Pathophysiology is the study of the disturbance of normal mechanical, physical, and biochemical functions, either caused by a disease, or resulting from a. 𝗣𝗗𝗙 | As Per PCI Regulations FIRST YEAR B. PHARM. Semester - II. A Textbook of Pathophysiology for Pharmacists. Book · January PDF | On Oct 12, , Almir Fajkic and others published A TEXTBOOK OF PRACTICAL PATHOPHYSIOLOGY.
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Porth's Pathophysiology pdf (9th edition) norinkgibipen.cf#!AdY12bCB! QtvG_Y1JfeGG7IQiOUaRcyXkA-p4Z52L6zL0Du4E. Pathophysiology/Lee-Ellen C. Copstead, Jacquelyn L. Banasik. . The student section of the book's website hosted on Evolve Unit XV: Integumentary System. a LANGE medical book Pathophysiology of Disease: An Introduction to Clinical Medicine Seventh Edition Edited by Gary D. Hammer, MD, PhD Millie.
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First published: Tools Request permission Export citation Add to favorites Track citation. Share Give access Share full text access. Share full text access. Please review our Terms and Conditions of Use and check box below to share full-text version of article. Summary A critical relationship exists among cardiac mechanics and atrial waveforms, the physiology of the venous circulations, and the dynamic effects of intrathoracic pressure ITP and respiratory motion on cardiovascular physiology, permitting a better interpretation of the waveforms to reflect pathophysiology.
Related Information. The mechanisms responsible for the reduction in intestinal vascular resistance that account for the changes in capillary pressure and capillary filtration coefficient that lead to enhanced capillary filtration in chronic portal hypertension involve the formation of vasodilator substances and other factors and are reviewed elsewhere [ 18 , 19 , 21 , 81 , , , ].
Nevertheless, the associated increase in transmicrovascular filtration rate largely accounts for the elevated transcapillary escape rate of proteins noted in this disorder through convective coupling of fluid and protein flux. Elevated capillary pressure and filtration rate occur early in the course of development of diabetes mellitus and is thought to be an important stimulus for capillary basement membrane thickening, the ultrastructural hallmark of diabetic microangiopathy [ 27 , ]. Microvascular rarefaction, or loss of capillaries, has been reported to accompany the development of arterial hypertension, diabetes mellitus, and the metabolic syndrome [ 8 , 27 , 32 , 70 , 73 , ].
The attendant reductions in the surface area available for exchange may partially offset the effect of capillary hypertension to increase interstitial fluid volume in these conditions.
Very large increases in venous pressure may induce increments in capillary filtration far in excess of what would be predicted from the associated increase in capillary pressure.
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This is due to pressure-induced increases in microvascular permeability that are manifest in the Starling equation by increases in hydraulic conductivity and reductions in the osmotic reflection coefficient. Organs such as the liver, which have discontinuous capillaries characterized by large gaps between endothelial cells and reflection coefficients approaching 0.
Large increases in venous pressure are thought to enlarge these pores in microvascular wall, which is referred to as the stretched pore phenomenon [ , , ]. Individual organs demonstrate a differential sensitivity to the effect of elevated venous pressure with regard to induction of the stretch pore phenomenon. For example, no increase in permeability occurs in microvessels of the feet during quiet standing, even though capillary pressure in the feet increases by more than 50 mmHg relative to values measured when supine, owing to the large hydrostatic column in arteries and veins.
However, pulmonary capillaries may demonstrate a stretched pore phenomenon during conditions such as left ventricular failure, an effect that exacerbates pulmonary edema formation in this condition [ ]. As noted above, myogenic constriction of arterioles in response to elevations in arterial or venous pressure constitutes an important safety factor against edema formation in hydrostatic edema by limiting the increase in capillary pressure and by reducing the number of perfused capillaries, and thus the available surface area for fluid filtration, that might otherwise occur in response to arterial or venous hypertension or increased venous resistance Figure 4.
However, it is important to note even modest increments in capillary pressure, which might appear to be small and inconsequential, can result in substantial increases in fluid filtration rates across the microvasculature.
This is because normal net filtration pressure is quite small, averaging 0. Thus, increasing capillary pressure by just 2 mmHg, as noted above in arterial hypertension, results in an initial fold increase in fluid movement from the blood into the interstitium.
Capillary hypertension results in the formation of a protein-poor ultrafiltrate that upon entry into the interstitial space raises interstitial fluid volume.
Owing to the compliance characteristics of the interstitium, small increments in interstitial volume produce very large increases in tissue pressure, which effectively reduces the transcapillary hydrostatic pressure gradient, thereby limiting further accumulation of fluid Figure 4. This effect is exacerbated in response to elevations in venous outflow pressure through the phenomenon of venous bulging. That is, the volume in veins increases immediately on elevation of venous pressure, which produces a coincident increase in interstitial pressure caused by expansion of engorged venules and veins into the interstitial spaces Figure 4.
In essence, venous engorgement shifts the interstitial compliance curve to the left, so that a smaller change in interstitial volume produces a larger increase in interstitial pressure.
Increased interstitial fluid pressure increases lymph flow by three mechanisms.
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First, increased tissue pressure provides the driving pressure for flow into initial lymphatics. Second, increased pressure in the interstitial compartment creates radial tension on the anchoring filaments connecting the extracellular matrix to lymphatic endothelial cells, locally increasing initial lymphatic diameter and opening gaps between interdigitating and overlapping junctions between adjacent lymphatic endothelial cells Figure 3.
These tensional forces create a small, transient suction pressure for movement of interstitial fluid through enlarged gaps between adjacent endothelial cells, which act as a second, one-way valve system to ensure unidirectional flow from the interstitium into lymphatics. Third, as fluid moves into initial lymphatics, it increases volume in upstream lymphangions, promoting their contractile activity and lymph flow.
The presence of valves between adjacent lymphangions assures one-way flow. As noted above, capillary hypertension results in the movement of protein-poor fluid into the interstitial spaces, reducing the concentration of tissue proteins and decreasing tissue colloid osmotic pressure Figure 4. Because solute is excluded from a large portion of gel water in the extracellular matrix, the rapidity of the decrease in tissue protein concentration that occurs in response to increased interstitial fluid volume is enhanced, thereby augmenting the effectiveness of protein washdown as an edema safety factor.
It is important to note that the effectiveness of decreases in tissue osmotic pressure as an edema safety factor is reduced in severe capillary hypertension, owing to the stretched-pore phenomenon discussed above, which increases convective-coupled protein transport into the tissue spaces. Marked reductions in the circulating levels of proteins, especially albumin, is another cause of edema that relates to intravascular factors Figure 4.
Hypoproteinemia may result from rapid loss of proteins across a compromised glomerular barrier in diseased kidneys, impaired hepatic synthesis of plasma proteins in liver disease, severe malnutrition or protein-losing enteropathy which limits the availability of substrate for protein synthesis , or from infusion of intravenous fluids lacking macromolecules.
Like capillary hypertension, this effect is opposed by elevations in tissue hydrostatic pressure, which increases lymph flow, both of which serve to limit the accumulation of tissue fluid Figure 4.
Enhanced capillary filtration also acts to dilute the concentration of proteins in the extracellular spaces, an effect that is magnified by increasing the accessible volume in the extracellular matrix gel Figures 2. The ensuing reduction in interstitial colloid osmotic pressure acts to reduce net filtration pressure, thereby minimizing edema formation. Unlike the response to vascular hypertension, there is no stimulus for myogenic arteriolar vasoconstriction and venous bulging does not occur in hypoproteinemia, which reduces the margin of safety for edema formation in response to this edemagenic stress.
As a consequence, tissues are less able to compensate for reductions in plasma colloid osmotic pressure that are equivalent to a given increase in capillary hydrostatic pressure. Disruption of the microvascular barrier is a pathologic sequela in a large number of disease states, commonly accompanies trauma, and can be induced by a wide variety of endogenously produced mediators and pharmacologic agents. In the Starling equation Equation 1.
Rapid reductions in the reflection coefficient decrease the effectiveness of the colloid osmotic pressure gradient in opposing filtration. The reduction in the restrictive properties of the endothelial barrier allows movement of a protein-rich filtrate into the tissue spaces, which increases interstitial colloid osmotic pressure Figure 4.
The resultant reduction in the colloid osmotic pressure gradient increases net filtration pressure, an effect that is exacerbated by the fact that many if not most of the mediators that increase microvascular permeability also act as vasodilators and reduce arteriolar resistance Figure 4. As a consequence, capillary pressure is elevated, which further increases net filtration pressure.
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In addition, vasodilatation tends to recruit capillaries, thereby increasing microvascular surface area available for fluid and protein flux into the tissues. The latter change contributes to a further increase in the capillary filtration coefficient which is equal to the hydraulic conductivity times surface area, L p S , thereby magnifying the effect of increased net filtration pressure to promote volume flux.
The marked enhancement in transcapillary fluid filtration results in increased convective transport of protein through the enlarged pores in the microvascular barrier Figure 4. Under such conditions, the effect of increases in interstitial fluid pressure and lymph flow to provide a margin of safety against edema formation are rapidly overwhelmed and marked swelling of the interstitial spaces ensues.
Permeability edema is exacerbated in inflammatory states that are characterized by leukocyte infiltration into the tissues Figure 4. Inflammation is a characteristic response to tissue injury and involves the release of a large number of mediators that not only increase microvessel permeability and cause vasodilatation, but also act to attract leukocytes to the damaged tissue Figure 4.
These phagocytic cells release a variety of hydrolytic enzymes as well as reactive oxygen and nitrogen species that degrade extracellular matrix components and the anchoring filaments that attach to lymphatic endothelial cells Figures 3. This reduces the radial tension on the valve-like overlapping and interdigitating cell membranes at the interendothelial junctions in initial lymphatics, which may compromise lymphatic filling.
Leukocyte-mediated disruption of the extracellular matrix components also increases interstitial compliance, which allows a larger volume of extracellular fluid to be accommodated within the matrix with little increase in interstitial fluid pressure, thereby attenuating the effectiveness of this edema safety factor.
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Filtration-secretion may compromise the absorptive function of the delicate intestinal mucosa and appears to occur as a result of the formation of large channels between mucosal cells in the villous tips when interstitial fluid pressure increases by greater than 5 mmHg [ 87 ].