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Pathology > Edema, Hyperemia, Congestion > Flashcards

Edema, Hyperemia, Congestion Flashcards

1
Q

Hemodynamics

A

Health of cells and organs depends on uninterrupted circulation to deliver oxygen, nutrients, and to remove waste
- requires normal fluid balance

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2
Q

What results in injury, while possibly maintaining an intact blood supply

A

Abnormalities in vascular permeability, or hemostasis

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3
Q

What components are a part of normal fluid homeostasis?

A
  • maintenance of vessel wall integrity
  • intravascular pressure
  • osmolarity within certain physiologic ranges
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4
Q

What affects the net movement of water across the vascular wall?

A

Changes in vascular volume, pressure, or protein content, or alterations in endothelial function

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5
Q

Body water composition

A

60% of lean body weight is water

  • 66% intracellular
  • 25% extracellular
  • 8% intravascular (blood plasma)
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6
Q

Edema

A

Increased fluid extravasation into interstitial/extracellular spaces
- includes body cavities

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7
Q

Recognizing edema

A

Easily recognized grossly, appears microscopically as subtle cell swelling, with clearing and separation of intracellular matrix elements

  • occurs in any tissue type
  • commonly seen in SQ, brain, lung
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8
Q

What prefix is used to indicate edema?

A

“Hydro” or “hydrops”

  • hydrothorax: pleural cavity
  • hydropericardium: pericardial sac
  • hydrosalpinx: uterine tube
  • hydrocephalus: brain
  • hydrocoele: fluid filled cyst anywhere in the body
  • hydroperitoneum: peritoneal cavity (ascities)
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9
Q

Anasarca

A

Severe and generalized edema, with profound SQ tissue swelling

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10
Q

Edema is considered to be a __________

A

Space displacing lesion

  • exerts pressure in a closed area such as brain or lung
  • easily resorbed in underlying cause is removed
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11
Q

Intracellular edema

A

Depression of metabolic systems of the tissues or lack of adequate nutrition to cells

  • depressed ionic pumps = Na and water leak in
  • inflammation = increased permeability of cell membranes = Na and water leak in
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12
Q

Extracellular edema

A

Abnormal leakage of fluid from blood capillaries

  • failure of lymphatic system to return fluid from interstitium
  • renal retention of salt and water
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13
Q

Transudate

A

Fluid accumulation due to hydrostatic imbalances between intravascular and extravascular compartments, despite normal vascular permeability

  • low protein levels
  • non inflammatory edema
  • clear, colorless, slightly yellow
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14
Q

Exudate

A

Increased endothelial permeability caused by leakage of plasma proteins (albumin) and leukocytes

  • high protein levels
  • inflammatory edema
  • opaque
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15
Q

Modified transudate

A

Between transudate and exudate

- FIP

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16
Q

Horse generalized edema

A

Usually in ventral abdomen and ventral thorax

- severe: distal extremities (stocking)

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17
Q

Bovine generalized edema

A

Usually in intermandibular space

- brisket area (thoracic inlet)

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18
Q

Cat generalized edema

A

Hydrothorax

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19
Q

Dog generalized edema

A

Ascites

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20
Q

Gross appearance of edema

A

Swollen, distended, gravitates ventrally

  • tissue pits on pressure and indentations remain after pressure is removed
  • tissue is cool to touch, unless inflammation is also present
  • tissue is not red/painful
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21
Q

SQ edema

A

Different distributions, depends on cause

- may be diffuse or more conspicuous at sites of highest hydrostatic pressure –> distribution is gravity dependent

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22
Q

Ascites

A

Recognized by presence of clear, yellow tinged fluid that distends loose connective tissues or accumulates in body cavities
- peritoneal, pleural, pericardial

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23
Q

Pig edema

A

Possible cause: septicemia with E. coli

- exhibit conjunctival edema, cannot open eyes

24
Q

Septicemia

A

Systemic bacterial infection

- bacterial toxins cause vascular leakage of protein = total body edema (anasarca)

25
Q

Micro appearance of edema

A

Separation of tissues by spaces that are clear (protein poor edema) or pink (protein rich edema) in hematoxylin and eosin stained slides
- dilation of lymphatic vessels (natural channel for removal of excess fluid)

26
Q

Pathogenesis of edema

A
  • increased intravascular pressure
  • decreased plasma colloid osmotic pressure
  • increased vascular permeability
  • lymphatic obstruction
  • heart failure/sodium retention
27
Q

______ and ____ leads to net accumulation of extravascular fluid

A

Increased hydrostatic pressure; diminished plasma osmotic pressure

28
Q

How do tissue lymphatics remove excess volume?

A

Returns it to circulation via thoracic duct

29
Q

Persistent tissue edema results when ______

A

The ability of the lymphatics to drain tissue is exceeded

30
Q

Hydrostatic pressure (blood pressure) vs osmotic pressure (protein)

A

High hydrostatic, low osmotic –> lose fluid out of vessels –> leads to high osmotic, low hydrostatic –> fluid out; proteins more concentrated

31
Q

Forces driving fluid out of a blood vessel

A

Hydrostatic pressure (bp) is the main factor in driving fluid OUT

  • interstitial fluid colloidal osmotic pressure –> IN
  • interstitium normally decreases protein, little impact on formation of edema
32
Q

Forces driving fluid into vessels

A

Intravascular colloidal osmotic pressure –> IN
- due to plasma protein in vessel lumen
- 25 mmHg
Tissue tension (tissue hydrostatic pressure) –> OUT
- 1-4 mmHg
- important in distribution of edema
- lax areas of body are more prone to edema

33
Q

Difference between areteriole capillary pressure and venous capillary pressure

A
  • arteriole hydrostatic pressure: 37 mmHg

- venular hydrostatic pressure: 17 mmHg

34
Q

Increased hydrostatic pressure is due to ______

A

Venous obstruction or impaired venous outflow
= increased hydrostatic pressure due to backflow of blood into venous system
= leakage of sodium and fluid into interstitial space
- no significant leakage of colloids

35
Q

Diseases that cause increased hydrostatic pressure

A
  • congestive heart failure
  • cirrhosis of liver
  • obstruction or narrowing of veins
36
Q

Decreased plasma colloidal pressure

A

Capillary blood contains decreased quantity of colloids due to

  • decreased hepatic synthesis of protein
  • increased protein loss thru kidney, or GIT
37
Q

Hypoproteinemia

A

Fluid and sodium are not reabsorbed at venous end of capillary = decreased colloidal pressure
- fluid accumulated in interstitium

38
Q

Diseases that cause decreased plasma oncotic pressure

A
  • kidney disease
  • cirrhosis of the liver/liver failure (hypoalbuminemia)
  • malnutrition/starvation
  • protein-losing gastroenteropathies
  • GI parasitism
39
Q

Increased vascular permeability

A

Endothelial cell damage results in increased capillary permeability to fluids, salts, and colloids
- increase in colloids within interstitium reduces reabsorption of fluid at the venous end of capillary —> colloids may eventually be drained away by lymphatics

40
Q

Lymphatic function

A

Normal: small quantities of fluids, salts, and colloids escape from capillaries and are drained from the interstitium by lymphatics
Lymphatic obstruction: materials accumulate

41
Q

Diseases that cause lymphatic obstruction

A
  • inflammation
  • neoplasia
  • post-surgical
  • post-irradiation
  • common occurance after lymph node disease, until collateral circulation can be established
42
Q

Heart failure/sodium retention

A

Increased tubular reabsorption of sodium

  • common in congestive heart failure and edema due to hypoproteinemia
  • reduced renal perfusion due to CHF
  • increased renin-angiotensin-aldosterone secretion
43
Q

Can you consume enough salt to cause Na retention edema?

A

No

- caused by heart failure or kidney disease, leading to increased plasma volume

44
Q

Heart failure

A

Hypoperfusion of the kidneys

  • renin: released from juxtaglomerular apparatus
  • angiotensin: causes secretion of aldosterone
  • aldosterone: causes increased absorption of Na in kidneys
  • water follows sodium!!
45
Q

Kidney disease

A
  • Na no excreted

- results in Na retention

46
Q

Active hyperemia

A

Active process resulting in increased tissue blood flow due to arteriolar dilation

  • excess blood of arterial origin (skeletal muscles during exercise, at sites of inflammation)
  • affected area is red due to engorgement with oxygenated blood
47
Q

Causes of active hyperemia

A
  • normal physiologic process (GIT gets blood for digestion)

- hallmark of inflammatory response

48
Q

Congestion

A

Passive process resulting from impaired outflow from a tissue

  • interference with venous drainage
  • may be systemic (heart failure), or local (isolated venous obstruction)
  • tissue has red-blue color (cyanosis) due to accumulation of deoxygenated blood
49
Q

Causes of congestion

A
  • heart failure: generalized slowing of blood everywhere
  • -> left heart: lung affected (chronic pulmonary congestion)
  • -> right heart: liver (chronic passive congestion)
  • venous occlusion (localized): thrombus, pressure, twisting
  • hypostasis: hypostatic congestion
50
Q

Hypostatic congestion

A

Blood pooling in organs and tissues on the lower side of a recumbent animal
- contrast to livor mortis: blood pooling on downside of animal after death

51
Q

Chronic passive congestion

A

Caused by any disease that results in right heart failure

52
Q

Chronic pulmonary congestion

A

Caused by any disease that results in left heart failure

53
Q

What is common between active and passive hyperemia?

A

Increased volume and pressure of blood in a given tissue with associated capillary dilation and a potential for fluid extravasation

54
Q

In _________, increased inflow leads to engorgement with oxygenated blood, leading to erythema

A

Active hyperemia

- tissue is bright red, warm to touch, and pulsating

55
Q

In ________, diminished outflow leads to a capillary bed swollen with deoxygenated venous blood, leading to cyanosis

A

Congestion

- tissue is blueish, blood is stagnant, slightly swollen, and cool

56
Q

How to microscopically distinguish active hyperemia from congestion

A

Histologically, they are difficult to distinguish

  • vessels full of blood
  • may see inflammatory cells during active hyperemia due to inflammation
57
Q

Chronic congestion

A
  • anoxic injury: stasis of blood with no new blood coming in due to atrophy (cell death and shrinking), fibrosis
  • thrombosis: expected because of decreased blood flow
  • edema
  • hemosiderin deposition

Pathology (19 decks)

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