Chapter 50 - Edema Flashcards
Describe the compartments through which water is distributed in a human body.
“About one-third of total-body water is confine to the extracellular space. Approximately 75% of the latter is interstitial fluid, and the remainder is in the plasma.”
What are the Starling foces? How can these contribute to edema formation?
“The forces that regulate the disposition of fluid betwen these two components of the extracellular compartment [intersticial and plasma] frequently are referred to as the Starling forces. The hydrostatic pressure within the capillaries and the colloid oncotic pressure in the interstitial fluid tend to promote movement of fluid from the vascular to the extravasular space. By contrast, the colloid oncotic pressure contributed by plasma proteins and the hydrostatic pressure within the interstitial fluid promote the movement of fluid into the vascular compartement. As a consequence, there is movement of water and diffusible solutes from the vascular space at the arteriolar end of the capillaries. Fluid is returned from the interstitial space into the vascular system at the venous end of the capillaries and by way of the lymphatics. These movements are usually balanced so that there is a steady state in the sizes of the intravascular and interstitial compartments, yet a large exchange between them occurs However, if either the capillary hydrostatic pressure is increased and/or the oncotic pressure is reduced, a further net movement of fluid from intravascular to the interstitial spaces will take place”
Name all the pathophysiological mechanisms that might lead to edema.
Abnormal Starling forces (increased hydrostatic pressure and/or decreased oncotic pressure in the intravascular compartment), increased capillary permeability, stimulation of the renin-angiotensinogen-aldosteron system, increased concentration of endothelin-1 hormone, resistance to the action of natriuretic peptides and increased arginine/vasopressin concentrations.
Give examples of situations associated with increased capillary permeability that might be associated with edema. Also, explain the features of this edema in correlation to causes of generalized edema.
“Edema may result from damage to the capillary endothelium, which increases its permeability and permits the transfer of proteins into the interstitial compartment. Injury to the capillary wall can result from drugs, viral or bacterial agents, and thermal or mechanical trauma. Increased capillary permeability also may be a consequence of hypersensitivity reaction and of immune injury. Damage to the capillary endothelium is presumably responsible for inflammatory edema, which is usually nonpitting, localized, and accompanied by other signs of inflammation - i.e., erythema, heat, and tenderness.”
Name the causes of nonpitting edema.
Inflammatory edema, lymphedema (late) and myxedema.
What is the correlation between underfilling and the sympathetic nervous system as well as the concentration of plasmatic renin? Explain the pathophysiology of these variables in contributing to edema.
“The dimished renal blood flow characteristic of states in which the effective arterial blood volume is reduced is translated by the renal juxtaglomerular cells (specialized myoepithelial cells surrounding the afferent arteriole) into a signal for increased renin release. Renin is an enzyme with a molecular mass of about 40,000 Da that acts on its substrate, angiotensinogen, an a2-globulin synthesized by the liver, to release angiotensin I, a decapeptide, which in turn is converted to angiotensin II (AII), an octapeptide. AII has generalized vasoconstrictor properties, particularly on the renal efferent arterioles. This action reduces the hydrostatic pressure in the peritubular capillaries, whereas the increased filtration fraction raises the colloid osmotic pressure in these vessels, thereby enchancing salt and water reabsorption in the proximal tubule as well as in the ascending loop of Henle.”
“The renin-angiotensin-aldosterone system (RAAS) operates as both a hormonal and paracrine system. Its activation causes sodiu and water retention and thereby contributes to edema formation Blockade of the conversion of angiotensin I to AII and blockade of the AII receptor enchance sodium and water excretion and reduce many forms of edema. AII that enters the systemic circulation stimulates the production of aldosterone by the zona glomerulosa of the adrenal cortex. Aldosterone in turn enchances sodium reabsorption (and potassiu excretion) by the collecing tubule, further favoring edema formation.”
Name two situations associated with increased aldosterone plasmatic concentration and explain the pathophysiology of this finding.
Heart failure and hepatic cirrhosis.
Both are associated with increased concentration of plasmatic aldosterone due to stimulation of the renin-angiotensinogen-aldosterone system (as a result of the underfilling). Moreover, in heart failure “not only is aldosterone secretion elevated but the biologic half-life of the hormone is prolonged secondary to the depression of hepatic blood flow, which reduces its hepatic catabolism”. In hepatic cirrhosis “The concentration of circulating aldosterone often is elevated by the failure of the liver in metabolize this hormone.”
Name the drugs that block the action of aldosterone.
- Aldosterone receptor antagonists: spironolactone and eplerenone.
- ENaC blockers: amiloride and trianterene.
What is the role of arigine vasopressin and endothelin-1 to edema formation in heart failure?
“The secretion of arginine vasopressin (AVP) occurs in response to increased intracellular osmolar concentration and, by stimulating V2 receptors, AVP increases the reabsorption of free water in the distal tubules and collecing ducts of the kidneys, thereby increasing total-body water. Circulating AVP is elevated in any patients with heart failure secondary to a nonosmotic stimulus associated with decreased effectve arterial volume and reduced compliance of the left atrium. Such patients fail to show the normal reduction of AVP with a reduction of osmolality, contributing to edema formation and hyponatremia.”
“This potent peptide vasoconstrictor is relased by endothelial cells. Its concentration in the plasma is elevated in patients with severe heart ailure and contributes to renal vasoconstriction, sodium retention, and edema.”
Explain the mechanism(s) of action of natriuretic peptides.
(1) excretion of sodium and water by augmenting glomerular filtration rate, inhibiting sodium reabsorption in the proximal tubule, and inhibiting release of renin and aldosterone; and (2) dilation of arterioles and venules by antagonizing the vasoconstrictor actions of AII, AVP, and sympathetic stimulation.”
In edematous states, resistance to the actions of natriuretic peptides may be increased, reducing their effectiveness.
True or False?
True.
Name the causes of generalized edema.
Heart failure, hepatic cirrhosis, renal causes (including nephrotic syndrome) and denutrition (including kwarshiorkor and marasmus).
Which physical findings might indicate a cardiac etiology of generalized edema?
“Elevated jugular venous pressure, ventricular (S3) gallop, ocasionally with displaced or dyskinetic apical pulse; peripheral cyanosis, col extremities, small pulse pressure when severe.”
One might find a low cholesterol in edematous patients with hepatic cirrhosis.
True or False?
True.
What is the severity of hypoalbuminemia associated with edema?
Less than 35g/L (3,5g/dL).
