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Common cause of pneumonia in immunocompromised pt

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

 

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Most common cause of atypical or walking pneumonia

Mycoplasm pneumonaie

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Common causitive agent for pneumonia in alcoholics

S. pneumoniae, Klebsiella, S. aureus 

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Can cause interstitial pneumonia in bird handlers

Chlymydia Psittachi

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

Histoplasma

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

Coccidiodes

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Pneumonia associated with currant jelly sputum

Klebsiella

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Q fever

Coxiella Burnetti

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Associated with pneumoniae acquired from air conditioners

Legionella pneumophilia

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

RSV

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Most common cause of pneumonia in neonate

Group B or E.coli

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

Mycoplasm pneumonaie

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Most common cause of viral pneumonaie

RSV

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Causes wool-sorters disease

Bacillis anthracis

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Common pneumonia in ventilator pts and CF pts

Pseudomonas aeruginosa and MRSA

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Pontiac fever

Legionella

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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?

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Pt has Pulmonary fibrosis (honeycomb lung)

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

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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. 

1. Nitric Oxide

2. Adenosine

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

What happened?

What's the pathophysiology responsible?

 

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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. 

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What is the MOA of Cromylyn?

when do we use it?

Inhibits mast cell degranulaiton thus prevents release of chemical mediators

Used to prevent acute asthma attacks

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How does emphysema and pulmonary fibrosis affect compliance differently?

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

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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 ______

end of bronchi.

beginning of terminal bronchioles, 

end of terminal bronchioles 

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What are all the funx of Type II pneumocytes?

 

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

Serve as precursors to type I cells and other type II cells.

ype II cells proliferate during lung damage. 

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

Club (Clara) cells 

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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 ____

INCREASED

week 26 

week 35. 

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Compare and contrast Left and Right Lung lobe

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. 

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What structures perforate the Diaphragm and at what levels?

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) 

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

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. 

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The common carotid bifourcates at C4. ƒ

The trachea bifourcates at T4.
ƒ The abdominal aorta bifourcates at L4. 

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How do you Determine physiologic dead space 

VD = physiologic dead space = 

VT = 
Paco2 = 

Peco2 = 

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. 

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What is the equation for physciologic dead space?

Taco, Paco, Peco, Paco (refers to order of variables in equation) 

VD = VT × (Paco2 – Peco2)/ Paco2 

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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 
 

deoxygenated Hb > 5 g/dL.

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When Hemoglobing DECREASES: 

Oxygen CONTENT of arterial blood will _____ 

 O2 SATURATION and PO2 will _______

Oxygen CONTENT of arterial blood will DECREASE

 O2 SATURATION and PO2 will STAY THE SAME

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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:

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)

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What happens in the setting of anemia to the following levels:

Hb levels:

%O2 saturation of Hb:

Dissolved O2 or (PaO2)

Total O2 content:

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)

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What happens to the following levels in the setting of POlycythemia:

Hb levels:

%O2 saturation of Hb:

Dissolved O2 or (PaO2)

Total O2 content:

Hb levels: INCREASED 

%O2 saturation of Hb: Normal (Hb fnx the same)

Dissolved O2 or (PaO2): Normal

Total O2 content: Increased bc more HgB

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Explain how the lungs are Perfusion limited and Diffusion Limited

When are people perfusion limited?

When are they Diffusion limited?

Perfusion limited—O2 (normal health), CO2, N2O. Gas equilibrates 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. 

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What effect does Emphysema have on the lungs?

What effect Pulmonary fibrosis have on the lungs?

In relastion ship to diffusion

IN emphysema we see DECREASED surface area for gas exchange 

In Fibrosis we see Increased thickeness in membrane thus Decreases diffusion of gas

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How do you measure the PVR?

Pulmonary vascular resistance?

What does this mean?

PVR = Ppurlmonary artery - PL.atrium / Cardiac Output

 

Pressure in L. Atrium = pulmonary wedge pressure

40

What situaitons lead to Hypoxemia or a low PaO2 pressure

 

HIgh altitude

HYPOventilation

Increasd A-a gradient

V/Q mismatch

Diffusion limitation

Right to LEft shunt

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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?

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. 

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V/Q = 0 = 

V/Q = ∞ = 

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. 

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What is the body's response to high altitude?

PaO2, PaCO2 

To EPO production and 2,3DPG

To renal function?

To the Heart?

 

?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 results in RVH. 

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What changes do we see in respose to excercise?

? 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. 

45

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

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

46

What Interstitial lung diseases can cause Restrictive lungs disease?

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) 

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

Disease and pathogenesis

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

 

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

Asbestos is from the roof (was common in insulation), but affects the base (lower lobes).

Silica and coal are from the base (earth), but affect the roof (upper lobes). 

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“Eggshell” calcification of hilar lymph nodes. 

silicosis

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Syndorme seen with acute onset respiratory failure, bilateral lung opacities,
DECREASED ? PaO2/FiO2, no HF.

Causes?

Patholophysiology?

Initial damage causes what?

 

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?--> INCREASE protein-rich leakage into alveoli and noncardiogenic pulmonary edema (normal PCWP)

4. Results in formation of intra-alveolar hyaline membranes

Initial damage due to release of neutrophilic substances toxic to alveolar wall, activation of coagulation cascade, and oxygen-derived free radicals. 

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