DISTURBANCES OF FLUIDS AND CIRCULATION
I. INTRODUCTION
II. INTERESTING CONNECTIONS
III. OBJECTIVES AND PRACTICE EXERCISES
THROMBUS
EMBOLUS
INFARCT
ISCHEMIA
CONGESTION
EDEMA
HEMORRHAGE
SHOCK
KEY WORDS:
Definitions:
Thrombus:
- A solid mass of blood elements formed within a blood vessel or cardiac
chamber, in a living organism (i.e., always formed antemortem).
Embolus:
- A detached intravascular mass (gas,liquid, solid) which travels
through the vascular system to lodge at a distant site.
Infarct:
- A localized area of ischemic necrosis in an organ or tissue.
Ischemia:
- Loss or decrease of blood supply to a tissue or organ. Often used
clinically to mean less damage than infarction. (e.g. "The chest pain
may be due to either infarction or ischemia".)
Collaterals:
- Alternate or parallel blood supplies. These may be native vessels
(as in the Arcade of Drummond in the mesentery, or the circle of Willis),
enlargements of existing vessels (as in collaterals in the diseased, ischemic
heart), or new vessels (as in areas of previous inflammation with scarring).
Congestion:
- Increased amount of blood in tissue, within blood vessels.
Hemorrhage:
- Escape of blood from the vascular system (outside of blood vessels.)
Edema:
- Excess serous fluid in a tissue or space.
Shock:
- A syndrome in which there is inability to maintain an adequate circulating
blood volume, causing inadequate perfusion of all tissues.
Know definitions for the following: (Use Robbins and your medical dictionary).
- hematemesis
- hemoptysis
- hematuria
- hematochezia
- hemothorax
- hemopericardium
- melen
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I. INTRODUCTION
In this section of the course, we will consider disturbances of fluid and
circulation. You will learn what happens when blood coagulates in vessels
and in cardiac chambers. Principles governing the formation and behavior
of thrombi will become second nature to you, as will vascular complications
such as embolism, ischemia, infarction, edema and congestion. You will learn
what factors determine the significance of hemorrhage and ischemia.
II. INTERESTING CONNECTIONS
Vascular intimal injury initiates not only a response in the blood (namely,
thrombosis) but also a response in the blood vessel (e.g., intimal thickening,
which can form the basis for atherosclerosis- see pp. 471-2). We will deal
with these processes again in Systemic Pathology.
III. OBJECTIVES AND PRACTICE EXERCISES
(Page numbers refer to Robbins.)
Read these, then read Robbins, then return after reading Robbins. If you
need help, see pages at end of this handout.
Be able to:
- Know the definitions in the handout, define and characterize the
terms in bold face type and italics in the reading.
- Explain how the vessel wall, platelets, and the plasma coagulation
system contribute to thrombosis. (See pp. 99 and following in Robbins.)
Note how abnormalities of each may also contribute to bleeding.
- Explain why thrombi form in arteries only after significant intimal
damage and/or luminal stenosis, but can form in veins which are only dilated.
(Clues: what is the major difference in blood flow? See alterations in
normal blood flow, p. 105).
- Explain why thrombosis is an expected complication of atherosclerosis,
a disease of arteries causing intimal damage and luminal narrowing (p.
105).
- Explain why thrombi form on walls of the left ventricle following
some large myocardial infarcts; on the wall of the left atrium in rheumatic
heart disease (in which there is usually mitral valve stenosis and atrial
fibrillation); and on the walls of aortic atherosclerotic aneurysms. (p.
105. See also sections on each entity - use your index).
- A patient's left leg is cool, pale, pulseless and painful. His right
leg is warm, purple, swollen and painful, but still has a pulse. Which
leg is more likely to have an arterial thrombus, and which a venous thrombus?
Explain. What are several causes (your differential diagnoses) for each
type of occlusion? (For causes, see p.110).
- An 84 year old woman presents with migratory thrombophlebitis (Trousseau's
sign) and phlegmasia cerulea dolens (swollen, painful blue leg). Studies
reveal multiple thrombotic occlusions in leg veins, inferior vena cava,
and pulmonary arteries, as well as pulmonary, splenic and renal infarcts.
Explain the findings. What neoplastic disease(s) do you suspect and why?
(Clues: first see p. 506 top left. Others are p. 106 top right, p.110,
p. 297 (top left), pp. 623-625, and p. 907 under clinical features).
- Your next patient has thrombophlebitis and pulmonary emboli. First
explain to your professor, using medical terminology, the pathogenesis
and natural course of these lesions. Then explain to the patient's family,
in lay terms, how these lesions developed and what will happen to the lesions
and to the patient. (Refer to pp. 111-112, and pp. 504-505, and pp. 679-680)
- Do varicosities of superficial veins usually result in pulmonary
emboli? (See p. 110 and p.111)
- Explain how pulmonary emboli might lead to pulmonary infarction
with hypoxia in one patient, but to sudden death without infarction in
another patient. (See p. 111.)
- Compare and contrast ischemia and infarction; thrombosis and embolism;
edema and congestion.
- Describe the sequence of inflammatory events occurring at the border
of an infarct. (See pink section, pp. 115-116.) Why does healing begin
first at the border of infarct with normal tissue rather than at the center?
(Review pp. 79 and 80.)
- Discuss possible pathogenetic mechanisms for edema in the lungs;
then do the same for peripheral tissues. (First, think of general mechanisms
of edema formation, and then explain how these mechanisms apply to the
pulmonary and systemic circulations. Refer to pp. 94-97 for clues.)
- (Refer to pp.117- 120 for this one.) A 27 year old male arrives
in the emergency room following a motor vehicle accident. He had several
bandaged lacerations of his left arm and face, and burns over 50% of his
body. His BP is 80/40 mmHg, hematocrit 38%. He may go into shock if not
treated. Why? What organs and systems would you anticipate to become affected
and in what ways? (pp.120-121) What complications of his burns do you anticipate?
(Look up Burns in your index.) The EMTs say he was bleeding profusely,
but his hematocrit is still nearly normal, at 38%. Then, over the next
two days, his hematocrit falls. Explain both observations. (Clue: p.587
- anemia of acute blood loss).
Click here for answers to objectives and practice
problems
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THROMBUS:
Definition:
Location:
Types:
Predisposing Factors: Virchow's triad:
1.
2.
3.
Effects:
Evolution:
EMBOLUS:
Definition:
Types:
Origins:
Effects:
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INFARCT:
Definition:
Types:
Morphology:
Clinical Significance:
ISCHEMIA:
Definition:
Factors influencing extent of damage:
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CONGESTION:
Definition:
Types:
Morphology:
Significance:
EDEMA:
Definition:
Mechanisms:
Morphology:
Clinical Significance:
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HEMORRHAGE:
Definition:
Causes:
Types:
Effects:
SHOCK:
Definition:
Types:
Effects on tissues:
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Outline
Questions?
Comments? Send a message to the CATS guru: jkessler@salus.uvm.edu