumonia)
    - pleuritic chest pain - sharp, stabbing pain on deep breath
  3. Physical findings - decreased tactile fremitus, dullness on percussion, decreased breath sounds on auscultation and egophony at upper levels of effusion (hyperresonance on auscultation due to consolidation)
  4. Difference
    A. Transudative - imbalance between production and absorption of fluid bc of systemic problem (MCC is CHF)
    - fluid has normal chemistry (pH, glucose, protein)
    B. Exudative - alteration of pleural fluid formation in response to inflammatory process eg secondary to pneumonia, PE, infection, malignancy
    - LIGHT’s criteria - protein fluid:serum ratio >0.5, LDH >0.6, or LDH more than 2/3 normal value
77
Q

[Pleural diseases]
Chylothorax
1. Pathophysiology
2. Treatment

Mesothelioma

  1. Pathophysiology
  2. Symptoms
A

Chylothorax

  1. Pathophysiology - lymphatic fluid (chyle) leaks into pleural space –> milky fluid on thoracentesis
    - leakage from thoracic duct, lymphoma, or trauma
    - triglycerides less than 135 does NOT have chylothorax
  2. Treatment - drainage, omit FFAs from diet, give somatostatin, do pleurodesis to close pleural space

Mesothelioma

  1. Pathophysiology - rare neoplasm from pleural epithelium (mesothelium); poor prognosis
  2. Symptoms - non-speciifc, insidious symptoms eg weight loss, cough, dyspnea, non-pleuritic chest pain
78
Q 
[Pleural diseases]
Pneumothorax 
1. Pathophysiology
A. Primary
B. Secondary
C. Tension
  1. Risk factors
  2. Physical findings
  3. Treatment
A

Pneumothorax
1. Pathophysiology - abnormal collection of air in pleural space –> surrounding lung collapses
A. Primary - spontaneously, usually in tall and thin men
B. Secondary - due to underlying lung disease eg COPD, CF, bronchiectasis
C. Tension pneumothorax - hemodynamic collapse of lung bc of pressure –> air can get into lung but not out –> 02 shortage and low BP

  1. Risk factors - smoking (dose dependent), respiratory bronchiolitis, family hx, CT disorders
  2. Physical findings - acute onset pain +/- dyspnea, at rest
    - decreased tactile fremitus, hyperresonant percussion, decreased breath sounds on auscultation
  3. Treatment - treat etiology, treatment depends on how big it is / hemodynamic compromise
    A. conservative - observe, aspirate
    B. intermediate - chest tube drainage, pleurodesis
    C. invasive - pleurectomy, VATS, thoracotomy
79
Q 
[Pulmonary Vascular Disease]
1. Describe types of pulmonary emboli incl setting and clinical picture
A. Fat
B. Amniotic fluid
C. Thrombi
  1. Explain how pulmonary emboli leads to abnormal imaging tests
  2. Explain diagnostic approach to DVT and PE
A

1A. Fat - due to fat from bone marrow (sickle cell pts) or closed fractures of long bones/pelvis –> ARDS
- supportive care
B. Amniotic fluid - rupture of amniotic sac –> fluid enters mother’s blood supply through placenta –> allergic rxn –> cardiopulmonary collapse
- supportive care
C. Thrombi - blood clots, 95% arise in lower extremities (in deep veins - DVT and PE are same condition); pulmonary emboli - blood clots that break off (embolize) and occlude pulmonary arteries

  1. CT - lack of contrast in occluded artery due to necrosis of occluded artery
    CXR - mostly normal or non-specific –> if pt has sx, think vascular cause; peripheral wedge-shaped opacity
    EKG - signs of RVH (eg RAD)

3A. Clinical + lab eval (D-dimer assays, ABG)
B. PE probability test eg Wells score
C. Diagnostic radiology (CT angio), sonography (looking for non-compressibility)

80
Q

[Pulmonary Vascular Disease]

  1. Explain how PE leads to impaired lung function
  2. Clinical findings
  3. Gas exchange abnormalities
A
  1. PE lodging in arterial system –> occluded blood supply to Type 2 pneumocytes –> no surfactant –> distal atelectasis (alveolar collapse) –> edema –> dyspnea and rales on exam
  2. V/Q mismatch (dead space ) –> hypoxemia (dont try to reverse bc its happening at distal level, allow hypoxic vasoconstriction)–> cyanosis
  3. Obstruction of pulmonary arteries –> increased pulmonary artery pressure (most dangerous thing!)–> increased P2 on heart auscultation
  4. Increased dead space ventilation –> increased alveolar ventilation –> tachypnea (air hunger)
  5. Classic signs often subtle/absent - dyspnea, pleuritic chest pain, hemoptysis; often obscured by coexisting disease
    - other signs/symptoms: leg swelling and pain, crackles, low grade fever
    * Patient with infarcted lung will be in more pleuritic pain and more breathless
  6. Gas exchange abnormalities - respiratory alkalosis (tachypnea) with increased A-a gradient
81
Q
  1. Diagnosis of pulmonary arterial hypertension PAH
  2. Signs/symptoms of PAH
  3. ID classification of pulmonary arterial hypertension
A
  1. Pulmonary arterial hypertension - based on right heart catheterization at rest
    mean PA pressure >/= 25 mm Hg AND normal
    pulmonary capillary wedge pressure PCWP (surrogate for pressure in LA) = 15 mm Hg
    *High PCWP tells you that patient also has LH disease, and RH disease is consequence

2A. Symptoms (sx late in disease - no prodrome) - dyspnea, fatigue, syncope; mostly F 20-30yo
B. Signs - increased P2, tricuspid regurg, RV heave, S4, peripheral edema, hepatic congestion –> cor pulmonale –> RH failure with ascites, cyanosis, JVD, boot shape on CXR

3i. Primary PAH - sporadic; remodeling and thickening of pulmonary arteries –> pulmonary arterial pressure increases but pulmonary capillary pressure normal (–> no pulmonary edema)
ii. PH with LH disease - most common, elevated PCWP –> elevated pulmonary capillary pressure –> pulmonary edema
iii. PH with lung disease or hypoxemia e.g. obesity - lower 02 at night, give 02
iv. PH due to chronic PEs - recurrent emboli, need surgical tx
v. Misc (HIV, sarcoidosis, IV drug use, etc)

M2 (11 decks)

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