Pathology: Abnormalities Of Blood Supply

Front 1

Define edema.

Back 1

Edema is the accumulation of excess fluid in interstitial tissue spaces or body cavities.

Front 2

What accounts for the fact that more fluid leaves the capillary bed at the arteriolar end than enters the capillary bed at the venous end?

Back 2

The difference enters the lymphatics.

Front 3

Under what four conditions will edema occur?

Back 3

1. Increased hydrostatic pressure (ie: CHF)
2. Decreased oncotic pressure (loss of plasma proteins due to renal disease)
3. Blocked lymphatics (surgical resection of lymph nodes)
4. Increased vascular permeability (inflammation)

Front 4

Name four causes of local edema and four causes of systemic edema.

Back 4

Local
1. Inflammation
2. Allergic reaction
3. Venous obstruction
4. Lymphatic obstruction

Systemic
1. Proteinuria
2. Decreased plasma protein synthesis
3. Decreased protein intake
4. CHF

Front 5

What is anasarca?

Back 5

Anasarca is massive, severe edema throughout the body.

Front 6

Differentiate between the etiology and appearance of hyperemia and congestion.

Back 6

Hyperemia is increased blood volume in the blood vessels due to arteriolar vasodilation, as in inflammation. Tissues will be red and warm.

Congestion is increased blood volume because of impaired venous outflow. Tissues will appear cyanotic due to lack of oxygenated blood, and eventually necrosis may occur. Capillary rupture may occur due to increased hydrostatic pressure.

Front 7

Describe the differences between acute and chronic pulmonary edema.

Back 7

Acute pulmonary edema occurs as a result of sudden left ventricular failure, as in an MI, and results in engorgement and overflow of the capillary beds. When the lymph drainage is overwhelmed, fluid spills into the interstitium and air spaces. A frothy, pink fluid may suffocate the patient.
Chronic pulmonary edema is a less severe increase in hydrostatic pressure which causes the alveolar walls to thicken and become fibrotic. Heart failure cells may be present.

Front 8

Describe the differences between acute and chronic liver congestion.

Back 8

Acute liver congestion may be secondary to shock or hepatic vein thrombosis. The sinusoids and central vein become distended, and centrilobular hepatocytes become vulnerable to hypoxic injury.
Chronic liver congestion is usually the result of right ventricular failure. Mid-lobular hepatocytes may undergo fatty change and centrilobular hepatocytes become atrophic or necrotic. Hemosiderin-laden macrophages are present, and the gross appearance is mottled (nutmeg liver) as a result of focal hemorrhage. This may be known as cardiac cirrhosis, although it is not true cirrhosis.

Front 9

What three factors must interact to produce hemostasis?

Back 9

1. Injured vessel wall
2. Platelets
3. Coagulation cascade

Front 10

What are the four basic events that result in hemostasis?

Back 10

1. Platelet exposure and binding to subendothelial collagen.
2. Platelet aggregation and formation of plug at injury site.
3. Activation of the coagulation cascade.
4. Thrombin activation of fibrin, which polymerizes and reinforces platelet plug to form the "definitive platelet plug".

Front 11

What three protein pathways must balance each other in the process of hemostasis?

Back 11

1. Coagulation
2. Anticoagulation
3. Fibrinolytic

Front 12

Describe the relationship between hemostasis and thrombosis.

Back 12

Thrombosis is pathological hemostasis.

Front 13

What is Virchow's Triad?

Back 13

Virchow's Triad is the three factors promoting thrombosis.
1. Endothelial injury
2. Stasis or turbulence of blood flow
3. Hypercoagulable state

Front 14

What three conditions might lead to platelet adherence and aggregation?

Back 14

1. Physical loss of endothelial cells
2. Denudation of endothelial cells (atherosclerosis)
3. Disturbance of local pro- and anti-coagulant balance

Front 15

Why do changes in blood flow increase thrombosis formation?

Which changes in blood flow favor arterial thrombi? venous thrombi?

Back 15

Under normal circumstances, platelets flow in the center of a blood vessel, and therefore do not frequently come into contact with the endothelium. When blood flow is slow or turbulent, platelets are more likely to come into contact with the endothelium and favor accumulation of clotting factors.

Stasis favors venous thrombi, while turbulence favors arterial thrombi.

Front 16

What conditions result in hypercoagulability?

Back 16

1. Platelet hyperreactivity
2. Prolonged immobilization
3. Surgery
4. Reduced cardiac output
5. Pregnancy
6. Cancer dissemination
7. Antiphospholipid antibody syndrome
8. Obesity
9. Oral contraceptives
10. Smoking

Front 17

What is the classic cause of arterial thrombosis?

Back 17

Atherosclerosis

Front 18

Where does turbulence of blood flow frequently arise?

Back 18

Arterial bifurcations (aortic, iliac, carotid bifurcations)

Front 19

Which three arteries are the most common sites of arterial thrombosis?

Back 19

1. Coronary arteries
2. Cerebral arteries
3. Femoral arteries

Front 20

Match the following with either arterial or venous thrombi.

White vs. red

Retrograde (against blood flow) vs. anterograde (with blood flow)

Back 20

Arterial: white, retrograde

Venous: red, anterograde

Front 21

Which types of thrombi are occlusive?

Back 21

Arterial and venous thrombi tend to be occlusive, while mural thrombi are not.

Front 22

Name four conditions that may lead to mural thrombosis.

Back 22

1. Myocardial infarction
2. Left atrial dilation (mitral valve stenosis)
3. Atrial fibrillation
4. Valvular disease

Front 23

Describe the gross appearance of a mural thrombus.

Back 23

A mural thrombus has a "laminated" appearance, which means that lighter areas of platelets may alternate with darker areas containing red blood cells (lines of Zahn). This appearance distinguishes a mural thrombus from a post-mortem clot.

Front 24

Where in a vein is a venous thrombosis most likely to occur? Why?

Back 24

A venous thrombus is most likely to occur within a valve because valves produce eddies and pockets of stagnant blood.

Front 25

Describe the five clinical features of superficial vein thrombosis. Give three examples of events that might cause an SVT.

Back 25

Clinical features:
1. Hyperemia
2. Warmth
3. Edema
4. Tenderness to palpation
5. Localized pain

Causes:
1. Infection
2. Trauma
3. Intravenous catheter

Front 26

In what group of patients is DVT of primary concern?

Back 26

Post-surgical patients, because they are hypercoagulable and immobile

Front 27

What clinical signs may be present in a patient with a DVT?

Back 27

Leg warmth, edema, swelling, cyanosis, distended superficial veins, tenderness along course of a vein, calf pain, positive Homan sign (forced dorsiflexion of foot).

However all of these signs may be absent when a DVT is present.

Front 28

What are the four potential fates of a thrombus?

Back 28

1. Dissolution (by fibrinolytic system)
2. Propagation (further platelet and fibrin accumulation, leading to vessel occlusion)
3. Organization/recanalization (conversion to vascularized connective tissue, possibly reestablishing blood flow)
4. Embolization (detachment and transport to distant site)

Front 29

How does aspirin prevent thrombosis?

Back 29

Aspirin prevents thrombosis by blocking the COX pathway and mitigating platelet aggregation. Therefore, if an atherosclerotic plaque were to rupture in a patient taking aspirin, the likelihood of platelets aggregating on the damaged endothelium would be greatly reduced.

Front 30

How does warfarin prevent coagulation?

Back 30

Warfarin acts as a vitamin K antagonist, which prevents coagulation cascade proteins from functioning normally.

Front 31

How does heparin prevent coagulation?

Back 31

Heparin prevents coagulation by binding to antithrombin III and increasing its antithrombin activity by 1000X.

Front 32

What natural fibrinolytic factor is utilized in thrombolysis? How is it activated in a therapeutic setting?

Back 32

Plasmin is the body's natural fibrinolytic protein. It is producted as plasminogen and is normally cleaved to its active form by tissue plasminogen activator (tPA). Streptokinase and urokinase used to be administered therapeutically to dissolve clots, but more recently a recombinant tPA has come into clinical use.

Front 33

Define embolism.

Back 33

An embolism is a detached solid, liquid, or gaseous mass that enters the circulation at one location and is carried to a distant location where it becomes lodged, resulting in partial or complete vascular occlusion.

Front 34

Name ten sources of emboli.

Back 34

1. Fragments of previously formed thrombi
2. Gas bubbles
3. Fat (broken bone)
4. Bone marrow
5. Pieces of atherosclerotic plaques
6. Runaway cardiac catheters
7. Foreign objects
8. Hair
9. Amniotic fluid
10. Tumor cell clusters

Front 35

Can arterial thrombi embolize to the venous circulation, and vice versa?

Back 35

No, with rare exceptions.

Front 36

What are the three most common sites for formation of thromboemboli in the heart?

Back 36

1. Left atrium
2. Left ventricle
3. Valves (vegetations)

Front 37

What are paradoxical emboli? How do they do what they do?

Back 37

Paradoxical emboli are those that manage to pass from venous circulation into arterial circulation. This is done through an atrial or ventricular septal defect.

Front 38

What is the name for thromboemboli traveling in the arterial circulation?

Back 38

Systemic thromboemboli

Front 39

Where do systemic thromboemboli most frequently lodge?

Back 39

Lower extremeties (75%)
Brain (10%0
Less often: kidneys, spleen, intestines

Front 40

What is the source of a pulmonary embolus in 95% of cases?

Back 40

DVT

Front 41

Name two causes of fat emboli.

Back 41

1. Broken bones
2. Blunt trauma

Front 42

Name five symptoms of fat emboli.

Back 42

1. Respiratory distress
2. Neurological symptoms
3. Thrombocytopenia
4. Anemia
5. Petechial rash

Front 43

What might atheroma emboli be a complication of?

Back 43

Catheterization and surgery on atherosclerotic arteries

Front 44

Where are emboli of fetal origin from an amniotic fluid embolism found?

Back 44

Lungs

Front 45

Typically, what volume of gas is required for a gas embolus to be clinically significant?

Back 45

50-100 mL

Front 46

Most infarction occurs as a result of arterial thrombosis or embolism. Name three locations of venous embolism that can also cause infarction.

Back 46

1. Renal vein
2. Superior sagittal sinus (drains superior cerebral hemispheres)
3. Mesenteric veins (this frequently results in wet gangrene)

Front 47

Describe white and red infarctions and their differences.

Back 47

White infarctions occur as a result of arterial blockage in solid organs, as blood is allowed to drain freely but new blood is not introduced.

Red infarctions occur in venous blockage, tissues possessing a dual blood supply, or reperfusion of necrotic tissues.

Front 48

What is DIC?

Back 48

DIC is disseminated intravascular coagulation. It is a condition in which patients develop microthrombi throughout the microcirculation, resulting in hemorrhage. It occurs secondary to an event that activates the clotting system.

Front 49

Why do patients with DIC hemorrhage?

Back 49

When the microthrombi of DIC form, they consume clotting components, rendering patients more vulnerable to bleeding. In addition to consumption of clotting components, the formation of microthrombi also activates the plasmin pathway, resulting in fibrinolysis and rendering the patient increasingly vulnerable to bleeding.

Front 50

Name four mechanisms that trigger DIC via thromboplastin activation.

Back 50

1. Endotoxin of G(-) sepsis
2. Obstetric complications
3. Malignancy (ie: pancreas and lung)
4. Traumatized or necrotic tissue

Front 51

Name three mechanisms that trigger DIC via widespread endothelial injury.

Back 51

1. Endotoxin of G(-) sepsis
2. Vasculitis (antigen-antibody complexes)
3. Temperature extremes (burns, frostbite)

Front 52

How does DIC present?

Back 52

There is a wide range of clinical presentations that may be observed with DIC. Some include thrombosis, hemorrhage, pulmonary edema, respiratory distress, neurological signs, acute renal failure, and circulatory collapse.
Common lab findings include thrombocytopenia, prolonged bleeding time, elevated fibrin split products, and anemia.

Front 53

What is the basic clinical definition of shock?

What are the three main types?

Back 53

Prolonged systemic hypoperfusion resulting from insufficient cardiac output or reduction in the effective circulating blood volume.

Types:
1. Hypovolemic
2. Cardiogenic
3. Generalized vasodilation

Front 54

What causes hypovolemic shock?

Back 54

Reduction of intravascular blood volume. May result from hemorrhage, vomiting, diarrhea, dehydration, or burns.

Front 55

What causes cardiogenic shock?

Back 55

Cardiogenic shock is a result of heart pump failure, resulting in compromise of cardiac output. It is usually associated with massive MI, but may also be caused by arrhythmias, interventricular spetal rupture, ventricular free wall rupture, or pulmonary embolism.

Front 56

Name three types of shock by generalized vasodilation.

Back 56

1. Anaphylactic shock
2. Neurogenic shock
3. Septic shock

Front 57

What factors are released by mast cells and basophils during anaphylactic shock?

Back 57

Histamine, bradykinin, leukotrienes

Front 58

What causes neurogenic shock?

Back 58

Spinal cord trauma, brain injury, general anesthesia.

Impairment of neural control of vasomotor tone, resulting in blood redistribution to periphery and reduced effective circulating volume.

Front 59

What type of bacteria is most commonly associated with septic shock?

Back 59

Gram negative bacteria, because endotoxin production stimulates cytokine release and inflammation.

Front 60

Describe the three stages of shock.

Back 60

1. Compensation/nonprogressive stage: Activation of sympathetic compensatory mechanisms, tachycardia, peripheral vasoconstriction, rapid shallow breathing, cold and clammy, cyanotic and pale, shallow pulse, low BP, diminishing urine output

2. Impaired tissue perfusion/progressive stage: Hypoxia and impaired fluid exchange due to prolonged vasoconstriction, lactic acidosis resulting in vasodilation, peripheral blood pooling, worsening cardiac output, necrosis (usually begins in renal tubules), alveolar damage (edema, hemorrhage, hyaline membrane formation), anoxic injury to liver and intestine, possible initiation of DIC

3. Decompensation/irreversible stage: loss of reflex vasoconstriction, kidney failure, cardiac output and BP drop to critical levels, cerebral hypoxia resulting in acute brain dysfunction, loss of consciousness, bowel ischemia resulting in bacterial seeding of blood stream, death is imminent