Circulation I Flashcards

1
Q

What are the four causes of edema?

A
  1. Increased intravascular hydrostatic pressure
  2. Decreased serum oncotic pressure
  3. Increased permeability of vessel walls
  4. Lymphatic obstruction or destruction
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2
Q

Explain the mechanism underlying increased intravascular hydrostatic pressure as a cause of edema. Give an example.

A

Pushes fluid out of vessels, not enough is reabsorbed

Example: heart failure, venous obstruction

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3
Q

Explain the mechanism underlying decreased serum oncotic pressure as a cause of edema. Give an example.

A

Not enough oncotic pressure to reabsorb fluid that leaks into interstitium

Example: low/absent protein synthesis, protein loss

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4
Q

Explain the mechanism underlying increased permeability of vessel walls as a cause of edema. Give an example.

A

More fluid leaks out than can be reabsorbed or carried away

Example: burns, inflammation, chemical injury

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5
Q

Explain the mechanism underlying lymphatic obstruction or destruction as a cause of edema. Give an example.

A

Lymph no longer able to carry away fluid that leaks into interstitium

Example: neoplasia, post-surgery, parasites

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6
Q

Distinguish a transudate from an exudate.

A

Transudate: fluid of low protein content (not from inflammation)

Exudate: fluid of high protein content (infectious, like pus)

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7
Q

Define hyperemia. Distinguish between active and passive hyperemia.

A

Congestion; increased volume of blood within a specific vascular bed

Active: increased flow into the area
Passive: decreased outflow from the area

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8
Q

Define hemorrhage. What morphological change would it cause?

A

Flow of blood FROM the vascular compartment

Change: see blood no longer contained in heart or in lumen of blood vessel

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9
Q

Name six local and two systemic causes for hemorrhage.

A

Local:

  1. Trauma
  2. Infection
  3. Inflammation
  4. Tumor
  5. Vascular malformation
  6. Focal tissue necrosis

Systemic:

  1. Coagulopathy
  2. Vascular defects (vasculitis)
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10
Q

Name the three factors determining the clinical significance of a hemorrhage.

A
  1. Volume of blood: larger amount worse than smaller
  2. Rate of bleeding: rapid worse than slow
  3. Site where hemorrhage occurs: including whether it leaves body or accumulates as a hematoma
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11
Q

Distinguish petechiae, purpora, hematoma, and ecchymosis.

A

Petechiae: minute hemorrhages in skin, mucous membranes, or serosal surfaces

Purpora: splotches of hemorrhage on surfaces

Hematoma: pool of extravascular blood trapped in tissues

Ecchymosis: large hemorrhages of surfaces deeper within tissue, normally with a known cause

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12
Q

Define anemia.

A

Reduction in number and/or volume of erythrocytes per unit volume of blood

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13
Q

What are the two major causes of anemia?

A
  1. Decreased production of RBCs

2. Increased loss of RBCs: slow blood loss, increased desctruction

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14
Q

Distinguish ischemia from infarction.

A

Ischemia: reduction or loss of the blood supply to a tissue or organ

Infarction: death of cells, a tissue, or an organ due to insufficient or absent blood supply

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15
Q

Describe the morphology of an infarct of the heart. (5 factors/stages)

A
  1. Muscle necrosis
  2. Neutrophil infiltration
  3. Macrophages
  4. Fibroblasts and capillaries
  5. Increased collagen (with healing) -> scar formation
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16
Q

Distinguish a thrombus from a clot.

A

BOTH are coagulated blood

Thrombus = “white clot,” composed of coagulation factors, always in vasculature

Clot = “red clot,” composed of clotted blood, normally outside of vasculature or in vasculature after death

17
Q

Define edema.

A

The presence of excessive fluid in the tissues or body cavities

Fluid in cavities = effusions

18
Q

Define anasarca.

A

Very severe generalized edema, especially of subcutaneous tissue

19
Q

Define dependent edema.

A

Distribution by gravity

20
Q

Define pitting edema.

A

Finger pressure leaves a depression

21
Q

Define ascites.

A

Excessive peritoneal fluid

22
Q

Define hydrothorax.

A

Excessive pleural fluid

23
Q

Define hydrarthrosis.

A

Excessive joint fluid

24
Q

List the gross (2) and microscopic (2) morphological changes associated with edema.

A

Gross:

  • -Organ or tissue swells
  • -Increased mass of the tissue due to an influx of fluid

Microscopic:

  • -Separation of tissue elements by pale, pink, protein-containing fluid
  • -No new cellular elements in the tissue (all interstitial)
25
Q

List three morphological changes associated with hyperemia.

A

Organ or tissue can appear redder
Blood remains within blood vessels
Vessels dilated, full of RBCs

26
Q

List the four factors affecting the development of ischemia and infarction.

A
  1. Supply of blood/O2 available
  2. Vascular pattern: single vs complex, collaterals
  3. Rate of decrease of blood supply
  4. Tissue vulnerability: metabolic rate, ability to survive on anaerobic glycolysis
27
Q

What is reperfusion injury? What causes it?

A

Damage to ischemic tissues once reperfused

Causes: toxic oxygen species, reperfusion of dead tissue -> hemorrhage

28
Q

What changes would you expect with an infarct of the myocardium? (3)

A

Changes:

  • Scars developing (Granulation tissue = collagen deposition, fibroblasts present)
  • Coagulative necrosis: ghost myocytes lacking nuclei, more eosinophilic
  • Blue basophilic granular debris = fragmented neutrophils and fibroblasts
29
Q

What changes would you expect with an infarct of the lung? (4)

A

Changes:

  • Ghosts of alveolar walls filled with degenerated RBCs and pink proteinaceous fluid
  • Congested capillaries
  • Boundary scar between dead and living lung
  • Hemorrhage into alveoli, with intact RBCs in acute infarcts
30
Q

What changes would you expect with a thromboembolus of the pulmonary artery? (4)

A

Changes:

  • Dusty rose color thrombus of aggregated fibrinogen
  • –Few enclosed lymphocytes and RBCs
  • –Some capillaries forming
  • –Many macrophages present
31
Q

What changes would you expect in a thrombus of a vein? (2)

A

Changes:

  • Dusty rose color thrombus of aggregated fibrinogen
  • –Few enclosed lymphocytes, fibroblasts, and RBCs
32
Q

What changes would you expect with an infarct of the testis? (2) What can cause this?

A

Changes:

  • Coagulative negrosis
  • Hemorrhage around infarcted tubules

Cause: venous thrombus

33
Q

What changes would you expect with pulmonary edema of the lung? (3) What can cause this?

A

Changes:

  • Lots of pink edematous fluid filling alveoli
  • Congested capillaries
  • Macrophages phagocytosing RBCs

Cause: left heart failure

34
Q

What changes would you expect with chronic congestion of the liver? (4) What can cause this?

A

Changes:

  • “Nutmeg liver”
  • Dying hepatocytes around central vein
  • —Replaced with fibroblasts and Kupffer cells
  • Congested sinusoids

Cause: increased hydrostatic pressure and reduced flow of blood

35
Q

What changes would you expect with atheroemboli in the brain, with infarct? (4) What can cause this?

A

Changes:

  • Liquifactive necrosis
  • Macrophages ingesting and removing dead tissue
  • Reactive astrocytes: enlarged, bright red, polygonal cells with spiky processes
  • Big, canoe-shaped clefts of cholesterol and foamy macrophages in atheroembolus

Cause: plaque from carotid artery

36
Q

What changes would you expect with an old infarct of the kidney? (3)

A

Changes:

  • Coagulative necrosis -> eosinophilic scar tissue
  • Absence of inflammatory cells
  • Recanalization of a well-organized thrombus