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Pulmonary Flashcards

1
Q

Why respiratory system - respiratory function

A

Gas transport for metabolism

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2
Q

Why respiratory system - non respiratory function

A

Filtering and metabolism

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3
Q

Stages of gas transport

A

Ventilation

Lung diffusion

Circulation

Tissue diffusion

Internal respiration

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4
Q

Stages of gas transport - ventilation

A

Movement of bulk airflow from atmosphere into lungs and vice evrsa

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5
Q

Stages of gas transport - lung diffusion

A

Gas exchange between respiratory zone and plasma/RBC across alveolar membrane

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6
Q

Stages of gas transport - Circulation

A

Blood flow carries gas to and from tissues

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7
Q

Stages of gas transport - tissue diffusion

A

Movement of oxygen from blood supply to tissue

CO2 from tissue to blood supply

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8
Q

Stages of gas transport - Internal respiration

A

Cellular metabolism using O2 and producing CO2 –> generates energy

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9
Q

Upper respiratory tract - function

A

Gas humidification, filtration, warming

Nasal passages

Air turbulence

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10
Q

Conducting airways function

A

Gas distribution to respiratory zone

No diffusion of gas

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11
Q

Airway patency based on structure: Trachea, bronchi, bronchioles

A

Trachea - cartialage arches (tracheal rings)

Bronchi - cartilage plates

Bronchioles - no cartilage, depend on lung recoil

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12
Q

Airway clearance mechanisms

A

Bronchi - Cilia and bronchial glands clear contaminants

Distal conducting airways - cilia and goblet cells

Defensins - innate lung immunity

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13
Q

Ventilatory pump contents

A

Rib cage and spine

Diaphragm

Intercostal muscles

Abdominal muscles

Accessory muscles

Visceral and parietal pleura and pleural fluid

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14
Q

Ventilatory pump - rib cage and spine

A

Walls of pump

Increase volume of chest cage during inspiration

Posture

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15
Q

Ventilatory pump - Diaphragm

A

Generates significant negative pressure for inspiration

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16
Q

Ventilatory pump - Intercostal muscles

A

External intercostals - chest wall expansion

Internal intercostals - Exhalation

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17
Q

Ventilatory pump - Abdominal muscles

A

Muscles of expiration

Utilized in lung disease or vigorous exercise

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18
Q

Ventilatory pump - Accessory muscles

A

Used in lung disease or exercise

Tripod sitting - Lean forward on table/desk to stabalize shoulder girdle and neck/shoulder to act on chest wall

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19
Q

Ventilatory pump - Parietal pleurae and pleural fluid

A

Visceral pleura - lies on lung, no pain fibers

Parietal pleura - covers inside of rib cage, pain fibers

Pleural space normally closed but can open/fluid filled in disease states

Pleural fluid acts as lubricant between two pleura

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20
Q

Quiet breathing

A

Diaphragm contracts –> thorax volumed expands –> pleural space pressure decreases below atmospheric –> lungs expand and alveoli increase volume (negative pressure) –> air flows down airways into alveoli

Inspiratory muscles relax –> lung recoils –> alveoli decrease volume (pressure increases) –> air flows out of lung

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21
Q

Exercise/lung disease breathing

A

Expiration may become active

Abdominal muscles and internal intercostals used –> further alveoli compression and expiration

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22
Q

Repiratory zone: Contents and characteristics

A

Respiratory bronchioles, alveloar ducts, alveoli - gas exchange

Large surface area

Large volume of gas maintain diffusion pressure gradient

Very thin membrane

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23
Q

Thin alveolar blood gas barrier contents

A

Respiratory epithelium

INterstitial space

Capillary endothelium

Plasma

Erythrocyte

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24
Q

Gas diffusion and heart pumping

A

Oscillating nature of heart provides energy to gas in small airways and increases diffusion

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25
Q

Non respiratory function of lung - Maintenece and defense

A

Keeps itself clean via cleansing mechanisms and innate/adaptive immunity

Constant turnover and remodeling

Surfactant to maintain alveolar compliance

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26
Q

Non respiratory function of lung - filtering

A

Small capillaries can filter out physical material (clots, foreign bodies etc)

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27
Q

Non respiratory function of lungs - chemical processing

A

Hormone production: ACTH, prsotaglandings, vasoactive peptides, GF, serotonin

ACE

Arachiadonic acid release after pulomnary endothelium damage

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28
Q

Physiological dead space

A

Sum of:

Anatomic dead space (conducting airways)

Gas in NON PERFUSED alveoli (no gas exchange occurs)

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29
Q

Alveolar ventilation and PaCO2

A

Inversely proportional

Double alveolar ventilation = halved arterial CO2

Halved alveolar ventilation = double arterial CO2

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30
Q

Driving force of oxygen between alveoli and capillary

A

60mmHg towards capillary

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31
Q

Driving force of CO2 between alveoli and capillary

A

5mmHg towards alveoli

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32
Q

Perfusion limitation

A

Diffusion is controlled by perfusion

No blood flow = equilibration of gasses and no more diffusion

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33
Q

Conditions that cause O2 transfer to become diffusion limited

A

Thickening of alveolar capillary membrane

High altitude/Low FIO2

Increased pulmonary blood flow

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34
Q

Diffusion limited O2 transfer - thickening of capillary membrane

A

Increases time for diffusion across membrane

Decreases rate of diffusion

Sever pulmonary diseases - pulmonary fibrosis

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35
Q

Diffusion limited O2 transfer - Low FIO2/high altitude

A

Decreased alveolar O2 pressure and decreased gradient across alveolar membrane

Decreases rate of diffusion

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36
Q

Diffusion limited O2 transfer - Increased pulmonary blood flow

A

Increased cardiac output = blood moves rapidly through lung and complete saturation is not achieved

Diffusion is not fast enough to keep up with perfusion

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37
Q

Amount of dissolved O2 in 1L of blood

A

3mL at PO2 of 100mmHg

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38
Q

Majority of oxygen in blood is located where…?

A

Bound to Hb

~96%

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39
Q

1g of Hb contains how much O2 when 100% saturated

A

1.34mL

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40
Q

Hb saturation in lung vs tissues

A

Hb in lung is almost 100% saturated

Hb in tissue is <60% saturated (O2 leaves Hb to go to tissue)

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41
Q

Left shift of HbO2 curve - causes and meaning

A

Hb has higher affinity for O2 at lower partial pressure

Decreased PC02

Increased pH (Decreased H)

Decreased temp

Decreased 2,3 BPG

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42
Q

HbO2 curve shifted to right - causes and meaning

A

Lower affinity to Hb given partial pressure of O2

Increase PCO2

Decrease pH

Increase temp

Increased 2,3 BPG

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43
Q

CO poisoning

A

Super high affinity to Hb, making it unavailable to carry Oxygen

When Hb binds to CO, P50 decreases and increases affinity for oxygen

Less oxygen carried and less oxygen released

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44
Q

Fetal hemoglobin

A

Higher affinity for O2

HbO2 shifted to left, decreased P50

Need to be able to take oxygen from placenta to fetus

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45
Q

Adequate delivery of oxygen to tissues requires:

A

Oxygen content in blood: Adequate PaO2 and hemoglobin

Cardiac output: Adequate delivery of oxygen to arteries

Vascular supply: Adequate delivery of oxygen to tissues

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46
Q

Hypoxemic hypoxia

A

Low PaO2 –> low oxygen saturation of Hb

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47
Q

Anemic hypoxia

A

PaO2 is normal

Oxygen carrying capacity is low –> low O2 content

Anemia

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48
Q

Circulatory hypoxia

A

Oxygen content normal

Blood flow to tissues reduced

Shock

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49
Q

Histotoxic hypoxia

A

Oxygen content and blood flow is normal

Tissue cannot use oxygen at cellular level

Cyanide poisoning

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50
Q

Carriers of CO2

A

Physical solution

Bicarbonate

Carbamino compounds (CO2 bound to NH4 on Hb)

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51
Q

Solubility of CO2

A

20x more solube than O2

.06mL CO2 dossolved/100mL blood per mmHg partial pressure

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52
Q

Major form of CO2 carried in blood

A

HCO3 in RBC

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53
Q

Deoxygenated Hb and Carbonic anhydrase equation

A

Deoxygenated hemoglobin accepts H+ –> reduces H+ –> drive reaction to HCO3

Tissues = deoxygenated Hb = H acceptance = CO2 pickup as HCO3

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54
Q

Oxygenated Hb and Carbonic anhydrase equation

A

Oxygenated Hb releases H+ and drives reaction towards CO2

Oxygenated Hb in lungs = released H+ = CO2 production

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55
Q

Difference between CO2 curve and O2 curve

A

Higher total content of CO2 in blood per mmHg partial presure

Steeper slope (more change in CO2 content per change in PCO2)

No effective plateau or max content

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56
Q

Haldane effect

A

As PO2 increases, CO2 dissociation curve shifts downward

Less CO2 carried in blood

Lungs: Blood takes up oxygen, CO2 released and expired

Tissues: Blood releases oxygen, increases capacity for CO2, takes up CO2 to transport ot lungs

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57
Q

Law of mass action and CO2: Lungs and tissue

A

Lung: PCO2 drop causes carbamino compounds and Bicarb to generate CO2 (In RBC)

Tissues: Increase in PCO2 forms HCO3 and carbamino compunds for transfer to lungs

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58
Q

RBC Carbonic anhydrase action in lungs

A

HCO3 decreases rapidly b/c forming H20 + CO2

Decrease in RBC HCO3 = HCO3 diffuses into cell = Cl exit from cell

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59
Q

RBC carbonic anhydrase in tissues

A

HCO3 rapidly increases inside RBC –> diffuses out of cell –> Cl entry

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60
Q

Ventilation/Perfusion (V/Q) ratio and CO2?O2 levels

A

Increased V/Q = increased ventilation = increased O2 and decreased CO2 (removal of CO2 and delivery of fresh O2)

Decreased V/Q = increased perfusion = decreased O2 and increased CO2 (Increased CO2 delivery with less O2, increased gas exchange)

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61
Q

V/Q at bottom/base of lung

A

Decreased V/Q

Perfusion higher than ventilation

Bottom of lung will have higher PCO2 and lower PAO2

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62
Q

V/Q at top/apex of lung

A

Increased

More ventilation relative to perfusion

Increased PAO2 and decreased PCO2

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63
Q

V/Q = infinity = ?

A

Highest amount of Oxygen and no CO2

Dead space, no perfusion, no gas exchange

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64
Q

V/Q = 0 = ?

A

No ventilation and complete perfusion

High CO2 and no O2

Shunt, blood does not get oxygenated

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65
Q

Compensatory response of hypoventilated part of lung

A

Other lung units can hyperventilate and lower CO2

Average all units CO2 to get CO2 of lungs

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66
Q

Compensatory O2 response of hypoventilated lung

A

Mixed blood O2 is NOT average of different units because hyperventilation of other units does not increase O2, saturation has already occurred

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67
Q

Central hypoventilation gas result and treatment

A

Central hypoventilation results in an increased PaCO2 which results in a decreased PAO2

Giving oxygen with an increased FIO2 can overcome this

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68
Q

Steps to find cause of hypoxemia

A

Calculate PAO2 and decide if hypoventilation is cause

If not hypoventilation –> measure diffusion capacity to see if there is diffusion limitation

If not diffusion limitation –> V/Q mismatch or shunt. Give oxygen: V/Q mismatch will resolve, R->L shunt will not

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69
Q

Tidal volume

A

Amount of air exchanged with each breath

~7.5L/min

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70
Q

Residual volume

A

Volume of gas left in lung after a complete expiration

Unable to completely empty lung because we cannot completely collapse chest

25% TLC

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71
Q

Inspiratory reserve volume

A

Volume of air that can be inspired from end of tidal inspiration to total lung capacity

Use if need to take deeper breath

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72
Q

Expiratory reserve volume

A

Volume of air we can exhale from end of tidal expiration

Forced exhale, dry cough

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73
Q

Total lung capacity

A

Total lung capacity

Volume at which inspiratory muscles are no longer strong enough to overcome expiratory recoil of lung and chest wall

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74
Q

Vital capacity

A

Volume of air that can be exhaled from TLC to RV

All volumes except RV

Measure by asking pt to inspire completely and expire into spirometer

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75
Q

Functional Residual capacity

A

Volume of gas in lungs at end of tidal expiration

Sum of ERV and RV

FRC prevent hypoxemia during exhalation

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76
Q

Inspiratory capacity

A

Complement of FRC

TLC = FRC + IC

Sum of TV + IRV

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77
Q

Non compliant lung

A

Require greater pressure change for each breath

Restrictive

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78
Q

Surfactant

A

Complex protein/phospholipid taht interrupts surface tension laws of lung

Low surface tension when area is small

High surface tension when surface area is large

Accounts for hysteresis in lung inflated with air

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79
Q

Surfactant and low/high volumes

A

Low volume inflation –> surfactant is in water layer and not at surface, does not reduce surface tenstion

High volume inflation –> surfactant spreads on surface and reduces surface tension

Lung more compliant at higher volume (inflated)

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80
Q

Pleural pressure gradient in lung

A

Occurs due to weight of lung

Top of lung: No weight added, pleural pressure at its most negative

Bottom of lung: Lung weight added and causes less negative pleural pressure

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81
Q

Pleural pressure gradient and alveoli

A

Alveoli at apex will be higher percent of max volume compared ot base of lung

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82
Q

Lung base: pleural pressure, alveolar volume

A

Pleural pressure is less negative

Alveoli at a lower volume

Alveoli are more compliant

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83
Q

Lung apex: Pleural pressure and alveolar volume

A

Pleural pressure is more negative

Alveoli at higher volume

Apex alveoli are less compliant

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84
Q

Pulmonary HTN definition

A

Resting mean pulmonary arterial pressure >25mmHg

Normal is between 8 and 20mm Hg

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85
Q

Pulmonary arterial HTN (PAH) definition

A

Mean pulmonary arterial pressure >25mm Hg

PUlmonary venous (pulmonary capillary wedge) pressure <15

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86
Q

Group 1 PAH

A

Pulmonary arterial HTN

Idiopathic PAH

Inherited

Connective tissue disease, HIV, portal HTN, congenital heart disease

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87
Q

Group 2 Pulmonary HTN

A

Pulmonary HTN due to left heart disease

Systolic dysfunction

Diastolic dysfunction

Valvular disease

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88
Q

Group 3 Pulmonary HTN

A

Pulmonary HTN due to lung disease and/or hypoxia

COPD

Interstitial lung disease

Sleep disordered breathing

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89
Q

Group 4 pulmonary HTN

A

Chronic thromboembolic pulmonary HTN

CTEPH

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90
Q

Components of pulmonary pressures

A

Pulmonary venous pressure/LA pressure

Pulmonary vascular resistance

Right sided Cardiac Output

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91
Q

Causes of increased pulmonary venous pressure

A

Left ventricular or diastolic dysfunction

MItral valve disease

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92
Q

Causes of increased pulmonary vascular resistance

A

Conditions that decreases area of pulmonary vascular beds (pulmonary emboli, CT disease, interstitial lung disease, COPD)

Conditions that induce hypoxic vasoconstriction

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93
Q

Causes of increased right sided cardiac output

A

L–>R ASD

L–>R VSD

Other systemic –> pulmonary shunts

Increases Right Ventricular volume

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94
Q

Pulmonary HTN sequence of events

A

Initiatl injury –> mild P HTN –> elevated pressure damages pulmonary vasculature –> narrowed pulmonary vascular bed –> RV hypertrophy to overcome increased resistance –> vascular injury accelerates with increased pulmonary arterial pressure –> increased RV afterload –> RV failure

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95
Q

Genetic predisposition to PAH

A

Genetic mutations in bone morphogenetic protein receptor type 2

BMPR2

Inuces apoptosis in certain cell types

Permits excess endothelial cell grownt and proliferation in response to injury

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96
Q

Sigaling pathways disturbed in PAH

A

Decreased prostacyclin and decreased Nitric Oxide pathways –> Inhibit vasodilation and increases proliferation

Increased endothelin pathway –> Vasoconstriction and increased proliferation

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97
Q

Pulmonary HTN clinical presentation and physical exam

A

Dyspnea on exertion and fatigue

RV failure = ankle swelling

Exertional chest pain, syncope can develop

Increased intensity of pulmonic component of S2

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98
Q

Community acquired pneumonias

A

95% due to viral, mycoplasma, pneumococcal, or Leigonella infections

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99
Q

Nonsocomial pneumonias

A

1% of hospital patients

ICU patients at highest risk

G(-) bacilli

Staph Aureus

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100
Q

Aspiration pneumonias

A

Caused by aspiration of infective material and/or gastric contents

Anaerobic bacteria

Chemical pneumonitis, necrotizing pneumonia, lung abscess, empyema

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101
Q

Pneumonia in immunocompromised hosts

A

Suppressed immune system due to disease or drugs

Opportunistic organisms

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102
Q

Pathogenesis of pneumonia

A

Loss of defense mechanisms

  1. Inhibition of normal cough reflex from NM disease, drug overdose, intubation, coma –> allows gastric contents/oropharyngeal flora to aspirate into lungs
  2. Injury of mucociliary apparatus prevents clearance of small inhale particles/microorganisms: Viral destruction, smoking, genetic disease
  3. Interference of phagocytic or bactericidal action of alveolar macrophages - alcohol, tobacco smoke, snoacia
  4. Bronchial obstruction - neoplasm, mucus plugging –> prevents clearance
  5. Decreased immunity
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103
Q

Alternative factors/mechanisms of pneumonia pathogenesis

A

Direct introduction of organisms into sterile lung by intubation/contaminated respiratory equipment

Hematogenous spread of infections

Bacteria common to hospital environments are often drug resistant

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104
Q

Bacterial pneumonia classification

A

Based on etiological agent and anatomic distribution pattern

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105
Q

Clinical presentation, PE, CXR of bacterial pneumonia

A

Malaise, fever, chills, pleuritic pain, productive cough (blood tinged)

Decreased breath sounds in affected lobes, expiratory rales

May have Leukocytosis with left shift

CXR - focal opacaties and occasionally pleural effusions

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106
Q

Most common organism causing pneumonia in ambulatory patients

A

Strep Pneumoniae

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107
Q

Most common cause of pneumonia in hospitalized patients

A

Gram(-) bacilli (Pseudomonas, Klebsiella, Proteus, E Coli)

Reach lungs via upper airways or through blood

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108
Q

Upper respiratory viral infections follwe dby…

A

Staphylococcal and Haemophilus

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109
Q

Legionella pneumophila

A

Associated with aerosols from cooling systems

Multiple small abscesses

Only grows on special media, may be missed on culture

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110
Q

Pathology: Bronchopneumonia

A

Lobular pneumonia

Gross: Patchy consolidation. Infiltrates associated with airways and represent extension of preexisting bronchitis/bronchiolitis

Microscopic: Alveolar spaces filled with suppurateive exudate composed of PMN, RBC, fibrin, edema, macrophages

Alveolar septa hyperemic and congested, not inflamed

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111
Q

Pathology: Lobar pneumonia

A

Gross/microscopic:

Consolidation by fibrinopurulent material is widespread and involves entire lobes/lobules

Rarely seen

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112
Q

Complications of bacterial pneumonia

A
  1. Abscess
  2. Empyema
  3. Organization
  4. Bacteremic dissemination
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113
Q

Complication of bacterial pneumonia: Abscess

A

Local suppurative process

Destruction of lung tissue and accumulation of neutrophils

Associated with aspiration, septic emboli, and bronchial obstruction

Strep Pneumoniae

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114
Q

Organism that most commonly causes abscess in pneumonia

A

Strep Pneumoniae, Pseudomonas aeruginosa, Staph aureus, anaerobes

Contain enzymes that liquify lung tissue

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115
Q

Complication of bacterial pneumonia: Empyema

A

Purulent inflammation of pleural space caused by spread of infection into pleural cavity

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116
Q

Complication of bacterial pneumonia: Organization

A

If fibrinous alveolar exudate is not broken down and reabsorbed –> organization

Formation of intraalveolar plugs of granulation tissue composed of fibroblasts, fibrin, and inflammatory cells

Can mature into fibrous tissue –> Scarring

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117
Q

Complication of bacterial pneumonia: Bacteremic dissemination

A

Sepsis

Spread to other organs

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118
Q

Viral pneumonias - more common in children or adults

A

Children

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119
Q

Clinical presentation of atypical pneumonias

A

Fever, headache, muscle aches

Dry, hacking, non productive cough

Most common complication is secondary bacterial pneumonia

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120
Q

Atypical pneumonia gross appearance

A

Discrete infiltrates, difficult to appreciate

Rare pleural effusions

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121
Q

Microscopic appearance of atypical pneumonias

A

Mononuclear interstitial inflammatory infiltrate within walls of alveoli

Alveolar septa widened and edematous, alveolar space may contain protein rich fluid

Type II pneumocytes are hyperplastic

Alveolar wals lined by hyaline membranes

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122
Q

Herpes, varicela, adenovirus atypical pneumonia microscopic appearance

A

Necrosis of bronchial and alveolar epithelium

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123
Q

CMV, herpes, and measles atypical pneumonia microscopic appearance

A

Viral inclusions within infected cells

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124
Q

Chronic Granulomatous infection categories

A

Fungal infections

TB

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125
Q

Pneumonial fungal infections

A

Coccidiomycosis

Histoplasmosis

Blastomycosis

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126
Q

Coccidiomycosis

A

Fungal infection caused by Coccidioides

Southwest US

Lung lesions, pleuritic pain, cough

Seen in tissue as large double walled spherules - filled with endospores

Granulomatous inflammation with giant cells and macrophages

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127
Q

Histoplasmosis

A

Fungal infection caused by Histoplasma

Central US

Usually asymptomatic until immunocompromised

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128
Q

Blastomycosis

A

Funcgal infection caused by Blastomyces

Eastern US

Granulomatous response

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129
Q

Tuberculosis

A

Mycobacterial infection caused by Mycobacterium tuberculosis

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130
Q

TB: Pattern of infection

A

Primary infection: Granulomas in lung and lymph nodes that frequently calcify

Secondary infection: Re activation. Usually in apices

Fibrocaseous disease: Upper lobe, cavities common

Miliary Spread: Hematogenous dissemination, innumerable micronodules in lungs, liver, spleen etc

Bronchopneumonia: Seen in overwhelming disease

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131
Q

TB clinical presentation

A

Primary infection - asymptomatic or flu like disease

Secondary infection - more severe symptoms

Erosion of lesions into blood vessels –> hemoptysis

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132
Q

TB pathology

A

Caseating granuloas

Epithelioid histocytes surrounded by lymphocytes, fibroblasts, giant cells

Central caseous necrosis

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133
Q

Progressive pulmonary TB

A

Active lesions may continue to progress –> cavitary fibrocaseous TB, miliary dissemination, TB bronchopneumonia

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134
Q

Opportunistic infections

A

Pneumocystis jiroveci

Aspergillus

Zygomycetes

Cryptococcus

Candida/torulopis

CMV, HSV

Actinomyces and Nocrdia

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135
Q

Pneumocystis jirovechi

A

Alveolar infiltrate of foamy material and mononuclear cells

Seen in HIV pts with CD4 <200

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136
Q

Aspergillus

A

Ubiquitous fungal organism found in soil and inhaled into lungs

Colonize old cavities from previous disease and grow as fungus ball

Can invade parenchyma and produce necrotizing pneumonia

Invades arteries and veins –> hemorrhagic infarcts

Septae hyphae branching @ 45 degree angle

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137
Q

Zygomycetes

A

Invade arteries and veins

Hyphae are pauciseptate and branch at 90 degree angle

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138
Q

Cryptococcus

A

Inhaled encapsulated yeast which causes mild pulmonary symptoms

Often spreads to CNS

Thick gelatinous capsule which appears as halo after tissue fixation

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139
Q

Candida and Torulopis

A

Produce bronchitis,bronchopneumonia, hemorrhagic pneumonia, acute abscesses

In immunicompromised patients

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140
Q

CMV and HSV

A

Hemorrhageic interstitial pneumonias

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141
Q

Actinomyces and nocardia

A

Filamentous branching bacteria which produce acute pneumonia with rapid progression to abscesses

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142
Q

FEV1/FVC less than LLN = ?

A

Obstructive defecit present

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143
Q

FVC less than LLN = ?

A

Restrictive deficit

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144
Q

Pulmonary circulation, pressure and resistance?

A

Low pressure, low resistance system

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145
Q

Gravity and pulmonary circulation

A

Apex: Low vascular pressure, collapsed vessels

Base: High vascular pressure, distended vessels

Interstitial pressure most negative at apex –> alveolar pressure is greatest at apex –> compresses vessels

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146
Q

Zone 1 of lung

A

Apex of lung

Palveoli > Parterial > Pvenous

No flow conditions, vessels collapsed shit

Alveolar dead space

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147
Q

Zone 2 of lung

A

Parterial > Palveolar > Pvenous

Arterial pressure is greater than alveolar so there is flow

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148
Q

Zone 3 of lung

A

Parterial > Pvenous > Palveolar

Continuous flow

Blood pressures at either end of system determine flow

Vessels completely distended

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149
Q

Extrapulmonary vessel distention at apex and base of lung

A

Apex: Fully distended b/c not exposed to alveolar pressure AND pleural pressure most negative

Base: Collapsed b/c pleural pressure least negative

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150
Q

Passive effects on pulmonary vascular resistance

A
  1. Vascular pressures
  2. lung volume
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151
Q

Vascular pressure effects on pulmonary vascular resistance

A

Increased vascular pressure = distended vessels = decreased resistance

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152
Q

Pulmonary vascular resistance during exercise

A

Increased CO = increased pulmonary artery pressure = Decreased pulmonary vascular resistance

  1. Vessels distended = decreased resistance
  2. Opening of closed (zone 1) vessels increases total cross sectional area = decreased resistance
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153
Q

Pulmonary vascular resistance during shock

A

Decreased cardiac output = decreased pulmonary vascular pressure = collapsed vessels = increased resistance

De-recruitment of upper zones due to drop in pressure and collapse of vessels

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154
Q

Lung volume and pulmonary vascular resistance

A

High lung volume: Intra-alveolar vessels = collapsed, extra-alveolar = distended

Low lung volume: Intra-alveolar vessels = distended, extra-alveolar vessels collapsed

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155
Q

Intra-alveolar vessels have lowers resistance at what volume

A

Residual volume (lowest volume)

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156
Q

Extra-alveolar vessels have lowest resistance at what volume

A

TLC, highest volume

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157
Q

Active regulation of pulmonary vascular resistance

A
  1. Neural
  2. Local
  3. Humoral
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158
Q

Local control of pulmonary vascular resistance

A
  1. Alveolar hypoxia causes vasoconstriction. Shunt blood to ventilated areas of blood
  2. Acidosis, hypercapnia, and prior smooth muscle hypertrophy accentuate the hypoxic vasoconstrictive response

Pulmonary vascular resistance is highest when alveolar hypoxia occurs in the face of acidemia

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159
Q

Pulmonary edema types

A

Hydrostatic edema

Non hydrostatic edema

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160
Q

Hydrostatic edema

A

Pulmonary edema due to increased pulmonary capillary pressure

Fluid backup:

Mitral valve stenosis

LV failure

Fluid overload due to renal failure

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161
Q

Non hydrostatic pulmonary edema

A

Chemical/thermal injury: Chemical inhalation, drowning, smoke inhalation

Humoral and immune injury: Endotoxin, prolonged shock, head injury

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162
Q

Receptors that monitor effects of breathing

A
  1. Chemoreceptors - respond to O2, CO2, and pH
  2. Mechanoreceptors - Respond to mechanical information from respiratory pump
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163
Q

Dorsal Respiratory Group

A

Inspiration

Controls basic rhythm of breathing

Quiescence –> crescendo of neuronal activity (inspriation) –> quiescence (expiration occurs here)

Input from CN IX/X

Output via phrenic nerve to diaphragm and other outputs to chest wall/upper airway muscles

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164
Q

Ventral Respiratory group

A

Expiratory area is inactive during normal respiration (expiration is passive during quiet breathing)

Exercise/lung disease - Activity in these neurons for active expiration

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165
Q

The Apneustic Center

A

Lower pons

Brainstem damage above this area results in apneustic breathing –> isolated from pneumotaxic center

Sends signals to DRG that prolong duration of excitatory ramping of diaphragm activity

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166
Q

Apneustic breathing

A

Prolonged inspiratory gasps with rapid expiration

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167
Q

Pneumotaxic Center

A

Upper pons

Responsible for ending inspiration, terminates inspiration activity

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168
Q

Central chemoreceptor

A

Primary chemical control of regular quiet breathing

Ventro-lateral medulla, close contact with CSF

Increased CO2 = increased ventilation

Chemoreceptor senses H+ difference (carbonic anhydrase equation)

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169
Q

Peripheral chemoreceptor locations and respond to ?

A

Carotid and aortic bodies

Respond to:

  1. Decreased PaO2
  2. Increased PaCO2
  3. Increased H+ (decreased pH)
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170
Q

Ventilatory response to hypoxia

A

Increase in peripheral chemoreceptor activity with PaO2 less than 500

NON LINEAR RESPONSE

Minimal increase until PaO2 less than 100

Dramatic increase when PaO2 less than 60

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171
Q

Pulmonary stretch receptors

A

Slowly adapting receptors that respond to stretching of airways

Transmit information via vagus

Responsible for vagal mediated inhibition of inspiration and promotion of expiration

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172
Q

Pulmonary irritant receptors

A

Extra-pulmonary airway epithelium

Rapidly adapting

Under conditions of continued irritation –> adapt and reduce activity

Respond to:

  1. Chemical irritation: Gas, antigens, inflammatory mediators
  2. Physical irritation: Airflow, particulates, bronchial smooth muscle tone
  3. Lung volume: Initiate sighs to maintain lung volume
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173
Q

Juxtacapillary Receptors

A

Located in alveolar walls near capillaries

Connect to central controllers via unmyelinated fibers, rapidly adapting

Stimulated by interstitial edema, inflammation

Also stimulated by increased left atrial and pulmonary venous pressure

Cause laryngeal closure and apnea, followed by shallow rapid breathing

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174
Q

Chest wall proprioceptors

A
  1. joint receptors
  2. Tendon receptors
  3. Muscle spindle receptors
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175
Q

Joint receptors

A

Ruffini, pacinian, golgi organs

Activity proportional to rate of rib movement

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176
Q

Tendon organs

A

PResent in intercostal and diaphragm muscle tendons

Monitor force fo contraction and inhibit inspiration

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177
Q

Muscle spindle receptors

A

Abundant in intercostals, rare in diaphragm

Stabalize rib cage and compensate for changes in body positions

Passive stretch –> increase afferent activity –> stimulate alpha motor neuron –> contract intercostal muscle

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178
Q

Respiratory control failure and disease states: Increased work of breathing

A

Obstructive diseases: COPD, obesity, sleep apnea

Causes response to CO2 to be blunted –> rise in CO2

Due to down regulation of response system due to maximum amount of work level reached

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179
Q

Respiratory control failure and disease states: Decreased efficiency of gas exchange

A

More work needed to achieve same result

Can lead ot diminished ventilatory drive

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180
Q

Respiratory control failure and disease states: Impaired ventilatory pump performance

A

Hyperinflation due to obstruction stretches inspiratory muscles and they become inefficient

Chest wall restriction (muscular dystrophy) also decreased ventilatory response

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181
Q

Respiratory control failure and disease states: Chronic CO2 retention

A

Leads to bicarb reabsorption in kidney causing metabolic alkalosis

Bicarb enters CSF over time and buffers change in H normally associated with CO2 increase

Abolishes central chemoreceptor drive

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182
Q

CFTR gene and mutation

A

DF508

Deletion of Phenylalanine at 508 position

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183
Q

CFTR protein

A

ATP binding anion channel

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184
Q

Pathophysiology of CF respiratory disease

A

Mucociliary clearance dysrupted due to inadequate hydration of airway surface liquid

Increased activity of ENaC –> Cl entry via electrochemical gradient –> water entry into cell –> decreased airway surface liquid

No mucociliary clearance = higher risk of infection, inflammation, obstruction –> chronic lung disease

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185
Q

Most common infective organism in CF

A

Pseudomonas

Staph aureus

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186
Q

CF is what type of lung disease?

A

Obstructive

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187
Q

Pathophysiology of CF GI disease: exocrine

A

Exocrine pancreatic insufficiency:

Autodigestion of pancreas w/ fibrosis, cysts, fatty replacement –> no enzyme production

–> Maldigestion of fats/proteins

Can cause bowel obstruction

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188
Q

Pathophysiology of CF GI disease: Other

A

CF Diabetes mellitus

Hepatobiliary disease: Inadequate bile flow, altered bile salts, inadequate bicarb concentration in bile –> Cholelithiasis, cholecystitis, biliary cirrhosis + portal HTN

GERD: Lung hyperinflation + reduced GI motility

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189
Q

Pathophysiology of CF genitourinary disease

A

Male infertility: Absence of vas deferens secondary to blockage/inflammation/fibrosis

Female reduced infertility: Failure of normal thinning of cervical mucus at ovulation

Nephrolithiasis: 5%

190
Q

CF salt loss in sweat

A

Normal sweat physiology: As sweat moves up duct, Na absorbed and Cl follows

CF sweat physiology: High sweat Cl values b/c Cl not reabsorbed

Increased Cl loss can lead to dehydration and metabolic alkalosis

191
Q

CF Sweat Test

A

Pilocarpine Iontophoresis

192
Q

Neonatal CF presentation

A

Meconium ileus

Prolonged jaundice (slow bile clearance)

193
Q

Positive newborn screen for CF

A

Immunoreactive trypsinogen elecated

If elevated then do genetic testing

Sweat testing

194
Q

CF presentation in infancy

A

Respiratory disease: Persistent wheezing/coughing, opacities on CXR, Staph pneumonia

Failure to thrive due to pancreatic insufficiency

Malabsorption/steatorrhea

Fat soluble (ADEK) vitamin deficiency (pancreatic insufficiency)

Metabolic alkalosis (Cl loss)

195
Q

CF presentation in childhood

A

Same as infancy

Greater risk for bronchiectasis/chronic sputum, digital clubbing, and airway obstruction on PFT

Rectal prolapse

Distal intestinal obstruction syndrome (thick dry stool)

Liver disease

Chronic/recurrent pancreatitis

Nasal polyps and sinusitis

196
Q

CF adolescence/adulthood presentation

A

Greater risk of advanced lung disease

Chronic pansinusitis

Bronchiectasis complications - pneumothorax/hemooptysis

More advanced liver disease

Azoospermia

197
Q

CF Diagnosis

A

One or more clinical features

+

Two CF mutations OR Two positive sweat tests OR abnormal nasal potential difference

198
Q

CF treatment categories

A

Lung treatment

Chest clearance

Anti infective

Anti inflammatory

Pulmonary exacerbations

Lung transplant

Chronic sinusitis

199
Q

CF treatment - Chest clearance

A
  1. Chest physiotherapy w/manual chest compression
  2. Bronchodilator
  3. Aerosolized hypertonic saline - Increase water, stimulate cough, shrink mucosa or airways
  4. Dornase alfa - Recombinant DNAse that breaks up DNA in sputum which liquefies it
  5. Exercise
200
Q

CF treatment - anti infective

A

Inhaled, Oral, IV antibiotics

Anti fungal

Anti mycobacterial

201
Q

CF treatment - Pulmonary exacerbations

A

Increased lung symptoms, loss of function, weight loss

Comprehensive therapy: IV antibiotics, chest clearance, nutrition, anti inflamm

202
Q

CF treatment - anti infective

A

Inhaled antibiotics - Psudomonas

Oral - Pseudomonas, Staph (mild exacerbations)

IV - Treat exacerbations

Anti fungal - aspergillus

Anti mycobacterial

203
Q

CF nutritional treatment

A

Good nutrition is essential

High calorie, high fat

Salt supplementation in infants

204
Q

CF enzyme replacement

A

Replace pancreatic enzymes

205
Q

Asthma definition

A

Chronic inflammatory disorder of airways

Mast cells, eosinophils, T cells, macrophages, PMN, epithelial cells

Bronchial hyper-responsiveness to normal stimuli

206
Q

Classic asthma pathogenesis

A

Th2 cell dependent, IgE mediated allergic disease

CD4 T cells, mast cells, eosinophils

Typical TH2 cytokines (IL-13, IL-4, IL-5)

207
Q

Asthma hygeine hypothesis

A

Increased hygiene and cleanliness reduces proper immune system development via environmental cues

Normally immune system shifted away from Th2 response

208
Q

Asthma triggers

A

Allergens

Infections

Exercise

Cold air

Air pollution

Cigarette smoke

Beta Blockers/NSAIDs

Emotions

209
Q

Clinical presentation for asthma diagnosis

A

Wheeze

Cough

Dyspnea

Chest tightness

Worse symptoms at night

210
Q

Chest exam during acute asthma attack

A

Expiratory wheezing

Hyperinflation

Prolonged expiratory time

211
Q

Early response of airway to asthma

A

Bronchospasm

Edema

Airflow obstruction

212
Q

Late response of respiratory system to asthma

A

Airway inflammation

Airflow obstruction

Airway hyper-responsiveness

213
Q

COPD definition

A

Airflow limitation that is not fully reversible

Progressive and associated with abnormal inflammatory response of lungs to noxious particles/gases primarily caused by cigarette smoking

214
Q

Obstructive lung disease - bronchospasm

215
Q

Obstructive lung disease - destruction of alveolar walls

216
Q

Obstrucive lung disease - small airways abnormalities

A

Chronic obstructive bronchitis

217
Q

Genetic cause of emphysema

A

Alpha-1 Antitrypsin Deficiency

SERPINA1 gene

Protease inhibitor that protects lung from neutrophil elastase and neutrophil mediated destruction

218
Q

Severity measurement of COPD

A

Level of FEV1 decrease

219
Q

Categories of obstructive lung disease drugs

A

Bronchodilators

Anti inflammatory agents

220
Q

Bronchodilator categories

A

Beta agonists

Anti cholinergics

Theophylline

221
Q

Anti inflammatory agent categories

A

Corticosteroids

Comolyn/Nedocromil

Leukotriene inhibitors

222
Q

Beta agonist overview

A

Most effective bronchodilators for asthma

Antagonize bronchosconstriction in airways of all sizes

Short acting so helpful for acute dyspnea and wheezing episodes

223
Q

Route of administration for Beta agonists

A

Inhalation

Decreases plasma concentration and reduces side effects

More rapid and effective

224
Q

Beta agonist adverse effects

A

Tremor - skeletal muscle stimulation

Palpiatation - Peripheral vascular vasodilation –> cardiac response

Hypokalemia in high doses

225
Q

Anti Cholinergics

A

Atropine use is limited by side effects

Tachycardia, blurred vision, dry mouth, urinary retention

226
Q

Ipratropium

A

Anticholinergic

Poorly absorbed into systemic circulation and produces no significant side effects

227
Q

Anti cholinergic MoA

A

Bronchodilation by anatagonizing ACh on M receptors in airway smooth muscle

228
Q

Tiotropium

A

Long duration of action and is used for COPD

229
Q

Theophylline

A

Second line therapy for asthma and COPD

Unclear MoA but, smooth muscle relaxation, improved diaphragmatic contraction, increased mucociliary clearance

230
Q

Theophylline pharmacokinetics

A

Metabolized by cytochrome system in liver

Affected by inhibtors/inducers of Cytochromes

231
Q

Theophylline toxicites/adverse effects

A

Nausea, tremor, headache, agitation, insomnia

Severe toxic effects at high doses - seizures and arrhythmias

232
Q

Theophylline indications

A

Second line therapy

Only after failure of primary drugs

233
Q

Corticosteroids

A

Bind to GR and prevent downstream effects ie inflammation

234
Q

Adverse effects of corticosteroids

A

General - Cushingoid, immune suppression, infection

Endocrine - Adrenal insufficiency, glucose intolerance

MSK - Osteoporosis/compression fractures, myopathy

Ophto - Cataracts, glaucoma

CV - HTN

Psych - Psychosis

GI - Pancreatitis

Cutaneous - Purpura, delayed wound healing

235
Q

Inhaled corticosteroids

A

Reduce symptoms, improve lung function, decrease bronchial hyperresponsiveness compared to inhaled B2 agonists

236
Q

Pharmacokinetics of inhaled corticosteroids

A

80-90% of inhaled drug and deposited in oropharynx and swallowed

Absorbed and causes systemic effects

10-20% reaches respiratory tract

237
Q

Inhaled corticosteroid drugs

A

Beclomethasone

Budesonide

Fluticasone

Mometasone

238
Q

Adverse effects of inhaled corticosteroids

A

Oropharyngeal candidiasis (high doses)

Dysphonia (myopathy of laryngeal muscles)

Slow growth in children

239
Q

Indications for corticosteroids

A

Most effective for treatment of acute exacerbations and chronic asthma

Inhaled corticsteroids are first line therapy for chronic asthma

Systemic corticosteroids are used for acute exacerbations of COPD

Chronic COPD - documented improvement with steroids or patients with severe COPD and repeated exacerbations

240
Q

Cromolyn sodium and nedocromil sodium

A

Anti inflammatory effects and improve bronchial hyperresponsiveness with chronic therapy

Protect against bronchoconstrictive stimuli (exercise)

241
Q

Cromolyn sodium and nedocromil sodium administration and side effects

A

Inhaled

No important side effects

242
Q

Leukotriene inhibitors

A

Prevent synthesis and action of leukotrienes

Block receptors OR block 5-lipooxygenase so no synthesis

Montelukast

Oral administration

243
Q

Asthma treatment

A

Step wise approach

All start with short acting Beta2 agonist for as needed

If not controlled then “controller agent” added - low dose inhaled corticosteroid

244
Q

Acute severe asthma exacerbation treatment

A

Inhaled short acting B2 agonist

Systemic corticosteroid therapy

245
Q

COPD treatment

A

Bronchodilator medications are most important: B2 agonists, anti cholinergic, theophylline

Prolonged inhaled corticosteroid treatment does not modify long term lung damage

246
Q

Acute COPD exacerbation treatment

A

Inhaled B2 agonist

Inhaled anti cholinergic

Systemic corticosteroid

247
Q

Etiologies of rhinitis

A

Allergic rhinitis - IgE mediated inflammation

Acute viral rhinitis - common cold

Non allergic noninfectious rhinitis - vasomotor rhinitis

248
Q

Classes of drugs for rhinitis

A

Decongestants

Antihistamines

Cromolyn

Corticosteroids

Anti cholinergics

Leukotriene inhibitors

249
Q

Decongestants

A

Alpha adrenergic receptor agonists

Produce vasoconstriction and decreases nasal congestion and blockage

250
Q

Decongestant adverse effects and contraindications

A

Restlessness and insomnia

Elevated BP

Urinary retention

USE WITH CAUTION: HTN, BPH, MAO inhibitors

251
Q

Topical decongestants

A

Repeated use leads to rebound congestion

Prolonged use may lead to chronic rhinitis, secondary hyperemia, tachyphylaxis, nasal mucosal irritability

Rhinitis Medicamentosa

252
Q

Antihistamines

A

HIstamine normally causes smooth muscle contractin, increased capillary permeability, glandular secretion

H1 antagonists selective for H1 only

253
Q

First generation H1 antagonists

A

Block muscarinic receptors producing anticholinergic side effecs

Also block H1 in CNS causing sedation

254
Q

Second generation H1 antagonists

A

More selective, no muscarinic side effects, poor BBB crossing

No sedation

255
Q

H1 antagonist symptom relief

A

Sneezing

Pruritis

Rhinorrhea

Less effective at relieving nasal blockade

256
Q

Cromolyn sodium and nedocromil sodium for rhinitis

A

Inhibit antigen induced release of histamine from mast cells

Maximal efficacy when used prophylactically before episodic allergen exposure

257
Q

Corticosteroids and rhinitis

A

Extremely effective in allergic rhinitis

258
Q

Anti cholinergics and rhinitis

A

Submucosal glands rich in parasympathetic innervation

Ach release –> nasal discharge

Anti cholinergics prevent nasal secretions

259
Q

Decongestant symptom relief

A

ONLY NASAL BLOCKAGE

260
Q

Cromolyn rhinitis symptoms relief

A

All, but not as effective as corticosteroids

Pruritis, blockage, sneezing, rhinorrhea

261
Q

Corticosteroid rhinitis symptom relief

A

Very effective at relieving all

Pruritis, sneezing, rhinorrhea, nasal blockage

262
Q

Anticholinergic rhinitis symptom relief

A

Effective and reducing rhinorrhea

263
Q

Clinical aspects of COPD

A

Non specific symptoms - sometimes cough/sputum.

Dyspnea

Slowing of forced expiration

264
Q

Emphysema definiton

A

Abnormal, permanent enlargement of air spaces distal to terminal bronchiole

Destruction of alveolar walls without obvious fibrosis

Natural elastic recoil (closing) of lung during exhalation is reduced because of destroyed lung tissue

265
Q

Types of emphysema

A

Centracinar

Paracinar

266
Q

Centracinar emphysema

A

Destruction of alveolar walls accentuated in center of acinus

Dilated air spaces

Microscopic - Round lesions, thin walls w/normal septa thickness but less protruding septa

20x more common

267
Q

Panacinar emphysema

A

Destruction of alveolar walls that is diffuse, entire acinus and thus entire lobule

Alpha 1 antitrypsin deficiency

All air spaces enalrged

Microscopic - Lesions have smooth thin walls without protruding septa

268
Q

Bulla

A

Emphysems lesion greater than 1cm

Usually subpleural

Can coexist with other epmysema or on its own

269
Q

Paraseptal emphysema

A

Distal acinus

Sub pleural lung zones

Rare, can cause spontaneous pneumothorax

270
Q

Protease-antiprotease emphysema pathogenesis

A

a1-AT neutralizes neutrophil elastase

Genetic defect can cause this

Smokers - Imbalance of proteinase and antiproteinase activity secondary to smoking

Smokers have more neutrophils in lung due to irritation, smoke inhibits a1-AT

271
Q

Chronic bronchitis definition

A

Chronic inflammation of airways (small ones)

Fibrosis, chronic inflammation, muscular hypertrophy, pigment accumulation, mucous plugging, epithelial abnormalities

Caused by smoking

272
Q

Simple chronic bronchitis

A

Involves large cartilaginous airways (bronchi)

Chronic cough and mucous production

Microscopic - chronic inflammation and enlarged bronchial mucous glands

Does NOT lead to rogressive disabling obstructive disease

Associated with more frequent infectious bronchitis

273
Q

Extrinsic Asthma

A

Type I hypersensitivity reaction to environmental allergen –> IgE coated mast cells bind –> release histamine, Ach, cytokines, leukotrienes

Late phase reaction: PMN recruited to irritated ariways, eosinophils damage epithelium –> bronchoconstriction

Can be familial: allergic rhinitis, eczema, urticaria

Drug induced and occupational asthma

274
Q

Intrinsic asthma

A

Triggered by viral infections

IgE elevated

More common in adults

275
Q

Gross and microscopic path of asthma

A

Gross: Obstructive mucous plugging, hyperinflation

Microscopic:

BM thickening and collagen deposition

Eosinophilic infiltrate

Mucous plugging

Variable smooth msucle enlargement, bronchial gland enlargement, chronic inflammation

276
Q

Complications of asthma

A

All uncommon

Sudden death

Pulmonary HTN

Bronchiectasis (abnormal, permanent dilation of bronchi)

277
Q

Obstructive disease PFT

A

TLC: Normal/high

FVC: Normal/low

FEV1: Low

FEV1/FVC: Low

278
Q

Major physiological features of COPD

A

Airflow limitation

Hypoxemia

CO2 retention

279
Q
A

Centracinar emphysema

280
Q
A

Centracinar emphysema

281
Q
A

Centracinar emphysema

282
Q
A

Centracinar emphysema

283
Q
A

Panacinar emphysema

284
Q
A

Panacinar emphysema

285
Q
A

Panacinar emphysema

286
Q
A

Panacinar emphysema

287
Q
A

Panacinar emphysema

288
Q
A

Panacinar emphysema vs normal

289
Q
A

Distal acinar emphysema

290
Q
A

Distal acinar emphysema

291
Q
292
Q
A

Chronic bronchitis w/ mucous plug

293
Q
A

Normal airway wall

294
Q
A

Chronic bronchitis

Increased mucous and inflammation

295
Q
A

Small airways disease

296
Q

Obstruction of small airwats in chronic bronchitis vs emphysema

A

Chronic bronchitis: INTRINSIC. Fibrosis, mucous plugging, inflammation

Emphysema: EXTRINSIC. Collapse of small airways in expiration due to lack of support

297
Q
298
Q
299
Q
A

Asthma

Eosinophils

300
Q

Acute Lung injury characteristics

A
  1. Abrupt decline in respiratory function
  2. Bilateral infiltrates
  3. Reduced lung compliance
  4. hypoxemia
  5. Absence of heart failure
301
Q

Acute lung injury causes

A

Caused by agents that diffusely injure lung parenchyma

Sepsis, aspiration, infection, trauma, radiation, inhalation of toxins, drugs

302
Q

ARDS definition

A

Clinical syndrome characterized by sever acute respiratory failure

Manifestation of severe ALI

303
Q

4 common causes of ALI and ARDS

A

Sepsis

Diffuse infections

Aspiration

Trauma

304
Q

Diffuse alveolar damage definition

A

Pathalogical term

Histological manifestation of severe ALI, generally in association with clinical ARDS

305
Q

Gross and microscopic path of DAD

A

Gross: Heavy, diffusely firm, red-tan lungs

Microscopic:

DIffuse damage to all parts of alveolar wall, including epi and endothelial injury

Hyaline membrane formation on surface of damaged alveoli

Hyperplasia of type II pneumocytes

Granulation tissue formation w/ influx of lymphocytes, macrophages, fibroblasts

306
Q

Pathogenesis of DAD

A

Endothelial injury w/ endothelial activation

Recruitment of neutrophils

Accumulation of fluid in alveolar spaces

Hyaline membrane formation

Cytokine release that perpetuates inflammatory response

307
Q

Treatment of ALI/ARDS

A

No proven treatments

Mechanical ventilation and supportive care

308
Q

Prognosis of ALI/ARDS

A

40-50% recover

Many die acutely

Few develop diffuse fibrosis and die in weeks-months

309
Q

Restrictive lung disease definition and settings

A

Characterized by reduced expansion of lung parenchyma

  1. Diffuse diseases of interstitium (pulmonary fibrosis)
  2. Chest wall disease w/ normal lungs (obesity, pleural disease, NM disease)

Results in DECREASED lung volume but airflow is normal or proportionally reduced

310
Q

Categories of restrictive lung disease

A

Fibrosis disease

Granulomatous disease

Eosinophilic disease

Smoking related disease

Miscellaneous

311
Q

Fibrosing idiopathic lung diseases

A

Idiopathic pulmonary fibrosis

Nonspecific interstiail pneumonia

Cryptogenic organizing pneumonia

Connective tissue disease associated interstitial lung disease

Drug reactions

312
Q

Granulomatous restrictive lung diseases

A

Sarcoidosis

Hypersensitivity pneumonitis

313
Q

Smoking related restrictive lung diseases

A

Desquamative interstitial pneumonia

Respiratory bronchiolitis associated interstitial lung disease

314
Q

Miscellaneous restrictive lung diseases

A

Pulmonary alveolar proteinosis

315
Q

Idiopathic pulmonary fibrosis definition

A

Clinical syndrome characterized by progressive interstitial fibrosis of lungs and respiratory failure

Associated with path pattern “usual interstitial pneumonia”

316
Q

Usual interstitial pneumonia

A

Pathalogical pattern of fibrosis

Heterogenous and peripherally accentuated fibrosis

317
Q

Clinical characteristics of IPF

A

Fibrosis only involves lungs

Smoking and metal fumes, wood dust increase risk

Prognosis worse than for all other types of chronic interstitial lung disease

318
Q

Pathogenesis of IPF

A

Unknown cause but immune related

Unregulated fibrosis

Mediators released –> fibroblast recruitment

319
Q

Gross and microscopic path of IPF (UIP pattern)

A

Gross: Small lungs, diffusely bumpy pleura, fibrous tissue in peripheral lung zones, dilated air spaces surrounded by dense fibrous tissue (honeycombing)

Microscopic:

Patchy destruction of lung architecture, accentuated in periphery of lobules

Dense mature fibrosis adjacent to foci of new fibrosis with proliferating fibroblasts

320
Q

Non specific interstitial pneumonia (NSIP) definition and characteristics

A

Chronic fibrosing interstitial lung disease that lacks characteristics of well characterized diseases

Diffuse homogenous thickening of alveolar walls by lymphocytes and fibrosis

Better prognosis

321
Q

Cryptogenic organizing pneumonia (COP) definition and characteristics

A

Unknown cause

Injury to lung that results in filling of alveoli and terminal bronchioles by plugs of proliferating fibroblasts

Good prognosis b/c no mature fibrosis

Steroids to treat

322
Q

Connective tissue disease associated ILD

A

CT disease if uncontrolled can cause lung fibrosis

RA

Scleroderma

Polymyositis

Sjogren

323
Q

Drug induced lung disease

A

Disease caused by drugs, esp antineoplastic drugs

Look like DAD, UIP, NSIP

324
Q

Sarcoidosis definition and characteristics

A

Multisystem granulomatous disease

Granulomatous inflammation and fibrosis

Lung involved in 90%

Non necrotizing granulomas distributed along lymphatic routes

CD4 T cells in lesions

325
Q

Hypersensitivity pneumonitis definition

A

Acute/chronic interstitial lung diseases caused by heightened sensitivity and inappropriate inflammatory reaction to inhaled antigens

Reversible, lack mature fibrosis

326
Q

Farmers lung

A

Spores of thermophilic bacteria in newly harvested hay

327
Q

Pigeon breeder lung

A

Proteins from serum, droppings, bird feathers

328
Q

Humidifier lung

A

Thermophilic bacteria in heated water resevoirs

329
Q

Clinical features of HP

A

Symptoms related to antigen exposure

Fever, dyspnea, cough, leukocytosis

Pulmonary infiltrates

330
Q

Path features of HP

A

Lymphoplasmacytic interstitial infiltrate in lungs

Small non necrotizing granulomas around airways

Chronic bronchiolitis

331
Q

Desquamative interstitial pneumonia definition and characteristics

A

Smoking related interstitial lung disease

Accummulation of many macrophages within alveolar spaces, mild interstitial fibrosis

Chronic dyspnea, dry cough, clubbing of digits

332
Q

Respiratory bronchiolitis associated interstitial lung disease

A

Smoking related interstitial lung disease

Milder than DIP, less macrophages

333
Q

Pulmonary alveolar proteinosis definition

A

Rare disease caused by accumulation of surfactant within alveolar spaces and bronchioles

Defect in Macrophage function or granulocyte-macrophage-colony-stimulating factor (GM-CSF)

334
Q

Types of PAP

A

Autoimmune: 90%. Anti GM-CSF autoantibody that neutralizes GM-CSF, alveolar macrophages cannot catabolize surfactant

Secondary: Caused by conditions that impair macrophage function

Hereditary: Mutations that disrupt GM-CSF

No chronic fibrosis

1/3 patient good, 1/3 bad, 1/3 same

Secondary infections can occur

Whole lung lavage

335
Q
A

Intersitial disease

336
Q

PFT in restrictive lung diseases

A

TLC: Low

FVC: Low

FEV1: Low

FEV1/FVC: Normal/high

337
Q
A

Diffuse Alveolar Damage

338
Q
A

DAD

hyaline membranes

339
Q
A

Organizing DAD

340
Q
A

Non spcific interstitial pneumonia

341
Q
A

Sarcoidosis

342
Q
A

Sarcoidosis

343
Q
A

Desquamative Intersitial Pneumonia

344
Q
A

Organizing pneumonia

Note spared lung and airspace filling

345
Q
A

Organizing pneumonia

346
Q
A

Hypersensitivity pneumonitis

347
Q
A

Hypersensitivity pneumonitis

Note poorly formed non necrotizing granuloma

348
Q
A

Hemorrhage

349
Q
A

Capillaritis

350
Q
A

Idiopathic hemosiderosis

351
Q
A

Pulmonary alveolar proteinosis

352
Q

Major types of primary neoplasms in lung

A

Carcinomas

Carcinoid tumors

Other

353
Q

Lung cancer demographics

A

3rd most common cancer, leading cause of cancer death

Age 40-70

5 year survival is 15%

354
Q

Major etiology of lung carcinomas

355
Q

Modern classification of lung carcinomas

A

Small cell

Squamous cell

Adenocarcinoma

Large cell

Other

356
Q

Histological distinctions of lung cancer that change treatment

A

Small cell vs non small cell

Adenocarcinoma vs squamous cell

357
Q

Gross appearance of primary lung cancer

A

Originate in large bronchi - Hilar (squamous or small cell)

  • Firm infiltrating sold gray-tan mass in intimate association with large bronchus

Peripheral lung cancers - Adenocarcinomas

358
Q

Small cell carcinoma histopathology

A

Invasive sheets or nests of small undifferentiated malignant epithelial cells

Contain chromatin but no prominent nucleoli, little cytoplasm

Originate from bronchial neuroendocrine cells

359
Q

Squamous cell carcinoma histopathology

A

Invasive sheets, nests, cords of large malignant epithelial cells w/ intercellular bridges and/or keratin pearls

360
Q

Adenocarcinoma histopathology

A

Large malignant epithelial cells forming invasive glandular structures

Adenocarcinoma in situ is slow growing, low grade variant - Large malignant cuboidal/columnar cells that grow across alveolar septal surfaces. Do not invade interstitium

361
Q

Large cell carcinoma histopathology

A

Invasive sheets of large, undifferentiated malignant epithelial cells

No squamous or glandular differentiation

362
Q

Complications of hilar tumor

A

Localized hyperinflation dur to partial bronchial obstruction

Atelectasis due to total bronchial obstruction

Bronchiectasis due to obstruction and inflammation

Post obstructive abscesses/pneumonia

Superior vena caval syndrome: Obstruction or SVC –> engorgement of veins in head and arms

363
Q

Complications of peripheral tumor

A

Pleural invastion and dissemination

Pleuritis and effusion

Invasion of vervical sympathetic plexus –> horners syndrome (Pancoast Tumors)

364
Q

Clinical course and prognosis of lung cancers

A

Cough, weight loss, chest pain, dyspnea

3/4 are unresectable at time of detection

365
Q

Carcinoid Tumor

A

Low grade malignant neoplasm derived from neuroendocrine cells

NOT CAUSED BY SMOKING

Locally invasive, most do not metastasize

Surgery

366
Q

Harmatoma

A

Benign mesenchymal neoplasm

Single, well circumscribed, spherical, peripheral lung nodule

Mature cartilage w/ other mesenchymal elements (fat, SM)

367
Q

Hematogenous metastasis

A

Carcinomas arising in other anatomic sites can spread to lung via vasculature

368
Q

Lymphangitic carcinomatosis

A

Invasion of lung via lympnatics

Linear, streaky tumor deposits

369
Q

Hematogenous metastasis to large airways

A

Carcinoma from body can spread to lung and involve large airway

Mimick primary lung cancer

370
Q

Aerogenous spread

A

Cancer that fragments off into aveoli and spread through airways to other parts of lung during breathing

371
Q

Pleaural metastasis

A

Carcinoma spread to pleural surface and dissemination through pleural space

Effusion with malignant cells

Poor prognosis

372
Q

Diffuse malignant mesothelioma

A

Malignant neoplasm arising from mesothelial lining of parietal or visceral pleura

Thick tumor rind that covers lung surface and inside of chest wall

Asbestos

Gland like/papillary structures

Spindle cells

Both

373
Q

Small cell carcinoma treatment method

A

Chemosensitive

Not treated surgically

374
Q

Non small cell carcinoma treatment option

A

Chemoresistant

Treat with surgery

375
Q
A

Invasive adenocarcinoma

376
Q
A

Invasive gland forming adenocarcinoma

377
Q
A

Adenocarcinoma in situ at periphery of invasive adenocarcinoma

378
Q
A

Adenocarcinoma in situ

379
Q

Mucinous adenocarcinoma

A

Invasive

Can present as lobar consolidation

Grows along alveolar septa and as invasive papillae

Cells contain abundant mucin

380
Q
A

Mucinous adenocarcinoma

381
Q
A

Mucinous adenocarcinoma

382
Q
A

Mucinous adenocarcinoma

383
Q

Adenocarcinoma in situ origin

A

Bronchiolar (goblet/Clara) cell or Type II pneumocyte

384
Q

Squamous cell carcinoma arise through sequence

A

Squamous metaplasia –> squamous dysplasia –> squamous cell carcinoma in situ –> invasive squamous cell carcinoma

385
Q
A

Squamous cell carcinoma

Central location

386
Q
A

Squamous cell carcinoma

Cavitation

387
Q
A

Squamous cell carcinoma

Keratin pearls

388
Q
A

Squamous cell carcinoma intercellular bridges

389
Q
A

Squamous metaplasia

390
Q
A

Invasive squamous cell carcinoma

391
Q
A

Large cell carcinoma

392
Q
A

Small cell carcinoma

393
Q
A

Small cell carcinoma

394
Q
A

Small cell carcinoma

395
Q

Types of Acute Respiratory Failure

A

Type I: Hypoxemic

Type II: Hypercapnic

396
Q

Causes of hypoxemic respiratory failure

A

Pneumonia

Cardiogenic pulmonary edema

Non cardiogenic pulmonary edema (ARDS)

397
Q

Causes of hypoxemia

A

V/Q mismatch

Shunt

Hypoventilation

Diffusion abnormalities

398
Q

Causes of hypercapnic respiratory failure

A

CNS depression

NM disease

Chest wall abnormalities

Upper airway obstruction

Obstructive lung disease

399
Q

Decreased alveolar ventilation = ?

A

Increased phsyiological dead space

Increased arterial CO2

400
Q

Pneumoconiosis definition

A

DIffuse interstitial lung disease caused by inhalation of inorganic dust

Asbestos, Beryllium, Coal, Silica

401
Q

Factors influencing pneumoiconosis development

A
  1. Amount of dust retained in lung
  2. Size and shape of particles
  3. Solubility and chemical reactivity of dust particles
  4. Presence of other irritants (cigarettes) or other disease
402
Q

Defense mechanisms of respiratory tract

A

Filtration and impaction in upper respiratory tract

Cough

Mucociliary transport

Phagocytosis and transport by macrophages

403
Q

Coal Workers Pneumconiosis definition and pathogenesis

A

Chronic lung disease caused by accumulation of inhaled coal dust

Poorly understood pathogenesis, fibrosis plays role

404
Q

Simple CWP

A

Small aggregates of coal dust-laden macrophages form in terminal bronchioles/respiratory ducts

  1. Little or not disturbance in ventilatory function
  2. Little to no fibrosis
  3. Associated with centracinar emphysema
  4. May progress to fibrous nodules
405
Q

Complicated CWP

A

Progressive massive fibrosis

Bulky fibrous nidules

Severe pulmonary symptoms and cor pulmonale

TB susceptible

406
Q

Silicosis definition and pathogenesis

A

Inhaled silica dust in lung, fibrosis

Macrophage plays pivotal role in development of fibrosis

Silica interact with membranes –> free radicals –> enzymes and inflammatory cells recruited

407
Q

Nodilar silicosis

A

1-5mm silicotic nodules, layers of acelular fibrous tissue and silica crystals

Lymph node involvement

Few symptoms

408
Q

Complicated (Conglomerate) Silicosis

A

Coaslescence of smaler silica nodules into large fibrous masses

Respiratory impairment, R HF, severe symptoms

TB infection increased risk

409
Q

Types of asbestos

A

Serpentine (white) asbestos

Amphibole (brown) asbestos

410
Q

Pathogenesis of asbestos related diseases

A

Inhaled deep into lung because of narrow shape

Coated with iron and proteins –> asbestos bodies

Lung parenchyma injured because of relseased chemical mediators when asbestos fibers phagocytized

411
Q

Asbestosis

A

Diffuse interstitial fibrosis of lungs

NO fibrous nodules or masses, diffuse fibrosis instead

412
Q

Asbestos pleural plaques

A

Thick deposits of fibrous tissue on surface of parietal pleura

No asbestos bodies!!

Marker for asbestos exposure, not specific though

413
Q

Asbestos and cancer

A

Increased risk for diffuse malignant mesothelioma, lung carcinoma, other cancers

414
Q

Latency of asbestos disease - carcinoma

A

Lung carcinoma develops in patients that are chronically exposed to large amounts

Several years before carcinoma

415
Q

Latency of asbestos - pleural mesothelioma

A

25-40 years after asbestos exposure

Initial exposure can be short

416
Q

Berylliosis definition

A

Accumulation of inhaled beryllium in lung

Variable degrees of granulomatous inflammation

417
Q
A

Simple CWP

418
Q
A

Progressive Massive Fibrosis

Complicated CWP

419
Q
420
Q
A

Silicotic nodule

421
Q
A

Asbestos bodies

422
Q
A

Pleural PLaque

423
Q
A

Diffuse malignant mesothelioma

424
Q
A

Granuloma in berylliosis

425
Q
A

Carcinoid tumor - endobronchial mass

426
Q
A

Carcinoid tumor

Nested growth pattern

427
Q
A

Carcinoid tumor

Regular nuclei

Salt and pepper chromatin

428
Q
429
Q
430
Q
A

Metastasis

Cannonball pattern

431
Q
A

Lymphangitic carcinomatosis

432
Q

Treatment summary: Non small summary

A

Stages I & II: Surgery

Stage III: Chemo/radiotherapy

Stage IV: Chemo vs targeted if adenocarcinoma has mutations

433
Q
A

Squamous cell carcinoma

Central

434
Q
A

Small cell carcinoma

Central location

Obstruct hilar vessels and bronhi

435
Q
A

Adenocarcinoma

Peripheral, lobulated mass

436
Q
A

Metastatic disease

Multiple random nodules

437
Q
A

Lymphangicitic spread

438
Q

P resistive

A

Flow x resistance

Pressure to overcome resistive forces is greater in obstructive diseases and faster breathing (higher flow)

439
Q

P elastic

A

Volume x elastance

Pressure to overcome elastic forces higher in larger tidal volumes and stiffer lungs (restrictive disease)

440
Q

Minimize work in Obstructive disease

A

Resistive work increased

Slow deep breaths (avoid increased flow)

441
Q

Minimize work in restrictive diseases

A

Compliance is low ie elastic work is increased

Breath with lower tidal volume

442
Q

Mechanisms of pleural fluid formation

A
  1. Increased capillary hydrostatic pressure
  2. Reduction in intravascular oncotic pressure
  3. Increased capillary permeability/vascular disruption
  4. Decreased lymphatic drainage or complete blockage
  5. Increased peritoneal fluid, with migration across diaphragm via lymph or structural defect
443
Q

Symptoms/physical findings of pleural effusion

A

Dyspnea

Chest pain

Cough

Decreased expansion

Dullness to percussion

Decreased breath sounds

Decreased tactile fremitus

Tracheal shift away from large effusion

Pleural friction rub

444
Q

Purulent pleural fluid = ?

445
Q

Putrid odor pleural fluid = ?

A

Anaerobic empyema

446
Q

Milky, opalescent pleural fluid = ?

A

Chylothorax

447
Q

Most common causes of transudate effusions and definition

A

Ultrafiltrates of plasma

CHF

Hypoalbuminemia

Nephrotic syndrome

Cirrhosis

448
Q

Exudate content and overall causes

A

Fluid with elevated protein content

Arise from:

Pleural/lung inflammation

Impaired lymphatic drainage of pleural space

Increased capillary wall permeability/

Vascular disruption

449
Q

Most common causes of exudates

A

Parapneumonic causes

Malignancy

Collagen vascular disease

TB

PE

450
Q

Exudate diagnosis ratios

A

Plural fluid protein:Serum protein > .5

Pleural LDH:Serum LDH >.6

Pleural fluid LDH > 2/3 upper limit of normal serum value

451
Q

Light criteria for exudates

A

PLeural fluid LDH > .45 upper limit of normal

Pleural fluid cholesterol level > 45,g/dL

Pleural fluid protein level greater than 2.9

452
Q

Respiratory distress syndrome definition

A

Clinical syndrome characterized by respiratoyr dysfunction in infants

Deficiency of pulmonary surfactant

453
Q

Respiratory distress syndrome pathology

A

Atelectasis and hyaline membranes in lung

454
Q

RDS complications

A

PDA

Interventricular hemorrhage of brain (due to hypoxia)

Necrotizing enterocolitis

Oxygen toxicity to lungs

Bronchopulmonary dysplasia

455
Q

Bronchopulmonary dysplasia

A

Chronic neonatal lung disease comlicating unresolved RDS –> persistant respiratory distress

New BPD caused by disrupted lung development and alveolar hypoplasia

456
Q

BPD pathology

A

Persistant lung immaturity

Chronic atelectasis

Alveolar hypoplasia

Interstitial fibrosis

457
Q

Bronchogenic cysts

A

Pinched off remnant of primitive esophagobronchial tissue that form benign cyst in lung, mediastinum, or next to gut

458
Q

Sequestrations

A

Portions of lung without bronchial connection with systemic arterial blood supply

Intralobar sequestrations are in visceral pleura

Extralobar sequestrations are invested by own pleura, separate from lungs

459
Q

Pulmonary hypoplasia definition + causes

A

Undevelopment of lung, lacks acinar development

Extrenal compression (rib cage anomalies or diaphragmatic hernia)

Renal agenesis or disease (Potters)

Oligohydraminoas

Anencephaly

Idiopathic

Association with complex malformation syndromes

460
Q

Bronchiectasis definition

A

Fixed dilation of large airways, usualy due to a previous necrotizing inflammatory process in airways –> permanent airway scarring

461
Q

Causes of bronchiectasis

A

Bronchial obstruction: Airway distended with secreted mucus, infection

Congenital or hereditary conditions

Immunodeficiency –> repeated infections

Ciliary abnormalities

Necrotizing bronchopneumonia

462
Q

Gross pathology of bronchiectasis

A

Dilated airways

Thin walls

463
Q

Microscopic pathology of bronchiectasis

A

Airway dilatation

Absence of normal bronchial wall structures (glands, muscle, cartilage)

Fibrosis and chronic inflammation of airways

464
Q

Clinical course of bronchiectasis

A

Chronic productive cough

Occasional hemoptysis

Episodes of acute infection

Eventually cor pulmonale and cyanosis

465
Q

Septum transversum

A

Grows from ventral body wall and separates heart and liver

Connects with esophagus/foregut

Develops into central tendon of diaphragm

466
Q

Stages of lung development

A

Embryonic

Pseudoglandular

Canalicular

Terminal sac stage

Post natal stage

467
Q

Embryonic stage

A

4-7 weeks

Primitive airways develop and lungs begin to fill pleural cavity

468
Q

Psudoglandular stage

A

8-16 weeks

Continuation of airway development - conducting airways

Lung arteries begin to form

469
Q

Canalicular stage

A

17-26 weeks

Formation of respiratory bronchioles

Cells in airways become ciliated cuboidal

Intense growth of blood vessels and formation of capillaries

470
Q

Terminal sac stage

A

26 weeks - birth

Alveoli form as buds

Type I and type II epithelium form

Surfactant is produced

471
Q

Postnatal stage

A

Birth-5 years

Significant increase in alveoli

CPR (3 decks)

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