Hemodynamic Disorders, Thromboembolic Disease and Shock

Question 1

Accumulation of fluid in tissues or body cavities.

Answer 1

Edema (tissues) or effusion (body cavities)

Question 2

Four main mechanisms of edema formation.

Answer 2

A. Increased hydrostatic pressure
B. Decreased oncotic pressure
C. Increased vascular permeability
D. Lymphatic obstruction

Question 3

General morphologic appearance of edema.

Answer 3

Clearing and separation of ECM, and subtle cell swelling

Question 4

It is an active process resulting from augmented blood flow due to arteriolar dilation; affected tissue is redder than normal, because of engorgement with oxygenated blood.

Answer 4

Hyperemia

Question 5

It is a passive process resulting from impaired venous return out of a tissue; tissue has a blue-red color due to accumulation of deoxygenated hemoglobin in the affected tissue.

Answer 5

Congestion

Question 6

Characterized by alveolar capillaries engorged with blood, with associated alveolar septal edema or focal minute intra-alveolar hemorrhage.

Answer 6

Acute pulmonary congestion

Question 7

Pulmonary septa are thickened and fibrotic, with hemosiderin-laden macrophages in alveolar spaces.

Answer 7

Chronic pulmonary congestion

Question 8

The central vein and sinusoids of the liver are distended with blood, with central hepatocyte degeneration; periportal hepatocytes are better oxygenated.

Answer 8

Acute hepatic congestion

Question 9

The central regions of the hepatic lobules are grossly red-brown, slightly depressed, and are accentuated against the surrounding zones of uncongested tan, sometimes fatty liver (nutmeg liver); presence of centrilobular necrosis with hepatocyte drop-out, hemorrhage, and hemosiderin-laden macrophages.

Answer 9

Chronic hepatic congestion

Question 10

Pathologic form of hemostasis.

Answer 10

Thrombosis

Question 11

Components of Virchow triad (abnormalities that lead to thrombus formation).

Answer 11

Endothelial injury, Stasis, Hypercoagulability

Question 12

It is a major contributor to the development of arterial thrombi.

Answer 12

Turbulence or endothelial injury

Question 13

It is a major contributor to the development of venous thrombi.

Answer 13

Stasis

Question 14

Any alteration of the coagulation pathway that predisposes to thrombosis; can be primary (e.g. Factor V Leiden, Protein C and S deficiency) or secondary (e.g. Cancer, atrial fibrillation, and prolonged immobilization)

Answer 14

Hypercoagulability

Question 15

Laminations composed pale platelet and fibrin deposits alternating with darker red cell_rich layers; signifies formation of thrombus in flowing blood; present in antemortem thrombosis.

Answer 15

Lines of Zahn

Question 16

Most common site of arterial thrombosis.

Answer 16

Coronary > cerebral > femoral

Question 17

Most common site of venous thrombosis.

Answer 17

Superficial or deep veins of the leg (Note: thrombi in superficial leg veins rarely embolize, while thrombi in deep leg veins are the most common sources of venous emboli)

Question 18

A detached, intravascular solid, liquid or gaseous mass that is carried by the blood distal to its point of origin.

Answer 18

Embolus

Question 19

Most common and most dreaded sequelae of deep venous thrombosis.

Answer 19

Pulmonary embolism

Question 20

Embolus occluding a bifurcation in the pulmonary tree; associated with sudden death due to acute right-sided heart failure.

Answer 20

Saddle embolus

Question 21

A venous embolus, which entered the systemic circulation through an interarterial or interventricular defect.

Answer 21

Paradoxical embolus

Question 22

Microscopic fat globules found in the circulation after fractures of long bones or after soft-tissue trauma; can lead to pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia.

Answer 22

Fat embolism

Question 23

Gas bubbles within the circulation obstructing vascular flow and causes distal ischemic injury; example: Decompression sickness (bends, chokes)

Answer 23

Air embolism

Question 24

Entry of amniotic fluid into the maternal circulation through a tear in the placental membranes and rupture of uterine veins; presence of marked pulmonary edema, diffuse alveolar damage, and presence of squamous cells in the pulmonary circulation shed from fetal skin, lanugo hair, fat, and mucin.

Answer 24

Amniotic fluid embolism

Question 25

Area of ischemic necrosis caused by occlusion of the vascular supply to the affected tissue.

Answer 25

Infarct

Question 26

Infarcts that tend to occur in loose tissues and in those with dual circulations, previously congested tissues, or when flow is reestablished after an infarction (i.e. after angioplasty of obstructed artery); examples: Pulmonary and Intestinal infarcts

Answer 26

Red infarct

Question 27

Infarcts that tend to occur in solid organs with end-arterial circulations; examples: Myocardial and Splenic infarcts

Answer 27

White infarct

Question 28

State of systemic tissue hypoperfusion due to reduced cardiac output and/or reduced effective circulating blood volume.

Answer 28

Shock

Question 29

This type of shock results from failure of the cardiac pump, which maybe caused by MI, ventricular arrhythmias, cardiac tamponade or outflow obstruction.

Answer 29

Cardiogenic shock

Question 30

This type of shock results from loss blood or plasma volume.

Answer 30

Hypovolemic shock

Question 31

This type of shock is caused by microbial infection, caused by Gram-negative and Gram-positive bacteria and fungi.

Answer 31

Septic shock

Question 32

Type of shock that occurs in the setting of an anesthetic accident or spinal cord injury as a result of loss of vascular tone and peripheral pooling of blood.

Answer 32

Neurogenic shock

Question 33

This type of shock represents systemic vasodilation and increased vascular permeability caused by an IgE-mediated hypersensitivity reaction.

Answer 33

Anaphylactic shock