Chapter 7 Flashcards

1
Q

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.

A

congestive heart failure, pulmonary edema

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2
Q

Diffuse alveolar damage with hyaline membranes is a feature of what syndrome?

A

adult respiratory distress syndrome

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3
Q

What is purulent exudate a feature of?

A

bacterial pneumonia

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4
Q

interstitial lymphocytes is a characteristic of what?

A

Viral pneumonitis

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5
Q

What is typically seen in patients with pulmonary hypertension?

A

Plexiform lesions

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6
Q

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.

A

Septic shock

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7
Q

A consequence of type I hypersensitivity reactions

A

Anaphylactic shock

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8
Q

Follows acute injury to the brain or spinal cord, which impairs the neural control of vasomotor tone, leading to generalized vasodilation.

A

Neurogenic shock

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9
Q

A feature of advanced heart failure. A feature of blood loss.

A

Cardiogenic and hypovolemic shock

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10
Q

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.

A

Sheehan syndrome, pituitary infarction

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11
Q

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.

A

Dissecting aortic aneurysm

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12
Q

This refers to widespread ischemic changes secondary to microvascular thrombi.

A

Disseminated intravascular coagulation

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13
Q

This is the engorgement of an organ with venous blood

A

Passive hyperemia

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14
Q

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.

A

Esophageal varices hematemesis

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15
Q

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,

A

Thromboembolism

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16
Q

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.

A

Fat embolism

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17
Q

When emboli arise in the venous circulation and bypasses the lungs by traveling through an incompletely closed foramen ovale, subsequently entering the arterial circulation

A

Paradoxical embolism

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18
Q

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.

A

Meningitis, septic shock

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19
Q

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).

A

Cerebral embolism, stroke

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20
Q

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.

A

Pulmonary embolism, talc embolism

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21
Q

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.

A

Amniotic fluid embolism

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22
Q

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.

A

DIC

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23
Q

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.

A

Congestive heart failure, nutmeg liver

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24
Q

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.

A

Chronic passive congestion of the liver

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25
A symptom of upper gastrointestinal bleeding. Blood from ruptured esophageal varices or a peptic ulcer is partially digested by hydrochloric acid. Hemoglobin is transformed into a black pigment (hematin), which imparts a typical "coffee-grounds" color to the stool.
Melena
26
Vomiting of blood
Hematemesis
27
Bleeding in to the biliary passagesas a complication of trauma or neoplasia
Hematobilia
28
The passage of bloody stools caused by lower GI hemorrhage
Hematochezia
29
Passage of fatty stools caused by pancreatic disease and malabsorption
Steatorrhea
30
Venous thrombosis is caused by the same factors that predispose to arterial thrombosis, namely endothelial injury, stasis, and a hypercoaguable state.
Deep venous thrombosis
31
Refers to bleeding into the joint cavity. Associated with joint swelling and is a crippling complication of hemophilia. Repeated bleeding may cause deformities and may limit the mobility of the joints.
Hemophilia, hemarthrosis
32
intracranial infusion of blood
Hematocephalus
33
coughing up blood
Hemoptysis
34
May be caused by hemorrhage, fluid loss from severe burns, diarrhea, excessive urine formation, perspiration or trauma. In the case of burns or trauma, direct damage to the microcirculation increases vascular permeability. Persons with third-degree burns weep large amounts of plasma.
Hypovolemic shock
35
Accumulation of fluid in the peritoneal cavity, protruding belly. Most commonly due to cirrhosis, severe liver disease or neoplasm
Ascites
36
May be confined to a limb or an organ as a result of localized obstruction to venous drainage. Examples include deep venous thrombosis of the leg veins, with resulting edema of the lower extremity, and thrombosis of the hepatic veins (Budd-Chiari syndrome) with secondary chronic passive congestion of the liver.
Passive hyperemia
37
An augmented blood supply of blood to an organ, usually as a physiologic response to an increased functional demand. The most striking active hyperemia occurs in association with inflammation.
Active hyperemia
38
Typically causes infarction
Arterial embolism
39
Extravascular accumulation of blood
Hematoma and hemorrhage
40
A larger superficial hemorrhage in the skin. Following hemorrhage, the initially purple discoloration of the skin turns green and then yellow before resolving. This sequence follows the progressive oxidation of bilirubin released from the hemoglobin of degraded erythrocytes. A "Black eye" is a good example of this.
Ecchymosis
41
pinpoint hemorrhages usually in the skin or conjunctiva. lesion represents the rupture of a capillary or arteriole and occurs in conjunction with vasculitis and coagulopathy. May also be produced by microemboli from infected heart valves (bacterial endocarditis)
petechiae
42
Diffuse superficial hemorrhage in the skin up to 1 cm in diameter
pupura
43
flat red area on skin covered in bumps
maculopapular rash
44
The pressure differential between the intravascular and the interstitial compartments is largely determined by the concentration of plasma proteins, especially albumin. Any condition that lowers plasma albumin levels, whether from albuminuria in nephrotic syndrome or reduced albumin synthesis in chronic liver disease, tends to promote generalized edema.
Decreased intravascular oncotic pressure
45
Increased hematocrit in the patient reflects hemoconcentration caused by dehydration, secondary to diarrhea. This hematologic condition, termed relative polycythemia, is characterized by decreased plasma volume with a normal red cell mass. When patients suffer from burns, vomiting, excessive sweating, or diarrhea, they not only lose fluid but also suffer electrolyte disturbances. Systemic blood pressure falls with continuous dehydration, and declining perfusion eventually leads to death.
Dehydration, relative polycythemia (proportion of RBC increases)
46
Inflammatory redness of the skin
Erythema
47
Embolism of an artery of the artery of the leg leads to sudden pain, absence of pulses, and a cold limb. In some cases, the limb must be amputated.
Arterial thromboembolism
48
Chronic failure of the left ventricle constitutes an impediment to the exit of blood from the lungs and leads to chronic passive congestion of the lungs. The pressure in the alveolar capillaries increases, and the vessels become engorged with blood. Microhemorrhages release erythrocytes into the alveolar spaces, where they are degraded by alveolar macrophages. The released iron, in the form of hemosiderin, remains in the macrophages, which are then labeled "heart failure cells."
Congestive Heart Failure
49
A large pulmonary embolus may lodge at the bifurcation of the main pulmonary artery (saddle embolus), obstructing blood flow to both lungs. With acute obstruction of more than half of the pulmonary arterial tree, the patient experiences severe hypotension and may die within minutes.
Deep venous thrombosis
50
What are examples of causes of arterial embolism?
Bacterial endocarditis, complicated artherosclerotic plaque, paradoxical embolization, right ventricular mural thrombus
51
Secondary to a pronounced decrease in vlood or plasma volume, caused by the loss of fluid from the vascular compartment. Hemorrhage, fluid loss from severe burns, diarrhea, excessive urine formation, perspiration, and traume are major mechanisms of fluid loss that can lead to hypovolemic shock.
Hypovolemic shock
52
In patients with severe aortic artherosclerosis, embolization of artheromatous debris into the renal arteries and vascular tree may cause acute renal failure.
Renal infarct, arterial embolism
53
Patients with this complain of shortness of breath (dyspnea) on exertion and when recumbent (orthopnea). They may be awakened from sleep by episodes of shortness of breath (paroxysmal nocturnal dyspnea). Physical examination usually reveals distended jugular veins.
left sided congestive heart failure
54
Persons with right-sided failure have pitting edema of the lower extremities and an enlarged and tender liver. Patients in congestive heart failure with pulmonary edema have crackling breath sounds (rales) caused by the expansion of fluid-filled alveoli.
right sided congestive heart failure
55
Myocardial infarction is the most common cause of mural thrombi in the left ventricle. These mural thrombi are a common source of arterial thromboemboli. Such emboli may occlude cerebral arteries and cause cerebral infarcts, known as strokes. Atrial fibrillation predisposes to the formation of mural thrombi.
Mural thrombus
56
Once formed, arterial thrombi may undergo 1. lysis, 2. propagation, 3. organization, 4. canalization, 5. embolization. Organization refers to the invasion of connective tissue elements, which causes a thrombus to become firm and appear grayish white. Canalization is the process by which new lumina lined by endothelial cells form within an organized thrombus. Propagation implies an increase in size.
The steps of mural thrombus
57
Cardiac myxoma is the most common primary tumor of the heart. one third of patients with left artial or left ventricular myoma die from tumor embolization to the brain.
Cardiac myxoma
58
Obstruction of lymphatic flow may occur in a number of clinical settings, but is most common because of surgical removal of lymph nodes or tumor obstruction. For example, the lymphatic system may be obstructed after axillary lymph node dissection for breast cancer. Prolonged lymphatic obstruction in the patient's shoulder causes edema, progressive dilation of lymphatic vessels (lymphangiectasia), and overgrowth of fibrous tissue,
Lymphedema
59
Represents an accumulation of lymphedema in the pleural space (chyle - lymph)
Chylothorax
60
This is caused by myocardial pump failure. This condition usually arises as a result of a large myocardial infarction, but myocarditis may also be responsible. Conditions that prevent left or right heart filling reduce cardiac output, resulting in obstructive shock. Such conditions include pulmonary embolism, cardiac tamponade, and rarely atrial myxoma.
Cardiogenic shock
61
In patients with congestive heart failure, venous engorgement of the lungs leads to accumulation of a transudate in the alveoli. Chronic left ventricle failure impedes blood flow out of the lungs and leads to passive pulmonary congestion. As a result, pressure in the alveolar capillaries increase (increased hydrostatic pressure) and these vessels become engorged with blood. Increased pressure forces fluid from the blood into the alveolar spaces, resulting in pulmonary edema, which interferes with gas exchange.
Pulmonary Edema
62
Volvulus is an example of intestinal obstruction in which a segment of gut twists on its mesentery, thereby kinking the bowel and usually interrupting the blood supply. Ischemia leads to infarction and intestinal gangrene.
Infarct
63
Myocardial infarcts are described as transmural (through the entire wall) or subendocardial. A transmural infarct results from complete occlusion of a major extramural coronary artery.
Transmural infarct
64
Reflects prolonged ischemia caused by partially occluding lesions of the coronary arteries when the requirement for oxygen exceeds the supply. Such a situation prevails in disorders such as shock, anoxia, or severe tachycardia.
Subendocardial infarction
65
Coughing up blood
hemoptysis
66
color of infarcts typically seen in the heart, kidneys, and spleen.
pale infarct
67
Results from either arterial or venous occlusion. They are distinguished from the other infarcts by bleeding into the necrotic area from adjacent arteries and veins. These infarcts occur principally in organs with a dual blood supply, such as the small intestine and brain. In the heart, this infarct occurs when the infarcted area is reperfused, as may occur following spontaneous or therapeutically induced lysis of the occluding thrombus. Grossly, these infarcts are sharply circumscribed, firm, and dark red to purple. Over a period of several days, acute inflammatory cells infiltrate the necrotic area from the viable border. The cellular debris is phagocytosed and digested by polumorphonuclear leukocytes and later by macrphages. Granulation tissue eventually forms, to be replaced ultimately by a scar.
red infarct
68
The pathogenesis of RDS of the newborn is intimately linked to a deficiency of surfactant. This material lowers the surface tension of the alveoli at low lung volumes and thereby prevent collapse (atelectasis) of the alveoli during expiration. Atelectasis secondary to surfactant deficiency results in perfused but not ventilated alveoli, a situation that leads to hypoxia and acidosis. Intraventricular cerebral hemorrhage is a major complication of RDS. The periventricular germinal matrix in the newborn brain is particularly vulnerable to hemorrhage because the dilated, thin-walled veins in this area rupture easily. The pathogenesis of this complication is believed to reflect anoxic injury to the periventricular capillaries, venous sludging and thrombosis, and impaired vascular autoregulation. Despite advances in neonatal intensive care, the overall mortality of RDS is about 15%, and 1/3 of infants born before 30 weeks of gestational age die of this order.
Respiratory distress syndrome of the neonate
69
present in the blood, especially in excess
-emia
70
lodging of a blood clot, fat globule, or gas bubble in the bloodstream which can cause blockage. May affect a body part away from the site of embolism
embolism
71
blood clot at the site of origin
thrombus