Edema Flashcards
Anasarca
Edema involving all aspects of the body: upper and lower extremities
and the face.
Lipedema
Edema caused by fluid retained in the interstitial space by lipids in
the dermis
Myxedema
Edema resulting from hypothyroidism.
Pretibial myxedema
Not technically edema, the swelling on the anterior shins
is due to coalescing of subcutaneous plaques due to Graves disease antibodies
infiltrating dermal tissue.
Unilateral extremity edema
is usually due to venous or lymphatic obstruction ,
deep venous thrombosis,
tumor obstruction,
primary lymphedema
Stasis edema
of a paralyzed lower extremity also may occur.
localized facial edema
Allergic reactions (“angioedema”) and superior vena caval obstruction
Bilateral lower-extremity edema
inferior vena caval obstruction,
compression due to ascites,
and abdominal mass
Periorbital edema
noted on awakening often results from renal disease and impaired Na
excretion
Edema typically results:
❑ when the pressure in the vessels (Pin) overrides the
semipermeable capillary membrane, pushing more volume into
the extravascular space.
❑ When the lymphatic drainage of the tissues is obstructed,
❑ When the capillary membrane permeability is increased (K).
❑ When the blood protein concentration is decreased (Oncin).
❑ Excess fat in the interstitium may draw and hold water into the
interstitial space causing edema (lipedema).
Pathogenesis In CHF
diminished cardiac output and arterial underfilling
result in both decreased renal perfusion and increased venous pressure
with resultant renal Na retention due to
renal vasoconstriction, intrarenal blood flow redistribution, direct Na-retentive effects
of norepinephrine and angiotensin II, and secondary hyperaldosteronism
leading to
distal tubular Na retention.
Pathogenesis In cirrhosis
arteriovenous shunts and peripheral vasodilation are the proximate causes
of Na retention.
Ascites accumulates when increased intrahepatic vascular resistance
produces portal hypertension.
As in heart failure, the effects of excess intrarenal and
circulating norepinephrine, angiotensin II, and aldosterone lead to renal Na retention
and worsening edema.
Reduced serum albumin and increased abdominal pressure also
promote lower-extremity edema.
Pathogenesis In acute or chronic renal failure
edema occurs if Na intake exceeds kidneys’
ability to excrete Na secondary to marked reductions in glomerular filtration.
Pathogensis In nephrotic syndrome
loss of protein into the urine also leads to primary Na
retention, through effects on tubular Na transport
idiopathic edema
a syndrome of
recurrent rapid weight gain