Pulmonary Disease and Facts

Question 1

Common cause of pneumonia in immunocompromised pt

Answer 1

S. aureus, enteric gram-negative rods, fungi, viruses, P. jirovecii (with HIV)

Question 2

Most common cause of atypical or walking pneumonia

Answer 2

Mycoplasm pneumonaie

Question 3

Common causitive agent for pneumonia in alcoholics

Answer 3

S. pneumoniae, Klebsiella, S. aureus

Question 4

Can cause interstitial pneumonia in bird handlers

Answer 4

Chlymydia Psittachi

Question 5

OFte cause of pneumonia in pt w/ hx of exposure to bats and bat droppings

Answer 5

Histoplasma

Question 6

Often cause of pneumonia in pt recently visited South California, New mexico or Texas

Answer 6

Coccidiodes

Question 7

Pneumonia associated with currant jelly sputum

Answer 7

Klebsiella

Question 8

Q fever

Answer 8

Coxiella Burnetti

Question 9

Associated with pneumoniae acquired from air conditioners

Answer 9

Legionella pneumophilia

Question 10

Most common cause of pneunomiae in children 1 year old or younger

Answer 10

RSV

Question 11

Most common cause of pneumonia in neonate

Answer 11

Group B or E.coli

Question 12

Most common cause of pneumonia in children and young adults (college and military)

Answer 12

Mycoplasm pneumonaie

Question 13

Most common cause of viral pneumonaie

Answer 13

RSV

Question 14

Causes wool-sorters disease

Answer 14

Bacillis anthracis

Question 15

Common pneumonia in ventilator pts and CF pts

Answer 15

Pseudomonas aeruginosa and MRSA

Question 16

Pontiac fever

Answer 16

Legionella

Question 17

See bilateral and diffuse pattern or small, irregular (reticulonodular) opacities, especially in the lower lobes. Pt has gradual onset dysnpea that was bad when she was working out but now all the time.

What changes would you expect to see in regards to:

FEV1, FVC and the FEV/FVC ratio?

Answer 17

Pt has Pulmonary fibrosis (honeycomb lung)

FEV and FVC are decreased proportionally thus normal or increased FEV/FVC ratio (restrictive disease)

Question 18

1. The most important mediator of coronary vascular dilation in large arteries and pre-arteriolar vessels. Made from arginine and O2 by endothelial cells. Causes vascular smooth muscle relaxation via guanylate cyclase mediated cGMP
2. byproduct of ATP that acts as vasodilatory element in small coronary arterioles.

Answer 18

1. Nitric Oxide
2. Adenosine

Question 19

70 yo woman had hip replacement surgery and devos acute SOB. Chest CT are as below

What happened?

What’s the pathophysiology responsible?

Answer 19

Saddle embolism; from DVT

DVT is d/t Virchows triad: endothelial injury, venous stasis and hypercoaguable state

Risk factors: old age, major lower extremetiy sugery immobility.

Question 20

What is the MOA of Cromylyn?

when do we use it?

Answer 20

Inhibits mast cell degranulaiton thus prevents release of chemical mediators

Used to prevent acute asthma attacks

Question 21

How does emphysema and pulmonary fibrosis affect compliance differently?

Answer 21

Compliance= Volume/change in Pressure

In Fibrosis we see DECREASED compliance: for any given volume the pressure will be signficantly decreased) and this is d/t reduced pulmonary parenchymal compliance

Emphysema shows INCREAESD compliance

Question 22

Large airways consist of nose, pharynx, larynx, trachea, and bronchi.

Cartilage and goblet cells extend to _____

Pseudostratified ciliated columnar cells (clear mucus from lungs) extend to ________then transition–> cuboidal cells.

Airway smooth muscle cells extend to ______

Answer 22

end of bronchi.

beginning of terminal bronchioles,

end of terminal bronchioles

Question 23

What are all the funx of Type II pneumocytes?

Answer 23

Secrete pulmonary surfactant and DECRASE ??alveolar surface tension and prevents alveolar collapse (atelectasis). Cuboidal and clustered .

Serve as precursors to type I cells and o_ther type II cells_.

ype II cells proliferate during lung damage.

Question 24

Nonciliated; low-columnar/cuboidal with secretory granules. Secrete component of surfactant; degrade toxins; act as reserve cells in lungs

Answer 24

Club (Clara) cells

Question 25

Alveoli have ______ ?tendency to collapse on expiration as radius?(law of Laplace). Surfactant synthesis begins around \_\_\_\_\_of gestation, but mature levels are not achieved until around \_\_\_\_

Answer 25

INCREASED week 26 week 35.

Question 26

Compare and contrast Left and Right Lung lobe

Answer 26

Right lung has 3 lobes; Left has Less Lobes (2) and Lingula (homolog of right middle lobe). Right lung is more common site for inhaled foreign body because the right main stem bronchus is wider and more vertical than the left.

Question 27

What structures perforate the Diaphragm and at what levels?

Answer 27

At **T8:** _IVC_ ƒAt **T10:** _esophagus, vagus_ (CN 10; 2 trunks) ƒAt **T12**: aorta (red), thoracic duct (white), azygos vein (blue) (“At T-1-2 it’s the red, white, and blue”) Diaphragm is innervated by **C3, 4, and 5** (phrenic nerve). Pain from diaphragm irritation (e.g., air or blood in peritoneal cavity) can be referred to shoulder (C5) and trapezius ridge (C3, 4)

Question 28

**I (IVC) ate (8) ten (10) eggs (esophagus) at (aorta) twelve (12).**

Answer 28

Number of letters = T level: T8: vena cava T10: “oesophagus” T12: aortic hiatus C3, 4, 5 keeps the diaphragm alive. Other bifurcations: ƒ The common carotid bifourcates at C4. ƒ The trachea bifourcates at T4. ƒ The abdominal aorta bifourcates at L4.

Answer 29

The common carotid bifourcates at C4. ƒ The trachea bifourcates at T4. ƒ The abdominal aorta bifourcates at L4.

Question 30

How do you Determine physiologic dead space VD = physiologic dead space = VT = Paco2 = Peco2 =

Answer 30

VD = anatomic dead space of conducting airways plus alveolar dead space; apex of healthy lung is largest contributor of alveolar dead space. Volume of inspired air that does not take part in gas exchange. ``` VT = tidal volume. Paco2 = arterial Pco2. ``` Peco2 = expired air Pco2.

Question 31

What is the equation for physciologic dead space?

Answer 31

Taco, Paco, Peco, Paco (refers to order of variables in equation) VD = VT × (Paco2 – Peco2)/ Paco2

Question 32

O2 content = (O2 binding capacity × % saturation) + dissolved O2. Normally 1 g Hb can bind 1.34 mL O2; normal Hb amount in blood is 15 g/dL. Cyanosis results when

Answer 32

deoxygenated Hb \> 5 g/dL.

Question 33

When Hemoglobing DECREASES: Oxygen **CONTENT** of arterial blood will \_\_\_\_\_ O2 **SATURATION** and **PO2** will \_\_\_\_\_\_\_

Answer 33

Oxygen CONTENT of arterial blood will DECREASE O2 SATURATION and PO2 will STAY THE SAME

Question 34

What happens to the following levels in the event of CO poisoning? Hb levels: %O2 saturation of Hb: Dissolved O2 or (PaO2) Total O2 content:

Answer 34

Hb levels remain the **same** %O2 saturation of Hb: DECREASE as CO compets with oxygen Dissolved O2 or (PaO2): _normal_ Total O2 content: Decreased (bc of increased CO)

Question 35

What happens in the setting of anemia to the following levels: Hb levels: %O2 saturation of Hb: Dissolved O2 or (PaO2) Total O2 content:

Answer 35

Hb levels: **DECREASE** (you're making less RBCs) %O2 saturation of Hb: **Normal** (the Hb you have funx fine) Dissolved O2 or (PaO2) = **Normal**, this NEVER changes bc) Total O2 content: **decreased** from less Hb content)

Question 36

What happens to the following levels in the setting of POlycythemia: Hb levels: %O2 saturation of Hb: Dissolved O2 or (PaO2) Total O2 content:

Answer 36

Hb levels: **INCREASED** %O2 saturation of Hb: **Normal** (Hb fnx the same) Dissolved O2 or (PaO2): **Normal** Total O2 content: **Increased** bc more HgB

Question 37

Explain how the lungs are **Perfusion** limited and **Diffusion** Limited When are people perfusion limited? When are they Diffusion limited?

Answer 37

**Perfusion limited**—O2 (_normal health_), CO2, N2O. Gas e_quilibrates early_ along the length of the capillary. Diffusion can be ?_INCREASED_ only if _INCREASE_ blood flow?. **Diffusion limited**—O2 (_emphysema, fibrosis_), CO. Gas does not equilibrate by the time blood reaches the end of the capillary.

Question 38

What effect does Emphysema have on the lungs? What effect Pulmonary fibrosis have on the lungs? In relastion ship to diffusion

Answer 38

IN emphysema we see DECREASED surface area for gas exchange In Fibrosis we see Increased thickeness in membrane thus Decreases diffusion of gas

Question 39

How do you measure the PVR? Pulmonary vascular resistance? What does this mean?

Answer 39

PVR = Ppurlmonary artery - PL.atrium / Cardiac Output Pressure in L. Atrium = pulmonary wedge pressure

Question 40

What situaitons lead to Hypoxemia or a low PaO2 pressure

Answer 40

HIgh altitude HYPOventilation Increasd A-a gradient V/Q mismatch Diffusion limitation Right to LEft shunt

Question 41

What is the normal V/Q of the apex of the lung? What is wasted here? What organims prefer this area? What happens here during exercise?

Answer 41

V/Q = 3 thus gets more ventilation then pefusion Wasted Ventialation TB is aerobic thus loves this area With exercise (Increased ?cardiac output), there is **vasodilation of apical capillaries**?--\> V/Q ratio approaches 1.

Question 42

V/Q = 0 = V/Q = ∞ =

Answer 42

V/Q = 0 = “oirway” obstruction (shunt). In shunt, 100% O2 does not improve Pao2. V/Q = ∞ = blood flow obstruction (physiologic dead space). Assuming \< 100% dead space, 100% O2 improves Pao2.

Question 43

What is the body's response to high altitude? Pa_O2, Pa_CO2 To EPO production and 2,3DPG To renal function? To the Heart?

Answer 43

?1.DECREASE atmospheric oxygen (PO2)??--\> DECREASE Pao2??--\> INCREASE ventilation??-- \>DECREASE Paco2 (blow off CO2) **Chronic? increase in ventilation.** 2. INCREAE ?EPO--\> INCREASE hematocrit and Hb (chronic hypoxia) and ?INCREASE 2,3-BPG (binds to Hb so that Hb releases more O2). ?3. INCREASE renal excretion of HCO3− to compensate for respiratory alkalosis (can augment with acetazolamide) . 4. Chronic hypoxic pulmonary vasoconstriction r**esults in RVH.**

Question 44

What changes do we see in respose to excercise?

Answer 44

? INCRAESE CO2 production. ?INCREASE O2 consumption. ?INCREASE ventilation rate to meet O2 demand. V/Q ratio from apex to _base becomes more uniform._ ?INCREASE pulmonary blood flow due to INCREASE ?cardiac output. ?DECREASE pH during strenuous exercise (2° to lactic acidosis). No change in Pao2 and Paco2, but see INCREASE ?in venous CO2 content and?in venous O2 content.

Question 45

Describe pulsus paradoxis. What respiratory disease do you see it in?

Answer 45

On inspiration you see increased blood flow to the RV which will push the LV in a bit. During inspiraiton normal to see decrese of systolic BP up to 10. When its more then 10 = pulsus paraxdoxis seen in **asthma**

Question 46

What Interstitial lung diseases can cause Restrictive lungs disease?

Answer 46

ƒ Acute respiratory distress syndrome (ARDS) ƒ Neonatal respiratory distress syndrome (NRDS; hyaline membrane disease) ƒ Pneumoconioses (e.g., anthracosis, silicosis, asbestosis) ƒ Sarcoidosis: bilateral hilar lymphadenopathy, noncaseating granuloma; ? ACE and Ca2+ ƒ Idiopathic pulmonary fibrosis A (repeated cycles of lung injury and wound healing with ?collagen deposition) ƒ Goodpasture syndrome ƒ Granulomatosis with polyangiitis (Wegener) ƒ Langerhans cell histiocytosis (eosinophilic granuloma) ƒ Hypersensitivity pneumonitis ƒ Drug toxicity (bleomycin, busulfan, amiodarone, methotrexate)

Question 47

Associated with foundries, sandblasting, mines. Incrases risk of TB and brochogenic carcinoma Disease and pathogenesis

Answer 47

**Macrophages** respond to silica and release f_ibrogenic factors,_ leading to **fibrosis**. It is thought that silica may **disrupt phagolysosomes and impair macrophages**, increasing susceptibility to TB.

Question 48

Where does Asbestos, silicosis and coal cause damage in the lung?

Answer 48

Asbestos is from the roof (was common in insulation), but **affects the base** (lower lobes). Silica and coal are from the base (earth), but a**ffect the roof** (upper lobes).

Question 49

“Eggshell” calcification of hilar lymph nodes.

Answer 49

silicosis

Question 50

Syndorme seen with acute onset respiratory failure, bilateral lung opacities, DECREASED ? PaO2/FiO2, no HF. Causes? Patholophysiology? Initial damage causes what?

Answer 50

**1. Acute respiratory distress syndrome** 2. May be caused by trauma, sepsis, shock, gastric aspiration, uremia, acute pancreatitis, amniotic fluid embolism. 3. Diffuse alveolar damage??alveolar capillary permeability?--\> I**NCREASE protein-rich leakage** into alveoli and noncardiogenic pulmonary edema (normal PCWP) 4. Results in _formation of intra-alveolar hyaline membranes_ Initial damage d_ue to release of neutrophilic substances_ toxic to alveolar wall, a_ctivation of coagulation cascade_, and _oxygen-derived free radicals._