Edema and congestion Flashcards

1
Q

what happens when hydrostatic pressure > oncotic pressure?

A

fluids enter interstitial space

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2
Q

what happens when oncotic pressure> hydrostatic pressure

A

net reabsorption of fluid

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3
Q

causes of increased hydrostatic pressure

A

impaired venous return

arteriolar dilation

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4
Q

causes of impaired venous return

A

CHF

constrictive pericarditis

Ascites

venous obstruction/ compression: thrombi, mass effect, lower extremity inactivity due to dependency

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5
Q

causes of arteriolar dilation

A

heat

neurohumoral dysregulation

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6
Q

how does L heart failure contribute to edema

A

increased hydrostatic pressure in pulmonary capillaries causes transudate to enter lung alveoli and interstitium and produce pulmonary edema

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7
Q

how does R heart failure contribute to edema

A

increased hydrostatic pressure in the vena cava causes and increase in transudate in the BLE and interstitium, producing pitting edema

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8
Q

causes of reduced plasma oncotic pressure

A

nephrotic syndrome

ascites

malnutrition

protein-losing gastropathy

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9
Q

how does nephrotic syndrome contribute to decreased oncotic pressure

A

increased salt/ water cant correct plasma volume deficits and plasma proteins continue to persist

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10
Q

consequences of decreased oncotic pressure

A

edema

reduced intravascular volume

renal hypoperfusion

secondary hyperaldosternism

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11
Q

causes of lymphatic obstruction

A

inflammation

neoplasm

postsurgical

postirradiation

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12
Q

how does lymph obstruction contribute to edema

A

normally, more fluid is filtered into the interstitial spaces than is reabsorbed into the vascular bed and is removed by the lymphatics.

when there is a lymph obstruction there is n reabsorption of fluid from the interstitial spaces and vascular beds

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13
Q

how does sodium retention cause edema?

A
  1. intravascular fluid expansion from water following sodium increases the hydrostatic pressure
  2. dilution of fluids causes decreased oncotic pressure
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14
Q

causes of sodium retention

A

excessive salt intake with renal insufficiency

increased tubular reabsorption of sodium

renal hypoperfusion

increased RAAS

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15
Q

how does inflammation contribute to edema

A

increases permeability of venules

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16
Q

what is myxedema

A

A collection of fluid caused by deposition of glycosaminoglycans (mucopolysaccharides) in various tissues.

17
Q

what causes myxedema

A

T cell cytokines stimulate fibroblasts to synthesize increased amounts of hyaluronic acid

18
Q

whats the difference between and edema and an effusion

A

Edema= fluid in interstitial spaces

Effusion: fluid in cavity

19
Q

how does edema present with renal impairment?

A

generalized edema

periorbital edema

20
Q

how does edema present in subQ tissues

A

influenced by gravity (dependent edema)

can impair wound healing

21
Q

how does edema present in the brain

A

narrowed sulci with distended gyri

grossly swollen with evidence of compression against the underlying skull

22
Q

how does edema present in the lungs

A

lungs 2-3x normal weight

frothy blood-tinged fluid made of extravasated cells, air and transudate

since it impedes oxygen diffusion, it makes a favorable environment for infection

23
Q

what do effusions typically look like

A

protein poor translucent straw-colored fluid

except peritoneal effusion caused y lymph obstruction, which appear milky due to the presence of lipids absorbed from the gut

24
Q

Differentiate between hyperemia and congestion

A

hyperemia is an active process that involves dilation leading to increased blood flow, turning tissues red

Congestion is a passive process caused by the decreased outflow of blood from a tissue

25
Q

What do congested tissues typically look like

A

dusky reddish-blue due to cyanosis and stasis f RBC;s

26
Q

differentiate the morphology of acute LVF and RVH

A

Acute LVF causes pulmonary edema: engorged alveolar capillaries, alveolar septal edema and focal intra alveolar hemorrhage

Acute RVF causes liver congestion: distended central vein sinusoids with centrilobular hepatocyte ischemic necrosis and periportal hepatocytes with possible fatty change

27
Q

differentiate the morphology of chronic LVF and RVH

A

chronic LVF: alveolar septae and interstitium become thick and fibrotic

microhemorrhages cause bleeding into the alveolar space, which is phagocytized and degraded by macrophages

chronic RVF: hemosiderin-laden macrophages with variable degrees of hepatocyte necrosis

centrilobular regions are grossly red-brown and slightly depressed due to cell death and are accentuated against the tan uncongested liver