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Cardiopulm Patho > Peripheral Edema > Flashcards

Peripheral Edema Flashcards

1
Q

what is edema

A

imbalance between capillary filtration and lymphatic reabsorption and drainage of interstitial fluid due to change in hydrostatic pressure, osmotic pressure, and cappilary permeability

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2
Q

discuss alterations in capillary hemodynamics

A

filtration rate exceeds reabsorption/transport and fluid moves from vascular space into the interstitial spaces
-hydrostatic pressure (blood) is high or wen colloid osmotic pressure is low (in the blood)

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3
Q

when does edema develop

A

when capillary filtration rates exceeds the lymph drainage rate either because the filtration rate is too high or the lymph drainage rate is too low or a combo of both

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4
Q

what are the causes of peripheral edema

A
  • INC in peripheral venous pressure (venous obstruction or reflux)
  • DEC in colloid osmotic pressure in blood
  • INC capillary permeability (inflam, vasodilation)
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5
Q

describe the four fluid forces that interact to maintain a balance between filtration and absorption

A
  • capillary hydrostatic pressure: higher in arterial end to favor filtration
  • interstitial hydrostatic pressure: very low values and increases w/ INC in fluid due to lymphatic blockage or INC capillary permeability
  • plasma osmotic pressure: high values favor absorption
  • interstitial osmotic pressure: low values
  • remember higher hydrostatic pressure forces fluid movement away from pressure and higher oncotic pressure draws fluid movement toward the pressure
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6
Q

give examples of why venous pressure or capillary permeability increase and vascular colloid osmotic pressure decreases

A
  • INC venous pressure: R ventricular failure, DVT, venous obstruction/reflux
  • DEC colloid osmotic: PRO loss from renal failure or hepatic failure
  • INC capillary perm: vasodilation or inflam
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7
Q

what are key elements of history and how are the related to a pathology

A
  • Is it unilateral or bilateral? Uni: lymphedema, DVT, venous insufficiency, compartment syndrome; Bilat: CHF, lipedema, kidney/liver failure
  • Duration of edema? Can progress from varicose veins to CVI to secondary lymphedema
  • Is it painful? Lipedema vs lymphedema vs CVI
  • Does it decrease w/ elevation or overnight? Venous vs early stage I lymphedema
  • Do you have hx of sleep apnea? Increased burden of right ventricle
  • Do you drink alcohol? Smoke? Liver disease
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8
Q

what are risk factors of varicose veins

A
  • age and weight
  • female
  • prego
  • DVTs
  • genetically defective valves
  • standing/sitting long periods of time
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9
Q

what are s/s of varicose veins

A
  • full, heavy, aching
  • swelling in ankles
  • itching
  • severe: leg swelling, calf pain, dry/scaly skin, hyperkeratosis
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10
Q

what is the pathophys of varicose veins

A

primary: genetic defect where INC type I collagen synthesis and DEC type III collagen synthesis, which contributes to weakness of vein wall and supporting fascia
secondary: deep venous obstructions, INC venous distensibility, or post-thrombosis can cause valvular incompetence

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11
Q

what that the med tests and treatment options for varicose veins

A

med tests: observation or duplex doppler US

treatment: elevation, ankle pumps, compression (20-30), aerobic and aquatic w/ garment

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12
Q

what are the risk factors for CVI

A
  • DVT
  • varicose veins
  • age, weight
  • female
  • prego
  • standing/sitting long time
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13
Q

what are the symptoms of CVI

A
  • swelling, aching, tiredness of leg
  • relieved with elevation
  • hemosiderin stains
  • hyperpigmentation or atrophic blanche
  • eczema
  • fibrosis
  • delayed wound healing
  • dilated veins
  • venous stasis ulcers
  • lipodermatosclerosis
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14
Q

what is the pathophys of CVI

A

valvular incompetence or obstruction and muscle pump impairment cause INC venous pressure, impairing return of blood and microcirculation hemodynamics

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15
Q

what med tests and treatments for CVI

A

med tests: observation and doppler

treatments: same as varicose veins, with thermal ablation of incompetent vein sclerotherapy, and vein stripping

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16
Q

general s/s of lymphedema

A

swelling or thickening and heaviness

17
Q

What are the s/s of each stage of lymphedema

A

stage O: reabsorption less than filtration, however not enough protein accumulated
stage 1: edema DEC w/ elevation or bed rest, edema is soft/pitting, no fibrosis or stemmer sign
stage 2: edema doesn’t DEC w/ elevation or night’s rest., fibrosis formation, non-pitting edema, positive stemmer’s sign
stage 3: fibrosis, sclerosis, fat deposits in deep sulci of joints, thickening of dermis, positive stemmer’s sign, trophic skin changes such as hyperkeratosis

18
Q

what can speed up change b/w one stage to another

A

-infection

19
Q

what is the pathophys of lymphedema

A
  • DEC in reabsorption of protein into the lymph system and decrease of rate of transportation
  • overload w/ protein, but normal reabsorption and transportation rates
20
Q

what is the pathophys of lipedema

A
  • lipid metabolism disorder, characterized by INC in fat storage and fat cell size
  • swelling occurs around puberty, during 2nd half of day b/c of orthostatic edema and diminished tissue resistance of fatty tissues that permits edema fluid to accumulate easily
  • INC capillary filtration and permeability
  • hemorrhages and swollen areas are painful
21
Q

describe the stages of lipedema

A
  • stage 1: subcutaneous tissue is thickened, but not viscous; superficial skin is smooth; fat tissue is nodular
  • stage 2: superficial skin is uneven, nodules are larger and feel like cotton balls
  • stage 3: increasing fat deposits w/ severe alteration in normal body contours
22
Q

what are the med test of lymphedema and lipedema

A
  • both are diagnosis of exclusions
  • rule out cardiac, liver, and kidney via blood work
  • rule out venous via US Doppler
  • lymphedema: lymphoscintigraphy, CT scan, and MRI
  • lipedema: negative Stemmer, tender to palpation, family hx, and clinical distribution of fatty tissue
23
Q

what are treatment options for lipedema

A
  • compression therapy
  • strengthening/hypertrophy exercises, so INC muscle mass will flatten out adipocytes
  • MLD due to orthostatic edema and if secondary develops
24
Q

what is the pathophys of peripheral edema as a result of CHF

A
  • inefficient cardiac pump results in increase in hydrostatic pressure, which results in increased interstitial fluid volume
  • in left ventricular failure, increase in hydrostatic pressure in pulmonary capillaries
  • in right ventricular failure, increase in hydrostatic pressure of systemic capillaries
25
Q

what is the pathophys of peripheral edema and renal failure

A
  • kidneys unable to filter/excrete fluid, so more fluid reaches venous system
  • blood plasma osmotic pressure decreases as a result, which increases plasma filtration and decreases absorption
  • this overloads lymphatics
26
Q

what is the pathophys of peripheral edema and nephrotic symdrome

A
  • damage to glomeruli in the kidneys, which are responsible for filtering blood
  • glomeruli allow too much protein to leave body, which decreases oncotic pressure, plus sodium is retained which increases water retention
27
Q

what is the pathophys of peripheral edema and liver disease

A
  • scarring of the liver (cirrhosis) leads to low albumin and other proteins in the blood, since liver responsible for producing proteins
  • decreased plasma proteins = low plasma oncotic pressure and a resultant increase in interstitial fluid

Cardiopulm Patho (4 decks)

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