Integrated Clinical Science: Cardiology I – Edema

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Twenty question-and-answer flashcards covering the definition, classifications, pathophysiology, and mechanisms of edema based on the lecture notes.

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20 Terms

1
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What is the medical definition of edema?

A palpable swelling produced by expansion of the interstitial fluid volume that collects in the small spaces surrounding the body’s tissues and organs.

2
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At approximately how much excess interstitial fluid does edema become clinically apparent?

When interstitial fluid volume increases by about 2.5–3 liters.

3
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Which major organ failures commonly cause edema?

Heart failure, kidney (renal) failure, and liver failure.

4
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How is a transudate distinguished from an exudate with respect to protein and cellular content?

Transudate has low protein content and few cells, whereas exudate has high protein content and more cells.

5
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What specific-gravity values differentiate transudate from exudate?

Transudate < 1.012; exudate > 1.020.

6
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Name the two main location-based categories of edema.

Localized edema and generalized edema.

7
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What are the two clinical (physical exam) types of edema?

Pitting edema and non-pitting edema.

8
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Give two examples of organ-specific or regional edemas of the central nervous and respiratory systems.

Cerebral edema (brain) and pulmonary edema or pleural effusion (lungs).

9
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What term describes free fluid accumulation in the peritoneal cavity?

Ascites.

10
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What is anasarca?

Massive, generalized edema of all subcutaneous tissues.

11
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Which form of cardiac-related edema involves fluid around the heart?

Pericardial effusion.

12
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What clinical test differentiates pitting from non-pitting edema?

Applying pressure with a finger to see whether an indentation (pit) persists.

13
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Which two opposing forces in Starling’s equation primarily govern capillary fluid exchange?

Vascular hydrostatic pressure and plasma colloid (oncotic) pressure.

14
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Explain how increased capillary hydrostatic pressure leads to edema.

When venular hydrostatic pressure exceeds plasma oncotic pressure, minimal or no reabsorption occurs, causing fluid to remain in interstitial tissues.

15
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Explain how reduced plasma oncotic pressure leads to edema.

Low plasma albumin (from liver disease or malnutrition) lowers oncotic pressure, allowing net fluid movement into interstitial tissues.

16
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How does lymphatic obstruction produce localized edema?

Impaired lymph drainage prevents removal of residual interstitial fluid, leading to its accumulation (e.g., after radical mastectomy or malignant blockage).

17
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Why do sodium and water retention promote edema formation?

Renal vasoconstriction, activation of the renin-angiotensin-aldosterone system, and ADH release cause the kidneys to retain Na⁺ and water, expanding plasma volume and raising hydrostatic pressure.

18
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Which inflammatory mediators increase capillary permeability and thereby cause edema?

Histamine, toxins, anoxia, and certain drugs that create endothelial gaps allowing plasma proteins to leak out.

19
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List the five major pathophysiologic mechanisms of edema formation.

1) Increased capillary hydrostatic pressure, 2) Decreased plasma oncotic pressure, 3) Lymphatic obstruction, 4) Increased capillary permeability, 5) Sodium and water retention.

20
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Is lymphatic fluid generally low or high in protein content?

High in protein content.