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Quick Scroll medicine-lung 07.10.08 (1 month ago) #1

SHOCK LUNG IS CHARACTERISED BY:
1.ALVEOLAR DAMAGE.
2.INTERSTITIAL THICKENING.
3.BOTH OFTHE ABOVE.
4.NONE OF THE ABOVE.
ANSWER GIVEN IS [1],BUT WHY NOT [2]?
HAVE A SAY FRIENDS.
THANKS.
REGARDS.
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Quick Scroll 07.10.08 (1 month ago) #2

shock lung is non cardiogenic pulmonary edema due to alveolar damage as a part of systemic inflammatory response syndrome(sirs).in the late stages it is accompanied by interstitial thickening but this is a complication of the disease not a part of the complications of shock
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Quick Scroll 07.12.08 (1 month ago) #3

so dear wisevision ,what is the answer here?
regards.
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Quick Scroll shock lung 07.14.08 (1 month ago) #4

Robbins Basic Pathology 8th Ed
The Lung > Acute Lung Injury> Acute Respiratory Distress Syndrome
ARDS is a clinical syndrome caused by diffuse alveolar capillary and epithelial damage. There is usually rapid onset of life-threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia that is refractory to oxygen therapy and that may progress to multisystem organ failure. The histologic manifestation of ARDS in the lungs is known as diffuse alveolar damage.

Morphology
In the acute phase of ARDS the lungs are dark red, firm, airless, and heavy. Microscopically, there is capillary congestion, necrosis of alveolar epithelial cells, interstitial and intra-alveolar edema and hemorrhage, and (particularly with sepsis) collections of neutrophils in capillaries. The most characteristic finding is the presence of hyaline membranes, particularly lining the distended alveolar ducts (Fig. 13-4). Such membranes consist of fibrin-rich edema fluid admixed with remnants of necrotic epithelial cells.
In the organizing stage there is marked proliferation of type II pneumocytes in an attempt to regenerate the alveolar lining. Resolution is unusual; more commonly there is organization of the fibrin exudates, with resultant intra-alveolar fibrosis. Marked thickening of the alveolar septa ensues, caused by proliferation of interstitial cells and deposition of collagen.

Clinical Course
Approximately 85% of patients develop the clinical syndrome of acute lung injury or ARDS within 72 hours of the initiating insult. The prognosis of ARDS is grim, and mortality rates have historically approached 100%. Despite improvements in supportive therapy the mortality rate among the 150,000 ARDS cases seen yearly is still about 60%. Should the patient survive the acute stage, diffuse interstitial fibrosis may occur and continue to compromise respiratory function. However, in most patients who survive the acute insult and are spared the chronic sequela, normal respiratory function returns within 6 to 12 months.

Rubin’s Pathology – Clinicopathological Foundations of Medicine - 5th Ed
Ch 13 – The Respiratory System

Diffuse Alveolar Damage (Acute Respiratory Distress Syndrome)
Diffuse alveolar damage (DAD) refers to a pattern of reaction to injury of alveolar epithelial and endothelial cells from a variety of acute insults (Table 12-1). The clinical counterpart of severe DAD is the acute respiratory distress syndrome (ARDS). In this disorder, a patient with apparently normal lungs sustains pulmonary damage and then develops rapidly progressive respiratory failure.
Importantly, the precise cause of DAD cannot be determined from the morphologic appearance of the lung alone, unless a specific infectious agent is identified. Some patients have an idiopathic form of DAD, in which no cause can be found. Idiopathic DAD is referred to clinically as acute interstitial pneumonia (AIP) and also includes cases historically referred to as Hamman-Rich disease.
If the patient survives the acute phase of ARDS, fibroblasts proliferate in the interstitial space and deposit collagen in the alveolar walls (Fig. 12-34). In patients who recover completely, lesions may heal, with resorption of the alveolar exudate and hyaline membranes and restitution of normal alveolar epithelium. Fibroblastic proliferation ceases, and the extra collagen is metabolized. It is well documented that patients with ARDS who recover do regain normal pulmonary function. In patients who do not recover, DAD can progress to end-stage fibrosis; remodeling of the lung architecture produces multiple cystlike spaces throughout the lung (honeycomb lung). These spaces
are separated from each other by fibrous tissue and lined by type II pneumocytes, bronchiolar epithelium, or squamous cells.

Considering the survival rate is very poor, the answer is taken as diffuse alveolar damage. This the other name for ARDS!!
The diffuse interstitial fibrosis is seen only if the patient survives the acute stage.
Hence the answer is taken to be only 1 and not both 1 & 2.
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Quick Scroll 07.15.08 (1 month ago) #5

THANK U A LOT.
REGARDS.
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