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Pulmonary > Pulm 1 > Flashcards

Pulm 1 Flashcards

1
Q

What is the function of the respiratory system?

A

Gas exchange (warm/humidify the air and filter and protect us from it)

Acid-base

Phonation

Metabolism of endogenous substances

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2
Q

How much blood passes through lungs each minute?

A

Entire blood volume (~5L)

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3
Q

How is the lung anatomically divided?

A
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4
Q

What are the functions of the airways (conducting zone)?

A

Serve as conduits of air

Provide for evacuation of foreign material

Provide immunologic and protective functions

Serve to warm and humidify the air as it enters

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5
Q

What are features of Respiratory Epithelium?

A
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6
Q

How do bronchi and bronchioles differ histologically?

A
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7
Q

What is the funcitonal subunit of hte lung?

A

Acinus

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8
Q

What are features that allow for efficient and rapid gas exchagne?

A

Large surface area

Short diffusion path

Concentration gradient

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9
Q

What does the lung look like at the alveolus?

A
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10
Q

What are Type 1 vs Type 2 pneumocytes?

A

Type 1 = cover ~95% of alveolus, but are only 40% of cells - cant’ divide

Type 2 - cover ~5% but account for 60% of cells. Divide to replace type I cells

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11
Q

What factors can influence anomalous funciton of thel ugns?

A

Gas exchange impairment in alveolar space

Increase in air flow resistance in bronchioles

Altered pulmonary mechnaics

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12
Q

What is ventilation-perfusion mismatch?

A

Area receiving blood isn’t the same as area receiving fresh air

E.g. neoplasm, mucous plugging, COPD, edema, pneumonia

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13
Q

What do we see here?

A

Mucus plugging in chornic bronchitis limits airflow to alveolar gas exchagne areas

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14
Q

What are alveoolar filling processes?

A

Pneumonia, edema

Fluid and inflammation occupies alveolar space preventing acess to the area of gas exchange

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15
Q

What do we see here?

A

Acute pneumonai - neutrophils fll alveolar spaces

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16
Q

How can you impair diffusing capacity?

A

Loss of alveolar or endothelial area (emphysema)

Thickening of alveolar wall (fibrosis)

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17
Q

What are two factors upon which diffusing capacity depends?

A

Alveolar and endothelial surface areas

Thickness of air-blood barrier

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18
Q

What do we see here?

A

Real bad emphysema - decreased alveolar surface

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19
Q

What do we see here?

A

Interstitial fibrosis - increased thickness of alveolar walls inhibits gas exchage

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20
Q

What are some obstacles to perfusion?

A

Destruciton of alveolar capillaries

Alteration of pulmonary blood flow (cardiac, pulmonary HTN)

Obstruciton of blood flow (PE, compression)

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21
Q

What are general features of the pulmonary vasculature?

A

Dual circulation:

Pulmonary arteries (low pressure, capacitance, gas exchagne)

Bronchial arteries (systemic pressure, nutrient vessels)

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22
Q

What do we see here?

A

Pulmonary HTN - increased htickenss of pulmonary vessels - decreased blood flow to gas exchange areas

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23
Q

What are structural mechanisms for defense in the lungs?

A

Nasal hairs

branching airways

Muco-ciliary escalator

Alveolar macrophages

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24
Q

A 55 year old man presented to the ED with shortness of breath. His exam shoes dullness to percussion, absence of breath sounds at the left base. The AP chest radiograph shows

opacification onf the left hemithorax. Fluid in the chest is suspected The next step is to order:

 A. Lateral decubitus film

 B. Apical lordotic film

 C. CT scan of the chest

 D. PA and lateral film

 E. Supine chest xray

A

Lateral decubitus film

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25
Q

What is the PA view?

A

Patient is upright and in full inspiration

XR tube is 6 feet from film

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26
Q

What is the lateral CXR?

A

Left side of patient against XR cassette

Helpful in visualizing lesions behind the heart the mediastinum or diaphragm

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27
Q

What is the AP view?

A

Portable XR unit on sick patients - supine or sitting in bed

XR passes from anterior to posterior

Less powerful, higher magnification, less sharp images (taken from shorter distance)

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28
Q

Which is PA, which is AP?

A
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29
Q

What is a lateral decubitus view?

A

Patient lies on his side in lateral position

Helps visualize free fluid in pleural cavity as it will gravitate and layers against dependent thoracic wall

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30
Q

What are expiratory views?

A

Help visualize free air in pleural cavity (pneumothorax) as the lung markings becoem more crowded which help delineate edge of lung

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31
Q

What is the apical lordotic view?

A

Frontal view taken with XR beam angled to project clavicles above the lung apex to display disease hidden behind the clavicles

Seen on right

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32
Q

Identify the structures on this xray

A
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33
Q

Identify the structures

A
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34
Q

What are demarcations of the right and left lung?

A

Right has RUL, RML, RLL

Left has LUL and LLL

Major fissure separates RUL and RML from RLL on right and the LUL from LLL on left

Minor fissure separates RUL from RML

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35
Q

what is lung compliance?

A

Volume/Pressure

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36
Q

What is the compliance of the chest wall?

A
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37
Q

What is the compliance of the respiratory system?

A

Combination of the chest wall and lungs

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38
Q

What is hysteresis?

A

The chest wall compliance is different in inflation than in deflation

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39
Q

Why is there hysteresis?

A

Surface tension increases the pressure needed to expand the lung

Surfactant helps

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40
Q

What are surface forces of the lung?

A

Air liquid interface adds to pressure to required to expand lungs

Saline filled lungs requrie less pressure

Surfactant reduces surface tension (decreases further when lungs get smaller) and prevents small airway and alveoli collapse

Surfactant is made by Type II pneumocytes

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41
Q

What cells make surfactatn?

A

Type II pneumocytes

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42
Q

What are tissue forces of elastic recoil/

A

Beyond a certain point of inflation, lungs get stiff

Below a minimum, alveoli stay open because of their structur

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43
Q

How does compliance change with disease?

A

ΔV/ΔP

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44
Q

What decreases lung compliance?

A

Pulmonary fibrosis

Pulmonary Edema

Pneumonia

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45
Q

What increases pulmonary compliance?

A

Epmhysema

Normal Aging

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46
Q

What do you see here?

A

Left: normal

Right: empnysematous lung - decreased elastic recoil, increased airflow resistance

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47
Q

What are pressures during tidal breath?

A

Pleural- always negative

Alveolar - correlates with flow

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48
Q

What is Reynolds number?

A

Density * diameter * velocity / Gas viscocity

Higher number => turbulent flow more likely

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49
Q

What characterizes air flow in large airways?

A

Turbulent flow

Resistance increases as flow increases

Helium/oxygen mixture decreases density and increases viscocity and is used to improve flow during turbulent flow conditions (upper airway obstuction)

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50
Q

How can you improve flow under turbulent flow conditions (e.g. upper airway obstruction)?

A

Provide a helium:oxygen mixture that decreases density and slightly increases viscocity improving the Reynolds number

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51
Q

What descries airflow in smaller airways?

A

Laminar flow and Poisseuille’s Law

Resistance is proportional to viscocity*length/radius^4

Airway radius is most impmortant factor in resistance

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52
Q

Where is there the most resistnace to airflow?

A

Larger airways - there are SO many smaller airways, that the laminar flow dynamics of the small radii doesn’t come into play

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53
Q

What does FEV1/FVC ratio decrease indicate?

A

Obstructive defect

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54
Q

What defines restriction?

A

Reduced lung volumes (not just spirometry)

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55
Q

What does reduced “diffusion capacity” indicate?

A

Gas transport defect, but not much else

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56
Q

What are spirometry measurements?

A
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57
Q

What are the lung volumes?

A
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58
Q

What should your FEV1 typically be?

A

~ 3/4 of full expiratory volume (vital capacity)

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59
Q

How do you measure FRC, and by extension reserve volume?

A

Helium dilution after equilibration

Body phlethysmography

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60
Q

Does diffusion limit oxygen transport?

A

No - a RBC spends more than enough time in the capillary to diffuse (1 second or so)

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61
Q

In a patient with emphysema, lung compliance would be expected to be

 A) Decreased

 B) Increased

 C) Generally unchanged

 D) Cannot predict

A

Increased - not necessarily a good thing

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62
Q

Most of the resistance to airflow in the lung comes from

 A) Large airways  B) Small airways  C) Alveoli

A

Large (not intuitive)

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63
Q

Functional Residual Capacity is the volume of the lungs

 A) When you take the biggest possible breath  B) When you let all your air out

 C) When you are dead

A

When you’re dead

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64
Q

What is physiologic dead space?

A

Total volume of lungs that doesn’t participate in gas excahnge

Anatomic dead space (conducting airways) + functional dead space (ventilated alveoli that do not participate in gas exchange)

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65
Q

What is the anatomic dead space?

A

Volume of conduncting airways (~150 mL)

Nose, mouth, trachea, bronchi, terminal bronchioles

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66
Q

What is functional dead space?

A

Abnormal to have

Ventilated alveoli that don’t participate in gas exchange

Due to mismatch of ventilation and perfusion (v and q)

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67
Q

How do we measure dead space?

A

compare partial pressure of CO2 in alveoli and partial pressure of CO2 in expired air

VD = VT X [(PaCO2 – PECO2)]/ PaCO2

You typically use Vd/Vt ratio: Vd/Vt = (PaCO2 - PeCO2) / PaCO2

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68
Q

What is minute ventilation?

A

Tidal volume * respiratory Rate

Ve = Vt * RR

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69
Q

what is normal tidal volume?

A

450-500mL

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70
Q

What is normal minute ventilation?

A

~6.3 liters/minute

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71
Q

What is alveolar ventilation?

A

Minute ventilation - dead space ventilation

Va = RR*(Vt - Vd)

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72
Q

What is the alveolar ventilation equation?

A

INverse relationship between alveolar ventilation and alveolar PACO2 when the rate of CO2 produciton is constant

PACO2 = VCO2 * K / VA

K = constant for body temp, ampbient pressure standard (863)

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73
Q

What does the alveolar ventilation equation tell us?

A

If VCO2 doubles (strenuous exercise) then the only way to maintain the normal value of PACO2 is for VA to double also

When VA is doubled then PACO2 is halved

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74
Q

What is the alveolar gas equation/

A

Describes relationship between alveolar CO2 and O2

PAO2 = PIO2 - PACO2/R

R is respiratory exchange ratio (CO2 produciton/O2 consumption); normal is 0.8

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75
Q

What ist he normal respiratory exchange ratio?

A

0.8

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76
Q

A man has a rate of CO2 production that is 80% of rate of O2 consumption. If his arterial PCO2 = 40 mmHg and PO2 in humidified tracheal air is 150 mmHg, what is his alveolar

PO2?

A

Assume arterial blood equilibrates with alveolar. So PaCO2 = PACO2

PAO2 = PIO2 - PACO2/R

150-40/.8 = 100mmHg

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77
Q

How is perfusion different in the lung?

A

Zone 1= apex

Zone 2 = middle

Zone 3 = base - best perfusion

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78
Q

How is ventilation different in different regions in the lung?

A

Also varies with gravity

Gravity produces differences in regional ventilation

V is highest in base of the lung

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79
Q

How is V/Q different throughout the lung?

A

Actually ends up being highest at the top of the lung!

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80
Q

Which area of the lung has best V/Q ratio, which has lowest?

A

Highest in zone 1 (top)

Lowest in zone 3 (base)

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81
Q

What is happening when V/Q = 0?

A

Shunt = perfusion without ventilation

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82
Q

What happens when V/Q => infinity?

A

Ventilation without perfusion

dead space

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83
Q

What is Dead space (V/Q = infinity)?

A

Since there is lack of blood flow, O2 can’t be received or CO2 cant be added to alveolar gas

E.g. Pulmonary Embolism

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84
Q

What occurs in a shunt?

A

Lack of ventilation

NO O2 from alveolar gas to deliver to blood ro CO2 from blood to be eliminated

E.g. airway obstruction or right to left cardiac shunt (ASD)

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85
Q

What is the fractional concentration of oxygen in the air?

A

21 % so partial pressure is 760 *.21= 160 mmHg

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86
Q

How does the partial pressure of oxygen change from atmosphere to lungs?

A

Humidified air includes vapor pressure of weather

Atmosphere is 21% oxygen so 760*.21, but humidified is 760 - vapor pressure of water

so its less

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87
Q

What is venous partial pressure of oxygen?

A

40

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88
Q

What is venous partial pressure of carbon dioxide?

A

46

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89
Q

What is arterial partial pressure of oxygen?

A

100

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90
Q

What is arterial partial pressure of carbon dioxide?

A

40

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91
Q

What is perfusion limited gas exchange/

A

Total amount of gas transported across alveolar/capillary barrier is limited by blood flow (perfusion)

Partial pressure gradient isn’t maintained, so only way to increase amoutn of gas transported is by icnreasing blood flow

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92
Q

How do O2, CO2, and N2O Gas exchange?

A

Perfusion limited

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93
Q

What is diffusion limited gas exchange?

A

Total amount of gas transported across the alveolar-capillary barrier is limited by diffusion process

As long as partial gradinet is maintained, diffusion will continue along the lenght of capillary

e.g. CO

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94
Q

How does CO gas exchange?

A

Diffusion limited

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95
Q

What are examples of diffusion limited gas exchange?

A

CO

O2 in emphysema, pulmonary fibrosis or exercise

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96
Q

How much oxygen/gm does hemoglobin carry?

A

1.34

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97
Q

What is the O2 content of blood?

A

O2 bound to HbA + Dissolved O2

Bound to HbA is Hb conc * 1.34 * % saturation

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98
Q

WhatisO2 contentofthe blood of a patient with anemia (Hb 10 gm/dL)?

 Assuming normal lungs hence normal PAO2 of 100 mmHg and normal PaO2 of 100 mmHg

 Hb is 98% saturated at PaO2 of 100 mmHg

A

O2 boundtoHb=10gm/dLx 1.34 mL O2 / gm Hb X 98% (saturation) = 13.1 mL O2/100 mL blood

 Total O2 content = above value + dissolved O2

 Dissolved O2 = PaO2 X solu = 100 mmHg X 0.003 mL O2/100 mL/mmHg = 0.3 mL O2/100 mL blood

 Total O2 content = sum of above = 13.1 + 0.3 = 13.4 mL O2/100 mL blood

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99
Q

What is the O2-Hb Dissociation curve?

A

Reversible binding of up to 4 molecules of O2

P50 = PO2 at which Hb is 50% saturated = 24 mmHg

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100
Q

What makes the O2-Hb dissociation curve shift to the right?

A

<!–anki–>

Decreased affinity of Hb for O2

 Increase in P50

 O2 unloading is facilitated

 Due to acidic pH or higher PCO2: BOHR effect (exercising skeletal muscles)

 Due to higher temp (exercise)

 Higher 2,3-DPG conc: byproduct of glycolysis in RBC, under hypoxic conditions, binds Hb & reduces affinity for O2

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101
Q

What makes the O2-Hb dissociation curve shift to the left

A

 Increased affinity of Hb for O2

 Decrease in P50

 Decreased unloading of O2 to tissues

 Decrease in PCO2 & increase in pH

 Decrease in temp

 Decrease in 2,3-DPG conc

 HbF: βchain replaced by γ chain and 2,3-DPG doesn’t bind as avidly to γchain

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102
Q

What occurs when carbon monoxied is in the blood?

A

Affinity for Hb is 250x that of O2

Presence of CO decreases available heme units, but ALSO shifts the curve to the left

Combined effects are catastrophic to tissues

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103
Q

How is CO2 transport in the blood carried out?

A
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104
Q

What is hypoxemia?

A

Decrease in arterial PaO2 (decreased oxygen in blood)

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105
Q

What is the A-a gradient?

A

Difference between alveolar and arterial O2 (PAO2 - PaO2)

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106
Q

How do we get measurements of PaO2?

A

blood gas machine

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107
Q

How do we get measurements of PAO2?

A

Alveolar gas equation

PAO2 = PIO2 - PaCO2/R

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108
Q

What is a normal A-a gradient?

A

< 12 mmHg

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109
Q

What are causes of hypoxemia?

A

High altitude

Hypoventilation
Diffusion defect

V/Q defect

R->L shunt

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110
Q

What is the effect of high altitude?

A

Low barometric pressure -> decreases PO2 of inspired and alveolar air

Diffusion is normal, and capillaries are normal, so PaO2 = PAO2 , so no A-a gradient defect

Supplemental O2 helps

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111
Q

What is the effect of hypoventilation?

A

Decreased alveolar PAO2

O2 equilibration is otherwise normal so A-a gradient is normal

Supplemental O2 increases alveolr PAO2 and helps

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112
Q

What are the effects of diffusion defects?

A

E.g. pulnoary fibrosis or pulmonary edema

Increases idffusion distance or decreases available surface area

O2 equilibration is impaired, so A-a gradient is increased

Supplemental O2 helps by increasing PAO2 and increasing driving force of diffusion

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113
Q

What are the effects of V/Q defects?

A

Increased dead space or high V/Q = clot in pulmonary artery

Increase shunt or low V/Q = area of alveolar flooding (pus in pneumonia or obstruction of airway)

A-a gradient is increased

Supplemental O2 can help by raising PO2 of low V/Q units where blood flow is highest

(Supplemental O2 can help, but may not in some cases)

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114
Q

What is the effect of a right-to left shunt?

A

Blood compeletely bypasses alveoli

Deoxygenated blood mixed with normally oxygenated non-shunted blood and dilutes it

A-a gradient is increased

Supplemental O2 doesn’t help because shunted blood keeps diluting normally oxygenated blood

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115
Q

What is Hypoxia?

A

Decreased oxygen delivery to tissues

O2 delivery has two coponents: Cardiac output * O2 content of blood

O2 content: biggest contributor is Oxy-Hb

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116
Q

What are causes of hypoxia?

A

Hypoxemia

Decreased cardiac output

Anemia

CO poisoning

CN poisoning

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117
Q

What is normal blood pH?

A

7.38 - 7.42

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118
Q

What is normal PaCO2?

A

40 mmHg

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119
Q

What is normal PaO2?

A

100 mmHg

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120
Q

What is the relationship between hydrogen ions (H+) and PCO2 and HCO3?

A

Directly proportional to CO2, indirectly to HCO3

H+ = 24 * PCO2/[HCO3]

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121
Q

How does hte body compensate acid-base disturbances acutely? chronically?

A

Pulmonary = acute (minutes)

Renal = Chronic (hours/days)

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122
Q

What are the primary acid-base disturbances?

A

Respiratory acidosis or alkalosis (PaCO2 too high or low respectivley)

Metabolic acidosis or alkalosis ([HCO3] too low or high respectively)

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123
Q

How do you approach acid-base analysis?

A

1) pH acidemic (<7.35) or alkalemia (>7.45)
2) Is primary metabolic or respiratory -> look at PCO2
3) If respiratory: acute or chronic: Acute: larger change in pH (0.8*(PCO2-40)/10) vs chronic: 0.3 *..)
4) If metabolic, compensated: Winter’s formula
5) If metabolic, anion gap?: Na - (Cl + HCO3) = anion gap elevated if > 12

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124
Q

What are soem causes of respiratory acidosis?

A

Chronic resp diseases: COPD, emphysema

Drugs: opiates, alcohol, hypnotics, anesthetics

Neuromuscular disease: Guillain-Barre, muscular dystrophy, myasthenia gravis

Obesity-hypoventialiton syndrome

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125
Q

What are potential causes of metabolic alkalosis?

A

H+ losses via GI or renal tract (vomiting or urine)

Intracellular movement of H+

Increased bicarb reabsorption by kidnesy (due to decrease in effective circulating volume (contraction alkalosis))

Exogenous alkali administration

Sustained elevated bicarb due to: volume depletion, chloride depletion, hypokalemia

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126
Q

What typically causes an elevated ion gap?

A

Rise in unmeasured anions:

MUDPILES

Methanol
Uremia
Diabetic Ketoacidosis

Paraldehyde or Metformin
Iron tablets or INH

Lactic acidosis

Ethylene glycol

Salicylates

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127
Q

What causes non-anion gap acidosis?

A

Loss of bicarb (diarrhea, or Gi tract)

Decreased H+ excretion in kidnesy (renal failure)

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128
Q

What is the compensation formula for metabolic acidosis?

A

PaCO2 = 1.5 * [HCO3] + 8 +/- 2

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129
Q

What is the compensation formula for metabolic alkalosis?

A

PaCO2 = 40 + [0.7*([HCO3]-24)]

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130
Q

What makes up the respiratory center?

A

Dorsal respiratory group (primarily responsible for inspiration, gets input from vagus and glossopharyngeal)

Ventral respiratory group (for inspiration and expiration, not as important)

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131
Q

What are inputs of ventilatory drive?

A

Chemoreceptors: medulla, carotid body, arotic arch

Lung receptors (stretch, J receptors, irritant receptors, chest wall)

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132
Q

What are central chemoreceptors?

A

Near surface of medulla (not same as medullary respiratory centers)

Responds to CO2 (pH)

On “brain side” of BBB

CO2 diffuses across quickly, charged particles (H+) do not

Very fast responses to small changes in PCO2

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133
Q

What are peripheral chemoreceptors?

A

Carotid bodies and aortic bodies

Thoguth to mostly respond to oxygen and some respond to CO2, especially in hypoxemia

Also respond to changes in arterial pressure

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134
Q

What is the hypercapnic drive?

A

~ 2 L/min/torr

Normal response to PCO2 of ~ 43 mmHg woudl be to more than double your minute ventilation

Elevated PCO2 is abnormal - you respond quickly and robustly

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135
Q

What is the hypoxic drive?

A

Mediated by peripheral chemoreceptors

Magnitude of response is smaller than hypercapnic drive

Not uncommon to be hypoxic with little to no dyspnea though

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136
Q

What are the role of lung receptors in breathing contorl?

A

Can give you normal blood gases with shortness of breath

“can’t do” or “won’t do”

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137
Q

What are stages of non-REM sleep?

A

Stage 1 : light sleep, easily arousable

Stage 2 : about 50% of sleep time

Stage 3 : “slow wave” or “delta” sleep -> deepest, most refreshing, most in children

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138
Q

What is the effect of sleep on ventilatory dirve?

A

Reduces

PCO2 rises about 2-6 mmHg on transition to sleep, and is associated with some respiratory irrregularity

Slow wave sleep (stage 3) - very regular breathing - body on autopilot

REM sleep - further decrease inv entilatory drive, greater dependence on diaphragm, decreased muscle tone

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139
Q

What is obstructive sleep apnea??

A

Common - more common in overwieght, family history

Major risk factor for MI, stroke, CHF

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140
Q

What is central sleep apnea??

A

Ventilatory drive problem

Seen in some obese patients (rare)

“Ondine’s curse” - rare in reality, common in textbooks - defect in PHOX2b gene - congenital central hypoventilation syndrome

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141
Q

How does Obstructive Sleep apnea occur?

A

Upper airway msucles normally contract ot actively keep airway patent

Sleep decreases muscular activity (especially REM)

Increased occurence with supine posture, obesity, or crowded airway

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142
Q

How do you asses the severity of obstructive sleep apnea?

A

Number of sleep related obstructive breathign events

Mild = 5-15 per hour of sleep

Moderate = 15-30

Severe > 30

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143
Q

What is cheyne-stokes respiration/

A

Periodic breathign with central apneas

Best example is CHF with increased circulation time (delayed thermostat)

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144
Q

What is exercise?

A

Increased oxygen consumption

Must increase cardiac output and increase minute ventilation

Can increase minute ventilation ~ 20x

ABGs are unchanged

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145
Q

What occurs to muscle oxygen extraction during exercise?

A

Increases from ~ 20% of cardiac output, to about 80% at maximal exercise

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146
Q

How do arterial blood gases change during exercise?

A

PaO2 same

PaCO2 same

pH declines during strenuous exercise

CO2 produciton increases from lactate metabolism (anaerobic threshold)

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147
Q

What typically limits exercise capacity?

A

Cardiac output (stroke volume) in most people

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148
Q

What is cough?

A

Non-specific symptom of respiratory disease, with broad DDx

Most common symptom world-wide for which patients seek medical attention

Protective physiologic reflex; defense mechanism for protecting airway and clearing foregin particles

Can spread disease and can represent serious medical disease or benign disease

Can be non-voluntary or voluntary

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149
Q

What are features of an effective cough?

A

Depends on capacity of respiratory muscles: increase intrathoracic pressures, dynamic compression of airways

Drives gas at high linear velocities (up to 100 mph)

Depends on effective interaction between flowing gas and mucus lining in the airways (loosens mucus, removes it from airways; works in concert with mucociliary escalator, abnormal mucus makes it difficult)

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150
Q

What are the three phases of coughs?

A

1) inspiratory: inspire any amount of air. larger => optimizes lenght-tension relationship
2) compressive: glottis is closed and expiratory effort ensuse - maintain lung volume and build pressure
3) expiratory: high expiratory flow rate and blast of turbulent flow ensues

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151
Q

What is the cough reflex?

A

Cough begins with stimulation of receptors in and under airway epithelium

Must abundant in larynx and large airways

Stimulated by irritants or inflammatory mediators by activating GPCRs (bradykinin B2, prostanoid EP3 receptors)

Two types of sensory afferents mediate it:

Aδ fibers: originate from nodose ganglia and are sensitive to mechanical stimuli

C-fibers: originate in jugular vagal ganglia and are chemosensitive (noxious chemicals)

Activation of these to vagus, synapse in solitary tract nucleus in medulla, to cough center via second order neurons

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152
Q

What are the afferents that mediate cough?

A

Aδ: originate in nodose ganglia, sensitive to mechanical stimuli

C-fibers: originate in jugular vagal ganglia and are chemosensitive (bradykinin and capsacin)

These then go to vagus, synapse in solitary tract in medulla to cough center via second order neurons

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153
Q

What are TPR channels?

A

Transient Receptor Potentail - superfamily of ion channels expressed in sensory neurons

TPRA and TPRV have been implicated in cough; open and activate afferent nerves and respond to noxious stimuli

In disease, these receptors can become sensitized and hyperresopnsive

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154
Q

What are the efferent components of the cough reflex?

A

Activated to produce cough:

Vagus- supplies larynx and tracheobronchial tree

Phrenic - supplies diaphragm

Spinal motor nerves - supply expiratory muscles

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155
Q

Why do we cough?

A

Excessive stimulation of cough receptors - too much mucus, foreign body

Stimulation of afferent vagus (rare) - mediastinal tumor, aortic aneurysm

Heightened sensitivity to cough receptors - ACE inhibitors, airway inflammation

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156
Q

What is the role of ACE inhibitors in cough?

A

Common side effect - proposed mechanism:

ACE also metabolizes bradykinina dn substance P - these molecules accumulate and produce cough

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157
Q

What are causes of acute cough?

A

Viral URT infection

Exacerbation of underyling lugn disorder

Acute environemntal exposure

Acute cardiopulmonary disease

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158
Q

What are subactue coughs?

A

Postinfectious cough

Non-postinfectuous

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159
Q

What are causes of chronic cough?

A

Active cigarette smoking or chronic irritant

ACE inhibitor use
Radiographically apparent disease process in lung

Other: upper airway cough syndrome, asthma, nonasthmatic eosinophilic bronchitis, GERD

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160
Q

What can cause impairment of cough?

A

Neuromuscular weakness (expiratory weakness, chest wall disorders, inspiratory weakness)

Vocal cord paralysis

Abnormal properteis of mucous (COPD, Cystic fibrosis)

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161
Q

What are complicaitons of cough?

A

Many many

Constitutional
Respiratory

CV

GI

GU

MSK

Neuro

Skin

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162
Q

25 y/o man presents with 24 hour history of non-productive cough. denies other symptoms. started after he chocked on chicken bone that he thoguht he swallowed. cough is initated by:

A- efferent neurons that supply larynx and trachea

B- Αδ fibers from nodose ganglia

C- medullary cough center

D- adrenergic nerve innervation of airways

E- inflammatory mediators bradykinin and prostaglandins

A

B - Aδ fibers from nodose ganglia - mechanical!

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163
Q

What is dyspnea?

A

Breathing discomfort; distressed feeling associated with breathing

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164
Q

What is tachypnea?

A

Increased respiratory rate - response to increased CO2 production, or CO2 elimination that exceeds CO2 production

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165
Q

What is apnea/hypopnea?

A

Absence of or inadequate ventilation (central or obstructive sleep apnea)

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166
Q

Where does the sensation of dyspnea arise from?

A

Periphearl receptors throughotu respiratory system

Sense of effort from cortex when efferent messages are transmitted to respiratory muscles

Psychological, social, and environmental factors

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167
Q

How is the intesnity of dyspnea modified by?

A

Relationship between expected airflow and displacement of lugns and chest wall for given motor command and the ACTUAL acheived output of the ventilatory pump

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168
Q

What can cause neuro-mechanical dissociation of expected and actual airflow?

A

Excess ventilatory drive

Decreased ability to perform work of breathing

Excessive work of breathing

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169
Q

What mediates dyspnea?

A

Mechanoreceptors (stretch, J, and irritant receptors)

Chemoreceptors (medullary, carotid, aortic bodies)

Sensation of respiratory effort in skeletal muscles of chest wall, etc)

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170
Q

How can you objectively assess dyspnea?

A

Use of accessory respiratory muscles, tachypnea, cyanosis, hyperinflation

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171
Q

What can cause dyspnea?

A

Increased ventilatory drive -> anxiety, pain, fever, sepsis, increased dead space, increassed CO2 production, metabolic acidosis, hypoxia, medications

Increased work of breathing-> chest wall deformity, pleural effusion, pneumothorax, pulmonary fiborsis/interstitial lung disease, pulmonary edema, pnemonia, lower and upper airway disease

172
Q

What is hemoptysis?

A

Coughing up blood from airways or lungs - from mild bronchitis to fatal cancer

have to exclude epistaxis, oral, esophageal or gastric sources

DDx is broad

173
Q

What are major sources of hemoptysis?

A

Pulmonary, bronchial, alveolar-cappillary interface, mucosal or peribronchial plexus, endobronchial lesions

174
Q

What is pleuritic chest pain?

A

Chest pain worsening with inspiration or movement

Originates form parietal pluera, which has pain fiber innervation (visceral pleura and lung parenchyma dont

Can be inflammatory or traumatic, well localized

175
Q

What are pulmonary causes of chest pain?

A

Infection (lung or primary pleura)

Inflammation
Infarction
Pneumothroax

Tumor (met, primary pleura, or lung tumor)

176
Q

what are non-pulmonary/cardiac causes of cehst pain?

A

MSK

Psychogenic
GI (GERD, motility disorders, splenic flexure syndrome, pancreatitis)

177
Q

What are mechanisms of lung defense

A

Mechanical barriers

Mucociliary transport

Cough and othe rreflexes

Innate immune system (secretory molecules, cellular components)

Adaptive immune system (antibodies)

178
Q

What is the funciton of the nose?

A

Air is warmed to within 1 degree of body temp

Almost completely humidified

Partially filtered

179
Q

How does the nose act as a filter?

A

Hairs at entrance filter out large particles

Air hits many obstructing structures (turbinates, septum, pharyngeal wall)

Particles cant change direction as rapidly as air and striek surfaces adn are entrapped by mucous and transported by cilia to be swallowed

180
Q

What is the most important determinant of how a foreing particle will interact with respiratory system?

A

Size

181
Q

How does the mucociliary transport work?

A

Cilia beat in a coordinated fashion

Mucous velocity can move at up to 25 mm/min

HIghly efficient mechanism that can clear mucous blanket of entire nose or sinus in 10 minutes

182
Q

How are cilia typically arranged on the microtubule level?

A

Circular

183
Q

What happens when protective mechanisms are overwhelmed?

A

Accumulations of mucus - can be large and block airways; can also become infected

184
Q

What is mucus?

A

90% water, 10% of protein, carbohydrates and lipid

Non-aqeuous constituents - sol or gel phase, or both, depending on solubility

Proteinc onstituents: mucin glycoproteins, proteoglycans, variety of proteins (MUC genes - glycoproteins)

185
Q

What are funcitons of mucus?

A

PReserves membrane (lubricates, humidifies, waterproofs, insulates, provides environment for ciliary action)

Acts as barrier (entraps microorganisms, particulates, provides sruface for Ig action, neutrolyzes toxic gases)

Transports trapped materials

186
Q

What is mucociliary clearance?

A

Defense mechanism of ciliated epithelial cells that propels airway secretions towards mouth

Normally: periceliary liquid layer (PCL) is the layer of fluid that bathes cilia - located between apical membrane of epithelial cells and base of overlying mucus must be of optimal depth

Water movement into and out of PCL is mediated by active ion tranpsort (where Cystic fibrosis comes into play)

187
Q

What is teh source of mucin

A

GOblet cells

Submucosal galnd cells

Intracellular granules

Submucosal gland cells are cholinergically innervated (unlike goblet cells); release mucus when innervated

188
Q

What is the sneeze reflex?

A

Very much like cough reflex, except applies to nasal passageways

Initiating stimulus is irritation of nasal passageways

Afferent impulses pass in CNV in medulla

Series of reactions similar to those for cough take place, however the uvula is depressed so large amounts of air pass through the nose, helping clear it of foreign matter

189
Q

What are secretory molecules of innate defenses of the lungs/airway?

A

Complement - lysis and opsonizaiton of bacteria

Lactoferrin/transferrin - bind iron and limit bacterial growth

Interferons - limit viral replicaiton

AMPs = antimicrobrial peptides (β-defensins, cathelicidins) - kill bacteria

NO - toxic ot microorganisms

Lysozyme - breakds down bacterial walls

Proteolytic enzymes and cathepsinG - break down proteins

Surfactant proteins (SP-D) bind ot microorganims

190
Q

What are the sentinel cells of the lower airway?

A

Pulmonary dendritic cells (just under epithelium with pseudopods inot airway - capture particles

Pulmonary macrophages reside in lumen and capture and engulf particles

191
Q

What is normal bronchoalveolar lavage fluid?

A

< 95% alvoelar macrophages

< 4% lymphocytes

< 2% granulocytes

< 2% monocytes

< 0.4% dendritic cells

192
Q

What molecules differentiate pathogen from non-pathogen in order to activate the immune system only when necessary?

A

TLRs

193
Q

A 19 year old man presented to the ED with pneumonia. Since age 6 months he has had recurrent pneumonia and sinusitis due to Streptococcus pneumoniae and Haemophilus influenzae. His immune status would likely reveal abnormal function of:

  • A. B Lymphocytes
  • B. macrophages
  • C. natural killer cells
  • D. platelets
  • E. T Lymphocytes
A

A - B lymphocytes

194
Q

A 68 year old miner has been inhaling coal dust for 45 years. His immune system has cleared the dust particles that he has inhaled. Which of the following cells is most abundant in the alveoli to begin this innate immune process?

A. Alveolar Macrophages

B. Lymphocytes

C. Granulocytes

D. Monocytes

E. Dendritic Cells

A

A - Alveolar macrohpages

195
Q

What is asthma?

A

Chronic inflammatory disease characteraized by recurrent episodes of wheezing, breathlessness, chest tightness and cough

Associated with widspread but variable ariflow obstruction that is partially reversible either spontaneously or as result of treatment

Inflammation also causes increase in bronchial hyperresponsiveness

196
Q

What are distinguishing features of asthma?

A

Diffuse airflow obstruction of large and small airways

Reversibility of airflow obstruction (spontaneous or result of therapy)

Bronchial hyperresponsiveness to challenge (with specific or non-specific inhalation agents)

197
Q

How do you physiologically measure asthma?

A

Spirometry

PEFR measurements with peak flowmeter

Lung volume determinations

ABG analysis

Bronchoprovocation testing

198
Q

What are the mechanics of asthma?

A

Poiseuille’s law - central problem is narrowed small ariways leadign to increased resistance that reduces air flow (flow proportional to radius^4)

Resistance is not constant: inhalation - low intrathoracic pressures open airways; exhalation: postivie pressures can cause airway collapse

EXPIRATORY obstruction -> like one way valves

199
Q

What is airtraping?

A

Some lung gets over-inflatted. Some lung gets compressed (hypoxia, hypercarbia)

Overall can become overinflated -> stretched diaphragm muscles, plus high ariway resistance -> increased work

200
Q

How do you mesure airway obstruction?

A

FEV1 (fractional expiration volume in 1 second)

201
Q

What is the effect of bronchodilators on asthmatic lugn obstruction?

A

REVERSES obstruction

202
Q

What are diagnostic criteria for asthma with respect to reversibility?

A

>12% improvement in FEV1 over after short-acting bronchodilator or after weeks of corticosteroid therapy or wtih spontaneous remission

20% variation in peak flow within 24 hour period (biurnal variation)

203
Q

What happens to lung volumes and ABGs in asthma?

A

Lung hyperinflation (TLC, and FRC increased)

Air trapping (increased RV)

V/Q mismatch (Low V/Q leads to hypoxemia)

Respiratory alkylosis (hypoxemia/anxiety/reflexes)

Respiratroy acidosis - late (Severe V/Q mismatch, respiratory muscle fatigue)

204
Q

What is bronchial hyperresponsiveness?

A

Exaggerated bronchoconstrictive response to specific (not everyone responds, e.g. allergen) or non-specific (everyone responds, eg. methacholine)

Can be quantified by bronchoprovocation tests (allergen, methacholine, histmaine challenge, cold air)

205
Q

Who has greatest prevalence for asthma?

A

Peak is in childhood (10%) -> declines to 5-6% in adolescents -> rises to 7-9% in adults

206
Q

What are risk factors for developing asthma?

A

Genetics and environment

Genetics: increased prevalence in 1st degree relatives, twins, association with atopy

Env: airborne allergens, viral respiratory infections, tobacco smoke, air pollution, occupation, lifestyle

207
Q

What is the pathobiologic etiology of asthma?

A

Basal chronic inflammaiton exacerbated by acute ifnlamation that leads to structual change sover time

208
Q

What occurs during the acute response of asthma?

A

Mediator release -> bronchoconstriction

Muscle contraction, muscle shortening, increased luminal resistance

209
Q

What occurs in chronic inflammaiton in asthma?

A

Cellr ecruitment, epithelial damage, early structural changes

210
Q

What is the relationship between allergy and astham?

A

Allergic astham is most common phenotype of astham

Sensitization in susceptible popoulations to indoor allergens -> housd-dust mite, animal dander, cockroaches, outdoor fungi)

Developing sensitivity to allergen can be cause of asthma (Declines with age)

Food allergens do not cause asthma

Reduce exposure to reduce asthma

211
Q

What is the atopic response?

A

Seen in asthma (Th2 phenotype)

212
Q

What is Th2 role in asthma?

A

Th2 response is atopic response to aeroalelrgens also toe extracellular pathogens such as helminths and certain bacteria

Th2 cells release IL-4, IL-5, IL-13, IL-9 which promote anitbody response and involves mast cells and eosinophils

213
Q

What do Th2 cells do? (as a result of their cytokines)?

A

Allergen specific synthesis of IgE (IL-4)

Recruits eosinophils (iL-5)

Recruit and promote growth of mast cells (IL-9)

AHR and mucus production (IL-13)

214
Q

What is the basis hygeine hypothesis?

A

Biases immune response to Th2 -> can see more asthma this way

215
Q

What happened in this asthmatic?

A

Lumen obstructed by secretions of mucus admixed with inflammatory exudates

Severe mucous plugging in acute severe asthma

216
Q

How does aireway remodeling occur in chronic asthma?

A

Smooth msucle mass increased

Mucous gland hypertrophy

Blood vessels engorge

Inflammatory cells persist

Collagen (Types 3 and 5) deposited in basement membrane (lamina reticularis) and in the extracellular space

217
Q

What are clinical manifesttions of asthma?

A

History of cough (worse at night), recurrent wheeze, recurrent difficulty breathing, recurrent chest tightness)

Wheezing - high pitched whistling sounds when breathing OUT: not necessary for diagnosis

Symptoms occur or worsen at night, waking the patient

218
Q

A 26 year old woman presents with shortness of breath on exertion. She was formerly able to play several sets of tenjis but lately gets shortness ofb reath after several games She has a history of allergic rhinitis and otherwise a negative past medical history. Her spirometry is normal. What test can best offer a diagnosis?

  • A. Post bronchodilator spirometry
  • B. Plethismography lung volumes
  • C. Methacholine challenge test
  • D. Serum IgE level
  • E. Total eosinophil count
A

C - methacholine challenge test (non-specific challenge)

219
Q

What is emphysema?

A

Abnormal permanent elnargement of air spaces distal to the terminal bronchiole, accompanied by destruciton of their walls

220
Q

What is chornic bronchitis?

A

Presence of chronci productive cough for at least 3 consecutive months in 2 consecutive years

221
Q

What is COPD?

A

Chornic obstructive pulmonary disease: disease characterized by airflow limitation that is not fully reversible

The ariflow limitation is progressvie and associated with abnormal inflammaotry response of the lungs to noxious particles and gases

222
Q

What are causative agents of COPD? (i.e. aggressors)

A

Cigarettes (developed world)

Fossil fuel burning (developing world)

223
Q

What is the association with smoking and COPD?

A

Major risk facotr

~90% of COPD patients ahve smoking history

However, only 15-20% of smokers develop COPD

224
Q

What are histopathological features of COPD?

A

Chronic bronchitis (bronchiolitis) - thickening of airway wall and infiltration with inflammatory cells

Emphysema (destruction of alveolar walls) -. loss of attachments and airway collapse

225
Q

What is the progression of COPD?

A

Normal -> hyperproduction of mucus -> inflammation and mucus -> end-stage

226
Q

Why is airflow limited in COPD?

A

Destruciton of attachments of alveoli to airways, mucus hypersecretion, fibrosis and inflammation

227
Q

What is the result of lung elastic recoil loss?

A

Airway obstruction

228
Q

What is the pathophysiology of COPD?

A

Funcitonal abnromalities in bronchitis (airway narrowing from inflammation -> diminished flow rates adn air trapping (increased Reserve volume))

Funcitonal abnromalities in emphysema (loss of fucntioning architecture - loss of recoil, collapsibility of airways, increased lung volumes)

Hyperinflation - chronic obstruction leads to air trapping, diaphragm flattens causes disadvantage and inefficiency in mechanics of breathing; increased work; higher lung volumes -> dyspnea

229
Q

What is the source of the decreased diffusing capacity of CO2 in COPD?

A

Loss of surface area for diffusion

230
Q

What are spirometric measurements in COPD?

A

High FEV1, Higher FVC

231
Q

How is COPD staged?

A

FEV1/FVC

232
Q

How do you perform spirometry for COPD testing?

A

Administer adequate dose of short-acting bronchodilator (e.g. salbutamol)

Post-bronchodilator FEV1/FVC of < 0.7 confirms airlfow limitation that is not fully reversible

233
Q

What findings do you see on CXR in COPD?

A

Emphysema - increased ucency, especially in upper lobes

Hyperinflation - flattened diaphragm (barrel chest)

234
Q

What are three types of emphysema?

A

Centrilobular -> holes in centrilobular area

Panlobular -> uniform dilatation of airspaces from respiratory bronchioles to alveoli

Paraseptal -> subpleural well-defined cystic spaces -> can be bullous lung disease

235
Q

What do we see ehre?

A

Normal lung

236
Q

What do we see here?

A

Centrilobular emphysema

237
Q

What do we see ehre?

A

Panlobular emphysema

238
Q

What do we see here?

A

Paraseptal emphysema

239
Q

What is the natural history of COPD?

A

Annual loss of FEV1 is ~ 50-100mL per year

Greater decline in patients with hypersecretion of mucus (chornic bronchitis)

Extertional dyspnea ~40% FEV1

Dyspnea at rest ~20% FEV1

Increased CO2/cor pulmonale ~ 25% FEV1

240
Q

Why does COPD only present after many many years of smoking, etc? (why does it present late)?

A

Affects small airways -> this provides the LEAST resistance since there are so many -> requires lots of involvvement ot begin to see symptoms

241
Q

What are causes of progressive airway obstruction in COPD?

A
  1. Proinflammatory mediators
  2. Proteolytic digestion of lung tissue
  3. Oxidative stress
242
Q

What is the primary inflammatory cell seen in the airways in COPD? How is it different than asthma?

A

Neutrophils!

Asthma has eosinophils

243
Q

What is the role of alveoolar macrophages in COPD?

A

Extremely important -> recruited, present in high numbers, survive longer, release numerous chemokines

Due to cigarette smoke, and other toxins

244
Q

What is the key cell for COPD pathogenesis?

A

Neutrophil

Recruited and activated via chemotactic factors (LTB4, IL-8). released form macrophage and epithelial cells as ar esult of stimluation by cigarette smoke

Release proteinases that break down connective tissue and stimulate mucus secretion

Release ROS and adhesion molecules taht potentiate inflammatory response and promote further neutrophil recruitment

245
Q

What ist he role of proteinases in COPD?

A

INvolved in alveolar wall destruction

Smokers ahve high levels of neutrophil elastase in BAL fluid; adn higher when emphysema is present

NE degrades elastin in elastic tissue

Collagen breakdown and synthesis is also a feature of emphysema

246
Q

What is alpha-1 antitrypsin (AAT)?

A

Elastase inhibitor that protects agains proteolytic degradation of elastin

Causes early COPD in smokers

Imbalance of neutrophil elastase and AAT causes COPD

247
Q

What are clinical features of α1 antitrypsin?

A

Early onset emphysema

Lowerlobe bulae/emphysema

Unexplained liver disease

248
Q

What are risk factors for COPD?

A

Smoking

Environmental factors, occupational exposure

Lugn growth

Airway hyperresponsiveness

Genetics

249
Q

What are clinical features of COPD?

A

Chronic productive cough commonly presents in 5th decade with acute chest disorder

Typically 1 pack per day smoker for > 20 years

Dyspnea on effort in 6th, or 7th decade

Mucoid sputum production in morning

Wheezing and dyspnea can lead to erroneous diagnosis of asthma

Poor quality of life and prognosis in later life

250
Q

What are acute exacerbations of COPD?

A

Acute event characterized by worsenign of patients respiratory symptoms that is beyond day-to-day variations and leads to change in medications

251
Q

What are potential causes of acute COPD exacerbations?

A

Bacterial or viral infection

Pollutants (NO, aprticulates, Sulfur dioxide, ozone)

Codl weather

Interruption of regular treatment

252
Q

What is AECOPD?

A

Acute exacerbation of COPD

253
Q

What are the common etiologies of AECOPD?

A

Infectious (non-infectious are ~ 20%)

254
Q

What are the pulmonary effects of chornic inflammmation in COPD?

A

Dyspnea

Cough
Sputum production
Exacerbations

Ankle Edema

255
Q

What are non-pulmonary (systemic) effects of the inflammation present in COPD?

A

Poor apetite/early satiety

Hypoxemia
Skeletal muscle dysfunction
CV increased risk of disease and death

Depression/anxiety/altered sleep
Osteoporosis

Anemia of chornic disease /GI bleed

256
Q

A 70 year old heavy smoker presented to his physician with shortness of breath that started 3 years ago. On exam he has prolonged exhalation, decreased breath sounds and has a barrel chest. The likely cause of his lung condition

  • A. Bronchospasm from cigarette smoke
  • B. Destruction of intra-alveolar septae
  • C. Deconditioning
  • D. Decreased CNS drive
  • E. Decreased work of breathing
A

B - Destruction of intra-alveolar septae

257
Q

What do you see here?

A

Thick airways, large airways (even at periphery)

Poor tapering of airways

Mucus clogs

Mismatch of airway size and adjacent vessel size

Representative of bronchiectasis - irreversible dilatiation of bronchi caused by destruction fo bronchial wall and elastic elements

258
Q

What is bronchiectasis?

A

Irreversible dilatation of bronchi caused by destruction of bronchial wall muscle and elastic elements

Obstructive: localized blockage and bronchiectasis occurs distal to this mechanical obstruction

Localized: used to be common, following childhood bronchopulmonary infections with measles, pertussis, or other bacteria

Generalized: secnodary to inherited impairment in host defense mechanisms, or acquired conditions that perrmit introduction of infectious organisms into airways

259
Q

How does bronchiectasis develop?

A

Interplay between external insult, impaired immune system, genetics

Causes bronchial wall inflammation and destruction, leading to ciliary dyskinesia or altered bronchial dynamics

This results in ineffective mucus clearance, leading to chronic or recurrent infection and perpetuating the cycle

260
Q

What are predisposing conditions for localized bronchiectasis?

A

Airway obstruction: foreign body, bronchial stricture, endobronchial mass

Non-obstructive (post infection) : bacterial, viral, mycobacterial

261
Q

What are predisposing conditions for generalized bronchiectasis?

A

Post infectious: measles, pertussis, mycobacteria

Congenital: cystic fibrosis, primary ciliary dyskinesia

Immunodeficiency: Ig deficiency, HIV/AIDS

Immune mediated: Allergic aspergillus, collagen vascular disease

GERD/Aspiration

262
Q

What are the most common pathogens seen in bronchiectasis?

A

H. flu

Pseudomonas aeruginosa

Moraxella catarrhalis

Staph aureus

Strep pneumo

Mycobacteria

263
Q

Who gets bronchiectasis?

A

Older individuals

264
Q

What are symptoms of bronciectasis?

A

Chronic cough

Dyspnea

Mucopurulent sputum production

Hemoptysis

Exacerbation of symptoms and need for antibiotic therapy several times a year for respiratory tract infection

265
Q

What are pulmonary function tests like in bronchiectasis?

A

In early or mild disease may be normal

As disease advances -> airflow obstruction

Late -> mixed obstruction and restriction

Depends on extent of involvement

266
Q

What do you typically see on x-ray in bronchiectasis?

A

Parallel line shadows (railroad track shadows), infiltrates, hyperexpansion (flattened diaphragm)

267
Q

What are three different classifications of bronchiectasis on CT?

A

Cylindrical (common)

Varicose

Saccular/cystic (most severe)

268
Q

What are typical CT findings in bronchiectasis?

A

“Tram lines” - horizontal course of bronchi and artery (red circle)

“Signet ring” sign: cross-section of dilated bronchi

“Tree bud” pattern - bronchiolar mucus impaction

269
Q

How do you traet patients with bronchiectasis?

A

Long term oral antibiotics

Aerosolized antibiotics (tobramycin inhalation solution)

Other measures: airway clearance measures

270
Q

Do you see hemoptysis in bronchiectasis?

A

Yes - major cause of hemoptysis

271
Q

What do we see here?

A

Situs inversus

Inflitrates

Cystic bronchiectasis

272
Q

What is primary ciliary dyskinesia?

A

Genetic disease in which you have defective ciliary structure and function

Chronic oto-sino-pulmonary disease; also have sterility (impaired ciliary mobility in vas deferens or fallopian tube)

Often seen with dextrocardia or with situs inversus (50% of individuals)

273
Q

What are features for diagnosis of primary ciliary dyskinesia?

A

Chronic upper and lower aireway disease

Slope-decline of lung function (FEV1) with age, but not as rapid as in cystic fibrosis

274
Q

What are the members of the sputum flora of patinets with primary ciliary dyskinesia?

A

H. flu/S. aureus

Smooth P. aeruginosa

Mucoid P. aeruginosa

Non-tuberculoid mycobacteria also isolated

275
Q

What do you see here?

A

Bronchiectasis - the balls seen are CLASSIC for aspergillus (aspergilloma)

Cystic bronchiectasis complicated by an aspergilloma

276
Q

What causes aspergillosis?

A

Aspergillus fumigatus is most common

Grows as septate dichotomous branching hyphae with actue angles and produce hundreds of spores

Can cause aspergilloma that can complicate bronchiectasis

277
Q

What is cystic fibrosis??

A

Mutations in gene encoding for CF transmembrane conductance regulator (CFTR) - most common is ΔF508; and results in dysregulation of transmembrane transport of small molecules

Abnormalities in epithelial ion transport (dysregulated salt and water transport)

Increased sweat chloride

Changes in airway surface liquid - impaired mucociliary clearance

Causes BRONCHIECTASIS

278
Q

What are common airway infections in cystic fibrosis?

A

S. aureus (first organism to infet young people)

H. flu (more common at younger age, uncommon in young adults)

Candida (most frequent, but considered harmless)

Aspergillus (seen in > 25% of pts)

Nontuberculous mycobacterium (MAC) - increasingly reported

279
Q

What is the issue with pseudomonas infections in cystic fibrosis?

A

Early isolates may be normal

Later mucoid strains are antibiotic resistant and can be encouraged by chronic antibiotics

Once establisehd may be impossible to eradicate (forms biofilms) and can develop tolerance to host defenses and antibiotics

280
Q

What is bronchiolitis?

A

INflammation in smaller conducting airways

Terminal to respiratory bronchioles

Intense repair process causes narrowing and distortion of small airways

INcomplete obliteration of lumen (constrictive bronchiolitis)

Complete obliteration (bronchiolitis obliterans)

281
Q

What are potential causes of bronchiolitis?

A

INfection

Inhalation injury

Collagen vascular disease is associated with this (RA, etc.)

Post transplant

Idiopathic

282
Q

How do patinets with bronchiolitis present clinically?

A

Infection: acute, with fever, cough, rhinorrhea, wheezing; viral in child respiratory syncytial virus; adults get it with adenovirus, influenza, parainfluenza, Legionella pneumophilia, Mycoplasma pneumonia

Inhalation exposures: may be delayed onset of cough adn breathlessness, subacute and progressive; NO2, Ammonia, Chlorine

Collagen vascular disease/post transplant: unexplained breathlessness, cough, or airflow obstruction; may be asymptomatic in early stages

283
Q

What do you see on CTs in bronchiolitis?

A

May be negative since it involves the smallest division of the pulmonary system

Centrilobular peripheral nodules and tree-in-bud opacities may be seen

Obstruction of small airways can cause air trapping or hyperinflation

284
Q

What do you see here?

A

Centrinodular nodules and tree-in-bud pattern of BRONCHIOLITIS

285
Q

What are indirect signs of bronchiolitis on CT?

A

Mosaic perfusion of lungs

286
Q

What do we see here?

A

Mosaic perfusion pattern in a patient with bronchiolitis

287
Q

A 35 year old man is known to have cystic fibrosis since birth presents with severe shortness of breath and increased sputum expectoration. The patient’s sputum is likely to show:

  • A. Resistant strains of Staphylococcus
  • B. Neutrophils without organisms
  • C. Mucoid strains of Pseudomonas
  • D. Pseudomonas sensitive to several antipseudomonals
  • E. Haemophilus organisms overtaking the petri dish
A

C - Mucoid Strains of Pseudomonas

288
Q

What are the major effector cells in asthma pathophysiology?

A

Mast cells/Eosinophils

289
Q

What are three types of asthma?

A

Extrinsic: type I hypersensitivity - atopic or occupational

Intrinsic: non-immune, due to aspirin ingestion, pneumonia, cold, stress, exercise, etc.

Status Asthmaticus: unremitting attacks due to exposure to previously sensitized antigen (can be FATAL)

290
Q

How does asthma present grossly on pathology?

A

Overdistended lungs, small areas of atelectasis, thick mucus plugs in proximal bronchi

291
Q

How does asthma present on microscopic pathology?

A

Mucus plugging

INflammation (eosinophils)

INcreased mucosal goblet cells and submucosal glands

Thickened basement membrane

Smooth muscle hypertrophy

Airway wall edema

292
Q

What is unique about the airway mucus in asthma?

A

Can form a cast of the airways

INcreased inflammatory cells

Increased inflammatory mediators

Increased mucin concentration

293
Q

What do we see here?

A

Mucus plugs

Denuded or altered respiratory epithelium

Eematous submucosa

ASTHMA

294
Q

What do we see here?

A

Sub-epithelial fibrosis

Bronchial smooth muscle hypertrophy/hyperplasia

Inflammation

Thickened basement membrane

ASTHMA

295
Q

What do we see here?

A

THICKENED BASEMENT MEMBRANE = ASTHMA

296
Q

What is emphysema??

A

Permanent enlargement of airwasy distal to the terminal bronchiole

Accompanied by destruction of walls without obvious fibrosis

Elastic component of the alveolar walls are destroyed -> decreased expiratory drive and tethering of small airways

297
Q

How is emphysema categorized pathologically?

A

Centriacinar (most)

Panacinar

Paraseptal

First two cause clinical significant airflow obstruction

Clinical severity is more important than histologic type for symptomatology

298
Q

What is centriacinar emphysema?

A

Central or proximal parts of acini are affected, distal parts are spared

See both emphysematous and normal airspaces within same acinus and lobule

Seen more in UPPER LOBES, due to its correlation with HEAVY SMOKERS

299
Q

What is panacinar emphysema?

A

Acini are uniformly enlarged from level of respiratory bronchiole to terminal blind alveoli

Associated with α1 ANTITRYPSIN (α1-AT) DEFICIENCY

300
Q

What type of emphysema is seen more commonly in heavy smokers?

A

Centrilobular emphysema

301
Q

What type of emphysema is seen with α1 antitrypsin deficiency?

A

Panacinar emphysema

302
Q

What is paraseptal emphysema?

A

Distal portion of acinus only involved (proximal areas are normal)

Involves lung tissue underneath the pleura

More severe in upper half of lungs

Air spaces can become very large

In young adults, can result in SPONTANEOUS PNEUMOTHORAX if otherwise healthy

303
Q

What is an association wtih a spontaneous pneumothorax in an otherwise healthy young adult?

A

Paraseptal emphysema (distal acinar emphysema)

304
Q

What do we see here?

A

Centriacinar emphysema

305
Q

What do you see here?

A

Centriacinar emphysema

306
Q

What are the alleles for α-1 antitrypsin deficiency?

A

ZZ homozygous individuals have full blown disease

MM individuals are healthy

307
Q

What do you suspect when a patient ahs early onset emphysema and unexplained liver disease and possible cirrhosis?

A

α1 Antitrypsin deficiency

308
Q

What does ZZ α1 antitrypsin alleles indicate?

A

Disease -

ZZ = disease

ZM = reduced functional levels

MM = normal

309
Q

What do we see on the left? right?

A

left - centriacinar emphysema

right - panacinar emphysema

310
Q

When do you begin to see symptoms in emphysema?

A

When 1/3 /of functional capacity is lost

311
Q

What are physical findings in emphysema?

A

Shortness of breath

Coughing

Wheezing

Weight loss

Barrel Chest

Breathing through pursed lips (pink puffer)

312
Q

What are sequellae of emphysema?

A

Secondary pulmonary vascular hypertension

Death due to respiratory acidosis adn coma

Pneumothorax

313
Q

What do we see here?

A

Bullous emphysema

314
Q

What are causes of chronic bronchitis?

A

4-10x more common in smokers, chronic irritation and infetions

Tobacco interferes with ciliary action, directly damages aireway epithelium, and inhibits ability of WBCs to clear bacteria; infections maintain but do not initiate chronic bronchitis

315
Q

How does chronic bronchitis appear grossly?

A

Boggy mucosa with excessive mucinous secretions, pus

316
Q

How does chronic bronchitis appear microscopically?

A

Early: hypersecretion of mucus in large airways with hypertrophy of submucosal glands in tracheobroncial tree

Late: increase in goblet cells in small airways causes excessive mucus production and airway obstruciton; increased Reid index

Reid index: ratio of thickness of mucus gland layer to thickness of wall between epithelium and cartilage (normal = 0.4) increased in chronic bronchitis

317
Q

What do you see here?

A

Chronic bronchitis

Reid INdex is close to 0.8-0.9 (80-90% of space is occupied by glands)

Enlarged mucus secreting apparatus

318
Q

What do you see here?

A

Bronchiectasis

Dilated, tortuous, easily collapsible airways that extend to the visceral pleural surface

Copious purulent secretions within dilated bronchi

May be generalized and bilateral or localized depending on etiology

319
Q

What do you see here?

A

Bronchiectasis

Markedly distended peripheral bronchi - can trace to pleural surface

Bronchial walls irregularly thickened

320
Q

What do you see here?

A

Bronchiectasis

DIlated airways that extned to visceral surface

Causes airflow eddies, and copious secretions

321
Q

What do you see histologically in bronchiectasis?

A

Chronic inflammation and ulceration of bronchial wall

Variable inflammation and fibrosis of adjacent alveoli

322
Q

What histology does this represent?

A

Bronchiectasis

323
Q

What are the small airways?

A

Less than 2mm internal diameter - NO cartilage

Membranous (terminal or respiratory)

Composed of epithelial cells (simple columnar, ciliated and nonciliated, as well as rare NE cells); connective tissue; and smooth muscle

324
Q

When do you see small airway disease?

A

Primary: constrictive bronchiolitis (obliterative bronchiolitis) - rare

Secondary: bronciectasis, asthma, COPD, etc. - more common

325
Q

What do you typically see in small airway disease microscopically?

A

Adjacent segment may have foamy macrophage accumulation and dilatation with mucostasis

326
Q

What is fibrotic small airway disease (constrictive bronchiolitis/obliterative bronchiolitis)?

A

Subepithelial collagen deposition with airway narrowing and constriction

Thought to be abnormal wound healing response

Seen with chronic transplant rejection, as part of GVHD following BM transplant; but also with toxin exposure, infection, collagen vascular disease, drugs, etc.

327
Q

What is this?

A

Constrictive bronchiolitis

Large amounts of connective tissue between airway and smooth muscle

Collagen and some inflammation hanging around

328
Q

What do we see here?

A

Constrictive bronchiolitis - big scar next to pulmonary artery

329
Q

What is bronchiolitis obliterans?

A

Not same as obliterative bronchiolitis (constrictive bronchiolitis)

In obliterans, you see luminal inflammatory exudates that forms plug of fibroblastic tissue (rare)

330
Q

What ist he difference between constrictive bronchiolitis and bronchiolitis obliterans?

A

Obliterans - buildup is WITHIN lumen

Constrictive - buildup of fibrosis is in wall, outside of lumen and constricts from outside in

331
Q

What is pneumonia?

A

Infection of the pulmonary parenchyma

332
Q

What are different routes that infections can take to the lower respriatory tract?

A

Inhalation - carried in small droplet particles inhaled into lungs

Aspiration - unable to protect ariways from secretions by glottic closure and coughing

Bloodstream - less common

333
Q

Why does pneumonia happen?

A

Defect in host defenses

Exposure to particularly virulent organism

Overwhelming inoculum

334
Q

What are host defenses that fail or are overcome in pneumonias?

A

Branching of airways and predisposition of airways to deposition by inhaled material

Antimicrobial peptides

Phagocytic/inflammatory cells

Adaptive immune responses

335
Q

What is the virulence factor of chlamydophilia neumoniae?

A

Ciliostatic factor

336
Q

What is the virulence factor of mycoplasma pneumoniae?

A

Shears off cilia

337
Q

What is the virulence factor of influenza virus?

A

Reduces tracheal mucus velocity

338
Q

What is the virulence factor of streptococcus pneumoniae?

A

Proteases that split secretory IgA and has a capsule taht inhibits phagocytosis

339
Q

What are the virulence factors of mycobacteria and legionella species?

A

Resistant to microbicidal activity of phagocytes

340
Q

What is strept pneumoniae?

A

Gram positive cocus in pairs or diploccoci

50% of pneumonias requiring hospitalization

Normal inhabitant of pharynx

Polysaccharide capsule protective from phagocytosis

341
Q

What is staph aureus?

A

Gram + cocus inc lusturs

Seen as secondary complication of influenza virus; seen in hospitalized patients; disseminated via blood

342
Q

What is haemophilus influenzae?

A

Small, coccobacillary gram-negative organism

Colonizes nasopharynx of normal individuals and lower airways of COPD patients

343
Q

What is Klebsiella pneumoniae?

A

Large gram - bacillus

Found in GI tract

Seen in alcoholics

Causes thick, bloody, mucoid sputum (currant jelly sputum)

344
Q

What is pseudomonas aeruginosa?

A

Gram - bacillus

Found in variety of environmental sources

Seen in debilitated, hospitalized patients previously treated wiht antibiotics

345
Q

What is legionella pneumonphila?

A

Cause of pneumonia typically associated with water reservoirs

Gram - bacillus

Poorly stained ; affets healthy and prior respiratory defense deficient individuals

NOn-respiratory manifestations: GI, CNS, Hepatic, Renal

346
Q

What is chlamydophila pneumoniae?

A

Obligate intracellular parasite

Not readily cultured

5-10% of pneumonias

347
Q

What is mycoplasma pneumoniae?

A

Smallest organism identified; intermediate between virus and bacteria

10-20% of all pneumonias

“Walking pneumonia” -> chest xray looks worse than clinical presentation

348
Q

What settings do anaerobic organisms cause pneumonia ins?

A

Aspiration of secretions (impaired consciousness due to coma, alcohol or seizures; or difficulty swallowing due to neuromuscular disease)

Poor dentition or gum disease are a risk factor (larger burden of organisms)

349
Q

What is the pathology of pneumonia characterized by?

A

Infection and inflammation of distal pulmonary parenchyma

Influx of neutrophils, edematous fluid, erythrocytes, mononucelar cells, fibrin

350
Q

What is bronchopneumonia?

A

Distal airway inflammation prominent along with alveolar disease

Spread of infection occurs through airways

Patchy distribution

E.g. staph aureus and gram - bacilli

351
Q

What is lobar pneumonia?

A

Infectious process throughot entire lobe of lung (dense consolidation)

Spread via alveolus to alveolus and from acinus to acinus via interalveolar pores (pores of Kohn)

E.g. strept pneumo, klebsiella pneumoniae

352
Q

What is interstitial pneumonia?

A

INflammatory process within interstitial walls rather than alveolar spaces

E.g. mycoplasma pneumoniae, influenza

353
Q

What do we see here?

A

Bronchopneumonia

354
Q

What do we see here?

A

Lobar pneumonia

355
Q

What do we see here?

A

Interstitial pneumonia

356
Q

How does pneumonia cause symptoms/disease?

A

Inflammaiton and infetion of distal air spaces leads to decreased ventilation

V/Q ratio decreased in diseased regions

If totally filled with inflammatory exudate, no ventilation : shunt -> hypoxemia

CO2 retention is not a common feature of pneumonia

Typically hyperventilate

357
Q

What are symptoms of pneumonia?

A

Fever

Cough (productive or not)

Shortness of breath

Pleuritic chest pain if process extends to pleural surface

358
Q

What do you find on exam in pneumonia?

A

generalized infection (tachycardia, tachypnea, fever)

Lung exam: opening/closing of distal airspaces = rales; consolidation = bronchial breath sounds, tactile fremitus, egophony, whisper pectorliquoy, dullness to percussion

359
Q

What are differences in typical vs atypical pneumonia?

A

Typical = acute, productive cough, lung exams with signs of consolidation, leukocytosis with neutrophilia, CXR shows consolidation, bugs include strept pneumo, h. flu, klebsiella pneumoniae, staph aureous, anaerobes

Atypical = gradula, non-productive cough, normal WBC, systemic compalints more than respiratory, bugs include mycoplasma pneumoniae, chlaidophyla pneumoniae, legionella, viruses

360
Q

What is histoplasmosis?

A

Histoplasma capsulatum

Dimorphic -> branching hyphae in soil, round, oval yeast in body

Mississippi or Ohio River Valley

Self limited in immunocompetent, lifethreatening in immunocompromised

COPD patients resembles tuberculosis

inhale sporesorganisms converts to yeast phaseinflammatory response in lung parenchymayeast may not be killed by macrophages and spreads to other organsdelayed hypersensitivity develops and immune response becomes granulomatous

361
Q

What is coccidiomycosis?

A

Coccidiodes immitis

Dimorphic - spherules in tissue, mycelia ins oil

San Joaquin valley

Inflammatory response is granulomatous

Immunocompetent = self limited

Immunocompromised = hematogenous spread and disseminated disaese

Can resemble TB

362
Q

What is blastomycosis?

A

Soil-dwelling blastomyces dermatidis

Midwestern and Southeastern US

Neutrophilic response but subsequently includes macrophages, and T cells; granulomas and pyogenic response

Resembles bacterial pneumonia

Self-limited

IMpaired immunity can be more rapid or severe disease

363
Q

What is aspergillus?

A

Widespread

Aspergillus fumigtus most common

NOT dimorphic, always mycelia (branching hyphal form)

Everyone exposed

364
Q

What is ABPA?

A

Allergic bronchopulmonary aspergillosis

Predisposing feature is asthma

Resides in airway and is important as antigen, not as pathogen

365
Q

What is aspergilloma?

A

Predisposing feature is preexisting cavity within pulmonary parenchyma (e.g. due to TB)

COlonzies cavity with little invasion

Presents as hemoptysis or with no symptoms but found on CXR

366
Q

What is invasive aspergillosis?

A

Predisposed by impaired immune resopnse

Invades and spreads through lung tissue

367
Q

What is chronic necrotizing pulmonary aspergillosis?

A

Predisposing feature is underlying lugn disease or impairment of immune system

Indolent, localized invasion of parenchyma

Necrosis of involved tissue -> cavity formation

368
Q

What do we see here?

A

Aspergilloma

369
Q

What is pneumocystis jiroveci?

A

Causes pneumonia in malignancy, organ transplant, or AIDS

Insidious onset fever and dyspnea

Alveolar filling -> hypoxemai is prominent clinical feature

370
Q

What are potential complications of pneumonia?

A

Abscess or empyema

371
Q

What is a lung abscess?

A

Localized collection of pus

Results form tissue destruction

Neutrophil rich

Etiologic agents are bacteria that cause necrosis (anaerobes, staph aureaus, gram negs)

372
Q

What is an empyema?

A

When pneumonia extends to pleural surface -> pus in pleural space

Thick, creamy or yellow fluid within space; enormous number of leukocytes and bacterial organisms

Need to drain and treat with antibiotics

373
Q

What do we see here?

A

Lung abscess

374
Q

What do we see here?

A

Empyema

375
Q

How do we base antibiotic therapy in pneumonia patients?

A

Where it was acquired

376
Q

How do we treat community acquired pneumonias?

A

Macrolides or doxycycline

Fluoroquinolone or β-lactam plus macrolide

377
Q

How do you treat nosocomial pneumonia?

A

Complex, depends on particular pathogens that are common in hospital, etc.

378
Q

What define bronchopneumonias?

A

Patchy consolidation of lung centered on bronchi

Neutrophils in bronchi, bronchioles, and adjacent alveolar spaces

379
Q

What define lobar pneumonias?

A

Affect entire lung lobe but are rare now due to antibiotics

Still seen wiht particularly virulent organism or immunosuppressed host

380
Q

What is the difference between bronchopneumonia and lobar pneumonia?

A


381
Q

What do we see here?

A

Bronchopneumonia

382
Q

What do we see here?

A

Lobar pneumonia

383
Q

What is the cell type seen in acute bacterial pneumonia?

A

PMNs, RBCs and fibrin (neutrophils!!!)

384
Q

What are symptoms of lung abscesses?

A

Cough

Fever

Foul-smelling sputum

Chest pain

Weight loss

385
Q

How do you treat lung abscesses?

A

Antibiotics

Resection may be required

386
Q

How does a lung abscess appear grossly?

A

Thick fibrotic walls and surrounding pneumonia in chronic abscesses

387
Q

What do we see here?

A

Lung Abscess

388
Q

What makes atypical pneumonias atypical?

A

Location of inflammation -> seen in alveolar septa and pulmonary interstitium (not in the airspaces)

Most commonly caused by mycoplasma pneumoniae, and viruses

Inflammation is comprised of LYPMHOCYTES, not neutrophils

389
Q

What cell type characterizes atypical pneumonia?

A

Lymphocytes

390
Q

What do we see here?

A

Atypical pneumonia (viral)

391
Q

What are pulmonary viral infections?

A

CMV

Herpes I and II

Adenovirus
Influenza and parainfluenza

392
Q

What do we see here?

A

Intranuclear and intracytoplasmic inclusions typical of cytomegalovirus

393
Q

What do we see here?

A

Intranuclear and intracytoplasmic inlcusions typical of cytomegalovirus

394
Q

What do we see here?

A

Intranuclear and intracytoplasmic inlcusions typical of cytomegalovirus

395
Q

What do we see here?

A

Multinucleate cells with intranuclear inclusions typical of herpesviruses

396
Q

What do we see here?

A

Single large intranuclear lesion characteristic of adenovirus infection (smudge cell)

397
Q

What is a Gohn Complex?

A

Pulmonary granuloma and hilar lymph node involvement

398
Q

What is miliary tB?

A

Disseminated TB resulting in multiple small granulomas and other organ involvement

399
Q

What do we see here?

A

Gohn Complex : granuloma + hilar LN involvement

400
Q

What are sites of tuberculous disease?

A

Lung

Meninges

Kidneys
Fallopian Tubes

Adrenals
Vertebrae

401
Q

When do you see mycobacterium avium intracellulaire (MAI)?

A

HIV/immunocompromised

Right middle lobe syndrome (Lady Windemere syndrome)

402
Q

Where is histoplasma located?

A

Mississippi + Ohio RIver Valey but also Carribean and Asia

403
Q

What do we see here?

A

Histoplasma - narrow based budding

404
Q

Where does coccidiodomycosis live?

A

Arizona, “San Joquin Valley”

405
Q

What do we see here on PAS stain?

A

Coccidiomycosis

406
Q

Where is blastomycosis live?

A

Deep south (Louisiana, Mississippi, etc)

407
Q

WHich organism causes broad based bud?

A

Blastomycosis

408
Q

What do we see here?

A

Broad based budding (blastomycosis)

409
Q

What do we see here?

A

Aspergillosis

410
Q

What do we see here?

A

Halo typical of cryptococcus

411
Q

What is unique about cryptococcus?

A

Mucamine capsule, highlighted by DPAS, Aclian blue, or micicarmine

412
Q

What do we see here?

A

Pink frothy material that is vacuolated space characteristic of PCP (Pneumocystis jirovecii)

413
Q

How are TB granulomas formed? What molecules are important for this?

A

TNFα and IFNγ and other cytokines activate foam cells to form granuloma

414
Q

Why may you get a false negative PPD?

A

Underlying disease with depressed cellular immunity

415
Q

Why might you get a false positive PPD?

A

Past infetion with other non-tuberculous mycobacteria (have shared antigens)

416
Q

What defines latent TB?

A

NAME?

417
Q

What defines TB disease (active TB)?

A

Presence of clinically active disease in one or more organ systems with confirmation of MTB organism

418
Q

What is primary tuberculosis?

A

Disease followign initial exposure

419
Q

What is proressive primary TB?

A

Reflects primary disease that has not been controlled by hose defense mechanisms and continues to be actie beyond hypersensitivity

420
Q

What is reactivation TB?

A

Disease that reactivates after a period of latency

421
Q

What is reinfection TB?

A

Disease in previously infected person that results from exposure to another source of organisms

422
Q

What is the characteristic location for reactivation of TB?

A

Apical regions of upper lobes, and to lesser extent, superior segment of lower lobes

High pO2 and less perfusion

423
Q

How does TB present?

A

Systemic symptoms (non-specific): weight loss, anorexia, fatigue, low-grade fever, night sweats

Pulm: cough, sputum, hemoptysis

Abnormal CXR but no clinical symptoms

424
Q

How do you diagnose TB?

A

Stained smears

Nucleic acid amplification

Culture (need for drug susceptibility testing)

425
Q

Who gets infected with non-TB mycobacteria?

A

Those iwth underlying lugn disease in which lung defenses are presumably diminished

AIDS

Pulmonary (2 decks)

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