Chapter 7 Flashcards
Left ventricular failure leads to chronic passive congestion of the lungs. Blood leaks from the congested pulmonary capillaries into the alveoli. Alveolar macrophages degrade RBCs and accumulate hemosiderin. Hemosiderin-laden macrophages are called heart failure cells.
congestive heart failure, pulmonary edema
Diffuse alveolar damage with hyaline membranes is a feature of what syndrome?
adult respiratory distress syndrome
What is purulent exudate a feature of?
bacterial pneumonia
interstitial lymphocytes is a characteristic of what?
Viral pneumonitis
What is typically seen in patients with pulmonary hypertension?
Plexiform lesions
This results from a systemic inflammatory response syndrome that leads to multiple organ dysfunction and hypotension. Clinical features include two or more signs of systemic inflammation (e.g. fever, tachycardia, tachypnea, leukocytosis, or leukopenia) in the setting of a known cause of inflammation. Processes progress to multiple organ dysfunction syndrome in critically ill patients. Gram-negative organisms are the most common cause of this.
Septic shock
A consequence of type I hypersensitivity reactions
Anaphylactic shock
Follows acute injury to the brain or spinal cord, which impairs the neural control of vasomotor tone, leading to generalized vasodilation.
Neurogenic shock
A feature of advanced heart failure. A feature of blood loss.
Cardiogenic and hypovolemic shock
Hypotension caused by postpartum bleeding can, in rare cases, lead to this. The pituitary is particularly susceptible at this time because its enlargement during pregnancy renders it vulnerable to a reduction in blood flow.
Sheehan syndrome, pituitary infarction
Pericardial fluid may accumulate rapidly, particularly with hemorrhage caused by a ruptured myocardial infarct, this, or trauma. In these circumstances, the pressure in the pericardial cavity exceeds the filling pressure of the heart, a condition termed cardiac tamponade. The term ‘electomechanical dissociation’ refers to a heart rhythm that should produce a beat, but does not. The most common cause of this condition is hypovolemia. The resulting precipitous decline in cardiac output is often fatal. The pathogenesis of this in most cases can be traced to a weakening of the aortic media (cystic medial necrosis). Most patients have a history of hypertension.
Dissecting aortic aneurysm
This refers to widespread ischemic changes secondary to microvascular thrombi.
Disseminated intravascular coagulation
This is the engorgement of an organ with venous blood
Passive hyperemia
Massive hematemesis (vomiting blood) is a frequent cause of death in patients with this. The patient with alcoholic cirrhosis has portal hypertension (increased hydrostatic pressure) and these are bleeding.
Esophageal varices hematemesis
Small pulmonary emboli rarely cause infarctions because of the dual blood supply to the lungs and because oxygen can diffuse from the alveoli into lung tissue. Symptoms depend upon the extent of blockage of the pulmonary arterial tree, whether there is already cardiopulmonary disease, and whether pulmonary infarction occurs,
Thromboembolism
These originate from adipose tissue in the medulla of fractured long bones. Fat carried by venous blood reaches the lungs, filters through the pulmonary circulation, enters arterial blood, and is disseminated throughout the body. The occlusion of cerebral capillaries is accompanied by petechial hemorrhages in the brain and is the most important complication of this.
Deep venous thrombosis and septic shock unlikely in short time frame.
Fat embolism
When emboli arise in the venous circulation and bypasses the lungs by traveling through an incompletely closed foramen ovale, subsequently entering the arterial circulation
Paradoxical embolism
Septicemia with Gram-negative organisms is the most common cause of septic shock. The invading bacteria are responsible for the release of endotoxin, a LPS. On entry into the circulation, LPS binds to the surface of monocytes/macrophages. The CD14 recognition complex mediates signalling through activation of nuclear transcription factor-kappa B (NF-kappa B) and upregulates the expression of TNF-alpha. In septic shock, this protein is released in great excess, resulting in effects that are often lethal.
Meningitis, septic shock
The heart is the most common source of arterial thromboemboli, which usually arise from mural thrombi or diseased valves. These emboli tend to lodge at points where the vessel lumen narrows abruptly (e.g, at bifurcations or in the area of an atherosclerotic plaque).
Cerebral embolism, stroke
Embolism is the passage through the venous or arterial circulations of any material capable of lodging in a blood vessel and, thereby, obstructing its lumen. Intravenous drug abusers who use talc as a carrier for illicit drugs may introduce it into the lung via the bloodstream (i.e. venous embolism)
None of the other choices exhibit birefringence under polarized light.
Pulmonary embolism, talc embolism
Amniotic fluid embolism refers to the entry of amniotic fluid containing fetal cells and debris into the maternal circulation through open uterine and cervical veins. It is a rare maternal complication of childbirth, but when it occurs, it is often catastrophic. This disorder usually occurs at the end of labor when the pulmonary emboli are composed of the epithelial constituents (squamae) contained in the amniotic fluid.
Amniotic fluid embolism
A thrombotic microangiopathy. Fibrin thrombi form in small blood vessels because of uncontrollable coagulopathy, which consumes fibrin and other coagulation factors. Once coagulation factors are depleted, uncontrollable hemorrhage ensues.
If someone overcomes this, they are at risk for acute respiratory distress syndrome.
DIC
A generalized increase in venous pressure, typically from chronic heart failure, results in an increase in the volume of blood in many organs (e.g., liver, spleen, and kidneys). The liver is particularly vulnerable to chronic passive congestion because the hepatic veins empty into the vena cava immediately inferior to the heart.
Congestive heart failure, nutmeg liver
In patients with chronic passive congestion of the liver, the central veins of the hepatic lobule become dilated. The increased venous pressure leads to dilation of the sinusoids and pressure atrophy of the centrilobular hepatocytes. Grossly, the cut surface of the chronically congested liver exhibits dark foci of centrilobular congestion surrounded by paler zones of unaffected peripheral portions of the lobules. The result resembles a cross section of a nutmeg. Longstanding passive congestion leads to bridging fibrosis; however, only in the most extreme cases is the fibrosis sufficiently severe to justify the label cardiac cirrhosis.
Chronic passive congestion of the liver