رسالة الماجستير فى الموجات فوق الصوتية

مشاركات: 11468
اشترك في: الخميس إبريل 04, 2013 10:28 pm

Re: رسالة الماجستير فى الموجات فوق الصوتية

مشاركةبواسطة دكتور كمال سيد » الأربعاء يوليو 30, 2014 3:04 pm

The renal cortex lies immediately beneath the fibrous capsule, arches over the bases of the pyramids, and dips in between adjacent pyramids towards the renal sinus as the renal columns, which provide passage of blood vessels and nerves
The inner cortex is divided from the medulla by a line of tangentially running blood vessels-the arcuate arteries and veins
The layers of cortex close to the medulla are termed the juxtamedullary cortex
Histologically, the kidney is composed of a very large number of tortuous, closely packed uriniferous tubules, bound together by a little connective tissue in which run the blood vessels, lymphatics and nerves. Each uriniferous tubule consists of two embryologically distinct parts namely, the nephron or secreting part which elaborates the urine, and the collecting tubule which carries the fluid from a number of renal tubules to a terminal papillary duct or duct of Bellini, which opens into a minor calix at the apex of a renal papilla
The nephron is the structural functional unit of the kidney of which each kidney contains about one million.
(Fig 3)
صورة
Nephron of the kidney. The labelled parts are 1. Glomerulus, 2. Efferent arteriole, 3. Bowman's capsule, 4. Proximal convoluted tubule, 5. Cortical collecting duct, 6. Distal convoluted tubule, 7. Loop of Henle, 8. Duct of Bellini, 9. Peritubular capillaries, 10. Arcuate vein, 11. Arcuate artery, 12. Afferent arteriole, 13. Juxtaglomerular apparatus.

The nephron comprises the renal corpuscle, which is concerned with filtration of substances from the plasma; and the renal tubule, which is concerned with selective resorption of substances from the glomerular filtrate until it approaches urine composition
The renal corpuscle (Malpighian) are small rounded masses about 0.2 mm in diameter which are visible in the renal cortex and columns of Bertin. Each is composed of a central glomerulus of vessels, and a membranous envelope termed the glomerular capsule(Bowman's capsule) which is the small pouch-like commencement of a renal tubule
The glomerulus is a lobulated tuft of convoluted, capillary blood vessels, held together by scanty connective tissue.
This capillary network is derived from a small afferent arteriole, which enters the capsule at a point opposite to that at which the capsule is connected with the tubule ; the efferent arteriole emerges from the capsule at the same point which is called the vascular pole of the capsule
The glomerular capsule(of Bowman) is the blind, expanded end of the renal tubule, deeply invaginated by the glomerulus. Its outer parietal wall is lined by squamous epithelium, while the visceral (glomerular) wall surrounding the capillaries and fixed to the basement membrane of the glomerulus, is lined by specialised epithelial podocytes
Thus, between the glomerulus and the outer layer of the capsule i.e. between visceral and parietal, there is a flattened cavity (capsular or urinary space) which is continuous with the lumen of the proximal convoluted tubule (PCT). It is the region within the glomerular capsule that collects the filtrate
A distinct basal lamina underlies the cells of the capsule and, in the glomerulus, this fuses with the basal lamina surrounding the capillary endothelial cells
The podocytes which surround the capillary loops consist of flattened stellate cells, the major dendrite-like processes of which are curved around the capillaries, interdigitating tightly with the processes of other podocytes. Where they approach neighbouring capillaries, many end-feet pedicels encroach on the basal lamina leaving narrow gaps between them. Each podocyte contains numerous mitochondria, microtubules, microfilaments, and vessels of various types, indicating a metabolic activity
The endothelium of the glomerulus is of the finely fenestrated type, the only barriers to the passage of fluid from the capillary lumen to the cavity of glomerular capsule are therefore, the fused basal lamina of the endothelium and podocytes
This layer, the glomerular basement membrane is~ 0.33 micrometer thick and is composed of three distinct layers, the first and third are the pale-staining laminae rarae interna and externa, and the middle dense, fibrous lamina densa. The glomerular slit diaphragm through which the filtrate must pass before it enters the urinary space covers the area between adjacent podocyte end- feet
(Fig 4)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3108006/
صورة
Scheme of filtration barrier (blood-urine) in the kidney
(A. The endothelial cells of the glomerulus; 1. pore (fenestra
B. Glomerular basement membrane: 1. lamina rara interna 2. lamina densa 3. lamina rara externa
C. Podocytes: 1. enzymatic and structural protein 2. filtration slit 3. diaphragm


The PCT is lined with simple cuboidal cells with highly folded basolateral membrane into numerous microvilli projecting into the lumen of the PCT called brush border. Microvilli are protoplasmic extensions of the plasma membrane and they greatly increase the surface area for absorption. They are permeable to water and solutes
Tight junctions are a type of cell to cell connection in which the cell membrane of adjacent cells form a very close binding and permit passage of water but limits escape of large molecules from tubular lumen into the interstitial space. The thin segment or the descending loop of Henle is formed of a single layer of simple flattened epithelium lacking brush border thus permeable ONLY to WATER but not to solutes. The thin segment extends from the PCT to the hair – pin turn in the loop of Henle.
The thick segment or the ascending limb of the loop of Henle becomes continuous with the distal or second convoluted tubule which is divisible into a straight and a convoluted section, between which is a special thickened region, the macula densa, after which the nephron straightens out as the junctional or connecting tubule which ends by joining a collecting or straight duct

The collecting ducts commence in the medullary rays of the cortex. They unite at short intervals with one another and finally open into wider tubes termed the papillary ducts or ducts of Bellini, which in turn open on the summit of a papilla, the numerous duct openings giving the tip of the papilla a perforated cribriform appearance.
The thick ascending segment and early distal convoluted tubules(DCT) are lined with similar cuboidal epithelium having a glycoprotein covering of the luminal membrane, with more tighter tight junctions than in the PCT, thus being permeable to SOLUTES only like Nacl but IMPERMEABLE to WATER. The DCT extends from the guxtaglomerular apparatus or JGA to the cortical collecting ducts.

As the thick ascending loop of Henle transitions into the early DCT the tubule runs adjacent to the afferent and efferent arterioles, and when these structures are in contact, they form the JGA formed by the macula densa or MD and the juxtaglomerular cells, which are modified smooth muscle cells of the afferent and efferent arterioles, namely the afferent. These enlarged cells serve as baroreceptors sensitive to blood pressure changes within the arterioles
صورة

مشاركات: 11468
اشترك في: الخميس إبريل 04, 2013 10:28 pm

Re: رسالة الماجستير فى الموجات فوق الصوتية

مشاركةبواسطة دكتور كمال سيد » الأربعاء يوليو 30, 2014 3:46 pm

The MD is a plaque of cells containing large tightly packed cell nuclei within the thick segment and is formed by the cells of the thick ascending limb of the loop of Henle in contact with the arterioles.
These cells monitor and respond to changes in the osmolarity of the filtrate in the tubule thus serving as osmoreceptors, and allowing changes in the tubule to influence the behavior of the adjacent glomerulus.

Fig 6

صورة
http://faculty.stcc.edu/AandP/AP/AP2pag ... ry/PCT.htm

The cuboidal cells of the late DCT and cortical collecting ducts or CCD are of two distinct functional types : the principal and the intercalated cells. The principal cells are sensitive to the hormone ADH which regulates the permeability to water and solutes like urea which is a waste product of protein deamination and it is the chief nitrogenous waste excreted in urine.

Fig 7

صورة

The renal arterial blood supply is through the main renal artery which arises as a lateral branch of the aorta just inferior to the superior mesenteric artery at the level of the 2nd lumbar vertebra, and venous blood is conveyed to the inferior vena cava(IVC) via the renal vein.
Each renal artery divides into five segmental arteries that enter the hilum, four infront and one behind the renal pelvis, and are distributed to different segments and areas of the kidney.
Segmental arteries give rise to lobar arteries, one for each renal pyramid, which again divide just before entering the kidney substance into 2-3 interlobar arteries which run radially to the corticomedullary junction on each side of the renal pyramids, where they give off the arcuate arteries which arch over the bases of the pyramids giving rise to the interlobular arteries that ascend in the cortex as far as the capsule
The afferent glomerular arterioles or AGA arise as branches of the of the interlobular arteries to supply the nephrons and glomerular capillary bed which drains into the efferent glomerular arterioles or EGA. EGA from the outer cortical glomeruli drain into a peritubular capillary network within the renal cortex and thence into increasingly larger and more proximal branches of the renal vein
Blood from the juxtamedullary glomeruli passes via vasa recta in the medulla and then turns back towards the area of the cortex from which the vasa recta originated. Vasa recta vessels possess fenestrated walls which facilitates movement of diffusible substances
Vasa recta drain the nephrons and coalesce to form the arcuate vein. Other small venules flow into the interlobular vein which in turn drains into the arcuate vein. The remainder of the venous drainage of the kidney corresponds to the arteries in the opposite direction.
The renal vein emerges from the hilum in front of the renal artery and drains into the IVC

Approximately 25% of humans possess dual or multiple renal arteries on one or both sides. The main renal arteries are solitary in ~60% of individuals, and multiple and smaller in the remainder. Renal arteries are more commonly multiple when the kidney is malpositioned or malrotated. Supplemental renal arteries may course directly into the polar regions of the kidney without coursing through the renal hilum.
Renal veins are usually solitary. The left renal vein is longer than the right, and for this reason the left kidney is usually chosen for live donor transplant nephrectomy

Anomalies of the kidney include: ectopic kidney, congenital fusion(horseshoe kidney), unilateral renal agenesis, hypoplastic kidneys, duplicated collecting system, extra renal pelvis, (persistent)fetal lobation,, junctional parenchymal defect, interrenicular septum, renal sinus lipomatosis, dromedary hump, renal column hypertrophy, medullary sponge kidney, ureteropelvic junction obstruction

Renal variants are those slight alterations in anatomy that may lead the sonographer to suspect that an abnormality is present while it is a normal variation. Renal variants include: Renal column hypertrophy, the dromedary hump, and the junctional parenchymal defect
Renal column hypertrophy is a common anatomic variant also termed hyppertrophy of the septal cortex or a prominent column of Bertin . It is a double layer of renal cortex that is folded towards the centre of the renal medulla, displacing a portion of the renal sinus. The echo texture is same as the adjacent renal cortex ; and the width of the mass is twice as great as the adjacent renal cortical thickness.
The dromedary hump is more common in the left kidney and demonstrates a lateral bulge at its mid portion . Sonographically it is identical to the renal cortex

The junctional parenchymal defect is more common in the left kidney. Embryologically, each kidney is formed from upper and lower units of parenchyma that fuse along an oblique line. The junction points of these limits may persist as a prominent indentation of the cortical surface. The parenchymal defect is triangular in shape with echogenic focus best demonstrated on longitudinal scans. It is commonly located anteriorly, at the junction of the upper and middle thirds of the kidney
صورة

مشاركات: 11468
اشترك في: الخميس إبريل 04, 2013 10:28 pm

Re: رسالة الماجستير فى الموجات فوق الصوتية

مشاركةبواسطة دكتور كمال سيد » الأربعاء يوليو 30, 2014 5:47 pm

CHAPTER TWO
Literature Review
contd


B )

RENAL PHYSIOLOGY


fig 8
صورة
1Human urinary system
2+3+4+5+6=
2Kidney
3Renal pelvis, 4Ureter, 5Urinary bladder, 6Urethra.

(Left side with frontal section)
7Adrenal gland

Vessels: 8 Renal artery and vein, 9 Inferior vena cava, 10 Abdominal aorta, 11 Common iliac artery and vein

With transparency: 12 Liver, 13 Large intestine, 14 Pelvis

The order of impurities being excreted from the kidneys: Kidneys → Ureters → Urinary Bladder → Urethra


The principal role of the kidneys is the elimination of waste material and the regulation of volume and composition of body fluids. In addition, the kidney has endocrine and metabolic functions producing erythropoietn, renin, prostaglandins and the metabolism of vitamin D and small molecular weight proteins
The kidney purifies the blood by excreting urine (excess water, salts and toxic metabolites), involving the processes of glomerular filtration, tubular reabsorption, and tubular secretion.
The hydrostatic pressure within the glomerular capillaries of ~ 45mm Hg results in filtration of fluid from plasma into Bowmans capsule. This filtrate is identical in its composition with plasma except that it normally contains no fat and very little protein. The filtrate then flows through the various parts of the renal tubule and is modified according to body needs to maintain homoeostasis by tubular selective reabsorption of its constituents and by tubular secretion.
About 65% of the water filtered by the glomerulus is reabsorbed by the PCT through active and passive transport processes. The remaining fluid passes through the DCT and collecting ducts
The filtrate is concentrated in the descending limb by reabsorbing (loosing) water and retaining solutes. The filtrate is diluted in the ascending limb where water is retained and solutes lost
This asymmetrical pattern of H2O & Nacl reabsorption in the descending and ascending limbs of the loop of Henle, creates an osmotic gradient within the medullary region
The Vasa recta circulates blood through the medulla to provide nutrients WITHOUT removing solutes, thus not weakening the osmotic gradient
The final processing of the filtrate in the late DCT and collecting ducts comes under direct physiological control, that membrane permeabilities and cellular activities are altered in response to the body needs to retain or excrete specific substances
This variability provides the mechanism for precisely regulating the balance of fluid and solutes returned to the blood. The principal cells of the late DCT and collecting ducts are sensitive to the hormones aldosterone and ADH. They perform hormonally –regulated Na & H2O reabsorption and potassium secretion. Thus Aldosterone precisely regulates the final amount of Na reabsorbed ; aldosteron levels remain low when the levels of Na & K in the blood are balanced

The Intercalated cells are specialized cells of the collecting ducts that are involved in Acid–base regulation, hence the pH of the blood, by secreting H+ ions into the filtrate through ATPase pumps in the luminal membrane.
A decrease in the level of Na+ ions or an increase in K+ ions will trigger the release of Aldosterone which will result in increase in the number and activity of Na / K pumps in the basolateral membrane and Na/K channels in the luminal membrane,( K channels are absent from the basolateral membrane). K+ ions enter the cell trough the basolateral membrane, but instead of diffusing back into the interstitium they diffuse through the luminal membrane and are secreted into the filtrate. Na+ excretion will be reduced leading to increased interstitial osmolarity and high water reabsorption hence reduced urine volume.
This permeabilty to water is only possible in the presence of ADH which occurs along with an increase in aldosterone under most normal conditions, that is because when stimulated by ADH, the principal cells quickly insert luminal water channels thereby increasing water permeability

The filtrate composition is altered as it passes up through the differing osmotic environments of the renal cortex and medulla (300 mosmoles in PCT–1200 mosmoles in interstitium) because filtrate concentration in the tubule is related to the interstitial osmolarity
The opposing flow and opposite activities of the descending and ascending segments of the loop of Henle is called the COUNTER CURRENT MULTIPLIER MECHANISM
The final step in urine formation occurs as the filtrate passes down the medullary collecting duct (MCD): Of the 125 ml / min of glomerular filtrate that entered the PCT from the glomerular capsule,95 % has been reabsorbed back into the peritubular capillaries into the blood, and only 5% (6ml/min) remains to enter the MCD
The medullary osmotic gradient (MOG) Is necessary for determining the final volume and concentration of urine through ADH release, and is constructed by the counter current multiplier mechanism, the chief substances being NaCl and Urea
Normal urine has an osmolarity of 600 mosm i.e. twice the normal body osmolarity. About 99% of the filtrate is reabsorbed into the blood leaving ~ 0.9% of the filtrate or (1.10ml/min) of concentrated urine to continue the passage into the renal pelvis and urinary bladder which equals~1.5liters/day in the normally hydrated person
Blood flowing through the kidneys is first filtered (all blood constituents are filtered except blood cells and plasma proteins) ; secondly the filtrate is modified so that useful substances including most of the filtered water are quickly reabsorbed back into the blood. Thirdly the unwanted substances that escape filtration are actively secreted into the tubular lumen
Filtration, reabsorption and secretion are the renal mechanisms undertaken for various homoestatic functions
The triple filtering membrane is composed of three layers namely the capillary endothelial layer with pores of about 100 micrometers in diameter, the tubular epithelium also called podocytes which contain slits of 25 nm in width and the basement membrane separating them ; it is made of mucopolysaccharides and contains no pores
The filtration membrane allows particles about 8 nm in diameter. The total surface area of the filtering membrane is about 0.4 m2 for each kidney. The PCT is 15 mm long and 5 microns in diameter with a well defined single layered luminal epithelial brush border which reabsorbs useful substances including Na+ and water
The descending limb of the loop of Henle is 12-14 mm in length and 15 microm in diameter, lined with flat epithelial cells. Only 15% of the nephrons have long loops descending into the renal pyramids and called juxta-medullary nephrons which play a major role in the urine concentration mechanism. The ascending limb of the loop of Henle is 12 mm long, the most distal part of which becomes thicker as it joins the DCT where it comes close to the afferent arteriole of the glomerulus and forms the juxtaglomerular apparatus which plays an important role in the regulation of the renin-angiotensin-aldosterone system
The DCTs are 5 mm in diameter, lined with microvilli lacking brush border. They join the collecting ducts which are 20 mm long and lined with cuboidal epithelium with no brush border. The collecting ducts open at the renal papillae into the minor calyces. Each collecting duct serves about 4000 nephrons ; thus the total length of one nephron is about 45-65 mm
Glomerular filteration is a passive physical process which does not require energy
The glomerular capillaries are 50 times more permeable than skeletal muscle capillaries. Glomerular filteration is controlled by the capillary hydrostatic pressure, capillary permeability, renal blood flow, plasma albumin concentration, pressure in bowman’s capsule and the number of functioning glomeruli
The glomerular capillary pressure is 60 mm Hg i.e twice that in skeletal muscle capillaries. The force of this pressure tends to help filtration of fluid through the filtration membrane into Bowman’s capsular space
There is an autoregulation system for the GFR that it hardly changes with changes of hydrostatic pressure from as little as 75 mm Hg to as high as 180 mm Hg : If GFR is too slow, the glomerular filtrate will flow slowly and most of its constituents will be reabsorbed and thus the kidney will fail to excrete the unwanted waste products. If the GFR is too fast, time will not be enough for tubular cells to reabsorb the vital substances of the glomerular filtrate
GFR is autoregulated by two mechanisms, namely the afferent arteriolar vasodilator feedback mechanism and the efferent arteriolar vasoconstrictor feedback mechanism : They are local myogenic responses of the vascular smooth muscle to the distending force of the blood flow :The renal blood vessels constrict in response to increased blood flow and dilate if blood flow is reduced. The combination of the two feedback mechanisms is called tubuloglomerular feedback, and are controlled by the juxtaglomerular cells(JGCs) which secrete renin, an enzyme which splits a decapeptide called angiotensin 1 from a plasma protein, alpha-2-globulin, called angiotensinogen. Angiotensin 1 loses two amino acids in the presence of a converting enzyme to become an octapeptide called angiotensin 11 which is a potent vaso-constrictor and also stimulates the adrenal cortex to secrete aldosterone
Renin secretion by the JGCs cells is stimulated by a high rate of flow in the DCT and a low Na+ concentration in the distal tubular fluid. Renin secretion activates the angiotensin-aldosterone system which produces constriction of the afferent arterioles thereby lowering the hydrostatic pressure in the glomerular capillaries resulting in lowering of the GFR
Glomerular and other renal diseases that damage the filtration membrane results in passage of large size molecules in the filtrate
صورة

مشاركات: 11468
اشترك في: الخميس إبريل 04, 2013 10:28 pm

Re: رسالة الماجستير فى الموجات فوق الصوتية

مشاركةبواسطة دكتور كمال سيد » الأربعاء يوليو 30, 2014 5:58 pm

In severe hemorrhage there is a reduction in systemic blood pressure and renal blood flow which result in serious reduction of GFR leading to acute shutdown and complete failure of urine formation and anuria
Plasma albumin increases in dehydration resulting in reduction of the GFR ; but those with hypoalbuminaemia usually have a high GFR, e.g. renal and liver disease

Passive tubular reabsorption depends on the concentration and/or electrochemical gradient e.g anions and water follow Na+ in the PCT and also 50% of the filtered urea passively diffuse from the tubules into the peri PCT capillaries

Active tubular reabsorption is the transfer of substances against concentration or electrical gradients and requires energy expenditure or specialized transport systems in the tubular cells. All filtered glucose is actively reabsorbed in the PCT
Transport maximum for glucose(Tm) is 300 mg / min i.e > 300 mg of glucose load in diabetes mellitus (DM) exceeds the Tm and the excess will appear in urine. Renal threshold for glucose is the level of glucose in the blood above which the Tm is exceeded resulting in glucosuria. Small amounts of albumin about 30-50 mg/day escape in the glomerular filtrate but reabsorbed in the PCT

Albuminuria may occur in renal diseases which cause an increase in glomerular capillary permeability. Standing for along time results in albuminuria due to increased pressure in the renal vein. 70-75% of the filtered water and sodium is reabsorbed in the PCT; Na+ reabsorption is active against an electrochemical gradient. Na+ and water are also reabsorbed in the DCTs and collecting ducts under the influence of the hormones aldosterone and ADH respectively; this enables the kidney to maintain homeostasis by regulating the excretion of Na+ and water in urine

When the filtrate passes down the descending limb of the loop of Henle, it looses water and regains urea from the surrounding more concentrated medullary interstitium
The fluid keeps it’s urea untill it reaches the collecting ducts where water is reabsorbed under the effect of ADH , resulting in a rise in urea concentration and as a result 40-50% of it diffuses back into the medullary interstitium and the rest is lost in urine
Due to it’s low Tm, phosphate is always found in urine where it acts as a main buffering system. Its absorption is related to glucose reabsorption as their transport mechanisms compete for a common source of energy, phloridzin, which blocks glucose reabsorption and increases phosphate reabsorption. Parathyroid hormone reduces the Tm for phosphate thereby increasing it’s excretion

Tubular secretion refers to the transport of substances from the peritubular blood, interstitium or tubular cells into the tubular lumen. It is a supplement to glomerular filteration since it removes from peritubular blood those substances which escaped total elimination by filtration at the glomerulus. Ammonia, salicylic acid and quinidine are passively secreted into the lumen. Creatinine, glucuronides, PAH, penicilline, chlorothiazide and diodrast are actively secreted
K+ and H+ ions are actively secreted by the tubular cells into the lumen by a mechanism which does not seem to be Tm- limited. K+ secretion in the DCT is reciprocally associated with the reabsorption of N+, so that when N+ reabsorption increases, K+ secretion also increases by an unknown mechanism
About 65% of K+ is reabsorbed in the PCT, 25% in the loop and 10% in the DCT and collecting ducts. In the PCT and loop, K+ moves in the same direction as Na+ i.e. both Na+ and K+ are reabsorbed

The amount of K+ secreted is directly related to aldosterone secretion and to Na+ reabsorption. A small increase in serum K+ directly stimulates the adrenal cortex to release aldosterone thereby enhancing K+ secretion which stops in the absence of aldosterone but reabsorption continues
Hypokalaemia results in alkalosis due to excess H+ ion secretion instead, indicating that the same carrier system is involved
The intercalated cells in the DCT and collecting ducts balance the blood pH by secreting H+ ions into the filtrate through ATPase pumps in the luminal membrane
The principal cells of the DCT and collecting ducts perform hormonally–regulated Na+ and water reabsorption, and K+ secretion
The loops of Henle of the juxtamedullary nephrons play a key role in the concentration of urine because they are responsible for the creation and maintenance of the high osmotic pressure in the interstitial fluid of the renal medulla
The descending limb is permeable to water which will be lost into the more concentrated medullary interstitium leading to gradual concentration of the fluid passing down the descending limb and becomes hypertonic as it descends
Some Na+ and chloride go into the descending limb adding further to the rise in their concentration. In the thick portion of the ascending limb, which is impermeable to water, chloride is actively pumped out of the tubule followed passively by Na+ into the interstitial fluid resulting in a hypotonic tubular fluid as it reaches the DCT
In the same way there is a similar change in the concentration of the interstitial fluid surrounding the loop. The osmotic pressure becomes progressively higher towards the tips of the renal papillae. This process of concentration is known as the counter–current multiplier mechanism for the concentration of urine
Vasa rectae are capillary loops descending from the cortex to the medulla with similar role as the loops of Henle. In the descending capillaries water escapes into the interstitial fluid while Na+ and urea enter the lumen increasing blood osmolarity as it descends
In the ascending capillaries water is reabsorbed and very quickly removed towards the cortex, as the capillaries rejoin the cortical circulation; thus the vasa rectae remove any water reabsorbed from the DCT and collecting ducts in addition to being the only blood supply to the medulla transporting oxygen and nutrients to it, and removing C2O and waste products from it
Up to 75% of Na+ in the filtrate, is actively reabsorbed in the PCT, in addition to a further amount in the loop; and only 10% reaching the DCT where fine regulation of Na+ reabsorption occurs under the influence of aldosterone
In the absence of aldosterone, most of the remaining Na+ is lost in the urine, while large amounts of aldosterone lead to reabsorption of almost all the sodium. The amount which passes in the filtrate is about 625 gm/day of which a very large amount is reabsorbed daily by the kidney
Na+ transport is greater than that of K+, which explains the negative intracellular potential. Na+ transport in the DCT is active against a concentration gradient from the tubular cells to the peritubular fluid; this net movement of Na+ creates a negative electrical gradient which tends to draw Na+ into the cell. Active Na+ transport also results in pumping K+ into the cell
Aldosterone acts by stimulating the synthesis of mRNA which is responsible for synthesis of protein carriers or enzymes necessary for the transport of Na+. Aldosterone secretion is regulated by means of the Na+ level in the extra cellular fluid
The GFR and concentration of urea in the blood determine the excretion of urea, which is normally 40-60%. Reduced GFR leads to less urea being filtered and more urea reabsorption due to the slow flow rate.
The pH of the urine produced by the kidneys varies from 4-8 according to internal environment requirements, where the pH should be constant at 7.4. This is achieved by the ability of the renal tubules to regulate the acid-base balance through secreting acid and reabsorbing bicarbonate. Blood buffers tend to minimize changes in pH while the lungs and kidneys excrete excess acid formed during metabolism

About 85% of the filtered bicarbonate is reabsorbed in the PCT, the rest in the DCT and collecting ducts which also secrete H+ ions. A fall of urine pH to 6.0 is achieved by reabsorption of HCO3 only, but below that requires active secretion of H+ ions. HCO3 is reabsorbed together with Na+. Na+ in the tubular lumen is present in the form of sodium bicarbonate( NaHco3), disodium phosphate (Na2Po4) and sodium chloride( Nacl) and other monovalent salts
Carbonic anhydrase(CA) in the brush border enhances the conversion of carbonic acid (H2CO3) into CO2 +H2O. CO2 diffuses into the tubular cell to combine with H2O forming H2CO3 enhanced by CA. H2CO3 dissociate yielding new HCO3 which is reabsorbed and added to the blood, while the H+ ion is actively secreted into the tubular lumen and picked up by either phosphate or ammonium buffers

The Tm for HCO3 is 2.9 mmol / min or 2.8 mmol per 10 ml of filtrate, i.e. above this level, it appears in urine indicating alkalosis. Under normal conditions of GFR 125 ml / min, up to 3 mmol / min of HCO3 are filtered and almost all of it is reabsorbed
صورة

مشاركات: 11468
اشترك في: الخميس إبريل 04, 2013 10:28 pm

Re: رسالة الماجستير فى الموجات فوق الصوتية

مشاركةبواسطة دكتور كمال سيد » الأربعاء يوليو 30, 2014 6:07 pm

The rate of formation of H+ ions by tubular cells is directly related to the concentration of CO2 in the extra cellular fluid i.e. the more CO2 is formed, the more of it passes into the tubular cells, and the more H+ is secreted
The excretion of H+ by tubular cells is achieved by means of their acceptance in urine by several buffers namely the combination with HCO3 in the filtrate thus facilitating the reabsorption of filtered HCO3, the conjugation with dibasic phosphate forming monobasic phosphate ions

Since all phosphate is filtered, its quantity is limited and therefore in acidosis it will readily be utilized as a buffer. The third buffer is ammonia (NH3) formed by the tubular cells ; it combines with H+ forming ammonium( NH4); NH3 also combines with chloride forming NH4CL which is excreted in urine. In hypo-natraemia more Na+ reabsorption takes place in exchange for K+, leaving little K+ to exchange with H+, leading to acidosis. In hypokalaemia more K+ is reabsorbed and more H+ is secreted, leading to alkalosis
Hyperkalaemia results in more K+ excretion and retention of H+ with the secretion of alkaline urine leading to acidosis
NH3 is formed in the renal tubular cells from glutamine which is broken down by the enzyme glutaminase to glutamic acid and NH3. NH3 is secreted into the lumen. H+ secreted by tubular cells into the lumen combines with NH3 to form NH4 which is an important buffer because it forms a weak acid, therefore can take large quantities of H+ with little change in pH
About two thirds of the H+ secreted by the renal tubules is excreted in this form. The rate of production of NH3 is proportional to the rate of H+ formation in the renal tubular cells
The more acidic the urine is, the more NH3 is produced; and the kidney can increase its NH3 production up to 50 times when there is excessive need for excretion of H+ Secretion can take place until its concentration in tubular lumen is 900 times that in the extra cellular fluid
This is the maximum transport gradient for H+ and corresponds to a urine pH of 4.5 (limiting pH). The acid excretion by the kidney is about 20-40 meq/day

The endocrine functions of the kidney include production of renin, erythropoietin, vitamin D and prostaglandins . Erythropoietin is produced by peritubular cells in the renal cortex, and released in response to hypoxia. It stimulates the bone marrow stem cells to promote erythropoiesis. Its half–life is 5 hours thus if large amounts are produced, polycythaemia follows. Low levels of erythropoietin are found in renal damage, which accounts for the anemia associated with kidney disease e.g. CRF.

Vitamin D3(1,25-dihydroxycholecalciferol) is synthesized in the skin or taken in food in an inactive form. It is hydroxylated in the liver at the C-25 position to give 25-hydroxycholecalciferol( calcidiol) which is the major form of vitamin D in the blood but is not active to act on the gut, kidney or bone
Calcidiol is hydroxylated at the C-1 position by a specific kidney enzyme to give calcitriol (1,25-dihydroxy-cholecalciferol) which is the active form that acts on the gut to regulate calcium and phosphate absorption, on the kidney to regulate calcium and phosphate excretion and on the bone to regulate calcium mobilization and exchange with serum calcium

All these actions are achieved together with the parathyroid hormone. Prostaglandins are a group of 20-carbon unsaturated fatty acids which are rapidly metabolized particularly by the lungs. They act as local hormones due to their short half life which is about few minutes
Renal prostaglandins (PGE) are released in response to renal ischemia due to sympathetic stimulation, catecholamine release or angiotensin11 release. PGE may be involved in the regulation of renal blood flow in these conditions; and may also modify the action of ADH by reducing the sensitivity of renal tubular cells to the effect of ADH
صورة

مشاركات: 11468
اشترك في: الخميس إبريل 04, 2013 10:28 pm

Re: رسالة الماجستير فى الموجات فوق الصوتية

مشاركةبواسطة دكتور كمال سيد » الأربعاء يوليو 30, 2014 6:18 pm

CHAPTER TWO
Literature Review
contd



C- I )

CLINICAL FEATURES OF CRF


There are few physical signs of ureamia per se and include: short stature in those with CRF in childhood, increased photosensitive pigmentation which makes the patient misleadingly healthy, scratch marks due to uremic pruritus, signs of fluid overload, pericardial friction rub, flow murmurs namely mitral regurgitation due to annular calcification; aortic and pulmonary regurgitant murmurs due to volume overload, rarely there is glove and stocking peripheral sensory loss

The symptoms and signs which constitute the clinical features of the uremic syndrome are multisystem and include mainly neurological manifestations, hematological disorders, cardiovascular disorders, pulmonary disorders, gastrointestinal manifestations, bone and calcium and phosphorous disorders, skin disorders, psychological disorders, and fluid and electrolyte disorders

In the majority of patients suffering from chronic renal failure, symptoms and signs are not referred to the anatomical site of the kidneys; clinical features commonly arise from abnormalities in the chemical composition of the body or from hypertension, anemia, metabolic bone disease manifestations; the origin of these manifestations may be suspected only after detection of urinary abnormalities

In the CNS, CRF causes an unusual combination of depressed cerebral function and decreased seizure threshold. However convulsions in CRF are caused by accelerated hypertension, drug accumulation and thrombocytopenic purpura. Patients suffer from fatigue, lethargy, sleep disturbances, peripheral neuropathy including the restless leg syndrome

Anemia and bleeding tendency is a common manifestation which is due in part to platelet dysfunction and abnormal coagulation. Anemia is universal as the glomerular filtration rate falls below 25 ml/min. Several factors contribute to the anemia namely depressed production of erythropoietin leading to reduced heme synthesis resulting in reduced end-organ response to erythropoietin; shortened red cell survival due to uremic toxins; marrow space fibrosis occurs with osteitis fibrosa of secondary hyperparathyroidism resulting in decreased erythropoiesis.
Pericarditis, hypertension, congestive heart failure, coronary artery disease, and myocarditis constitute the cardiovascular manifestations. Hypertension occurs in 80-90% of those with renal insufficiency and is due to expansion of extra cellular fluid volume from the reduced ability of the kidney to excrete ingested sodium; increased activity of rennin-angiotensin system; dysfunction of the autonomic nervous system with increased sympathetic tone and insensitive baroreceptors; diminished presence of vasodilators such as prostaglandins
Patients also develop pleuritis and uremic lung
Anorexia, nausea, vomiting gastroenteritis, gastrointestinal bleeding, and peptic ulcer are the main manifestations in the gastrointestinal tract

Metabolic–endocrine disorders manifest as glucose intolerance, hyperlipidemia, hyperuricemia, malnutrition, sexual dysfunction, and infertility. Fluid and electrolyte disorders consist of hyponatremia, hyperkalemia, hypermagnesemia, metabolic acidosis, and volume expansion or depletion

Skin features of uremia include pruritus, pigmentation, easy bruising, and uremic frost

The kidneys are usually impalpable unless enlarged as a result of polycystic disease, obstruction, diabetes mellitus, amyloid, myeloma or tumours ; in addition to the physical signs of the underlying diseases which may have caused the CRF. An assessment of the central venous pressure and blood pressure are also made
صورة

مشاركات: 11468
اشترك في: الخميس إبريل 04, 2013 10:28 pm

Re: رسالة الماجستير فى الموجات فوق الصوتية

مشاركةبواسطة دكتور كمال سيد » الأربعاء يوليو 30, 2014 6:41 pm

CHAPTER TWO
Literature Review
C- I )
contd


CRF is a permanent reduction in GFR sufficient to produce detectable alterations in well-being and organ function. This usually occurs at GFR below 25ml/min
: There are four stages
Stage 1 (silent) : GFR is up to 50 ml/min
Stage11 (renal insufficiency): GRF is 25-50 ml/min
Stage111 (renal failure) : GFR 5-25 ml/min
Stage1V (end-stage renal failure): GFR less than 5ml/min

Uraemia (azotaemia) implies the manifestations of organ dysfunction seen in stages 111 & 1V
Azotemia, the accumulation of nitrogenous waste products, chiefly UREA, in the blood IS THE HALL MARK of renal failure. It is a clinical syndrome resulting from multiple factors namely Retained metabolic products, Overproduction of counter-regulatory hormones e.g. parathyroid hormone in response to hypocalcaemia and the natriuretic hormone in response to volume overload, Underproduction of renal hormones e.g. decreased erythropoietin causes anaemia and the decreased 1-hydroxylation of vitamin D3 contributes to bone disease

Anaemia is universal as GFR falls below 25ml/min ; it is due to reduced erythropoietin production, reduced red cell life span, blood loss from decreased platelet function and abnormal coagulation, marrow space fibrosis from osteitis fibrosa of secondary hyper- parathyroidism resulting in decreased erythropoiesis
Hypertension occurs in 80-90% of patients with renal insufficiency and is produced due to reduced ability to excrete ingested Na+ leads to expansion of extra cellular fluid volume; Increased activity of the renin–angiotensin system; Autonomic dysfunction occurs with insensitive baroreceptors leading to increased sympathetic tone; Decreased renal generation of prostaglandins and other vasodilators of the kallikrein–kinine system
As GFR decreases there is a slight retention of phosphorus which leads to hypocalcaemia which stimulates PTH. This causes phosphaturia till eventually the renal tubule can no longer respond to higher levels of PTH with a further decrease in phosphorus reabsorption .When this occurs hyperphosphatemia develops, hypocalcaemia becomes prominent and PTH increases to very high levels which can cause bone disease with severe osteitis fibrosa
Altered vitamin D metabolism occurs secondary to decreased renal mass or to phosphorus retention, with decreased synthesis of 1,25(OH)2 D3. Eventually these events can lead to secondary hyperparathyroidism and osteomalacia
Therefore on mangement always be in the look up for reversible factors and their correction, mainly, hypertension, urinary tract infections, urinary tract obstruction, reduced renal perfusion due to water and salt depletion in addition to cardiogenic and septic shock and hemorrhage, infections which increase urea production, and nephrotoxic medication

When plasma creatinine consistently exceeds 300 micromol/l (3.4 mg/dl), dietary protein should be restricted to 40 gm per day in adult with adequate intake of carbohydrate(250 gm) and 60 gm of fat thus providing energy value of at least 1700 kcal. Fluid restriction is necessary only when the glomerular filtration rate is less than 5 ml/min or with congestive heart failure

The excretory function of the kidney can be partially replaced by dialysis, but dialysis cannot replace the endocrine and metabolic functions of the failing kidneys which can be achieved by a successful renal transplantation
When creatinine level is consistently exceeding 600 micromol/l an arteriovenous fistula is performed in the forearm to go for hemodialysis for 4-6 hours three times weekly
,There will be gradual reduction of uremic symptoms during the first six weeks of dialysis,
[color=#BF0000] but plasma creatinine and blood urea do not return to normal
صورة

مشاركات: 11468
اشترك في: الخميس إبريل 04, 2013 10:28 pm

Re: رسالة الماجستير فى الموجات فوق الصوتية

مشاركةبواسطة دكتور كمال سيد » الأربعاء يوليو 30, 2014 7:44 pm

C- II)

NORMAL RENAL SONOGRAPHY AND TECHNIQUE


Sonography is used primarily for anatomy, the IVU,CT for anatomy and function and nuclear medicine for function
Evaluating kidneys with U/S is a non-invasive approach. It delineates retroperitoneal masses or fluid collections such as haematomas or abscesses. It rules out hydronephrosis in those with renal failure since U/S is supreme in showing fluid filled structures. It determines the renal size and parenchymal detail, detects hydroureter, and images renal congenital abnormalities

Patients are given nothing by mouth except water to fill the bladder before examination. If over hydrated, the internal collecting system will become also distended. If dehydrated, the infundibula and renal pelvis will be collapsed

The examination begins with the patient in the supine or decubitus position.. Scans are performed in the sagittal and transverse planes from the anterior approach using the liver and spleen as acoustic windows for the right and left kidneys respectively
Scanning is always done in deep suspended inspiration.. Start with a longitudinal scan over the right upper abdomen and then follow with a transverse scan
Next, rotate the patient to the left lateral decubitus position, to visualize the right kidney in this coronal view
To visualize the left kidney, scan in the left upper abdomen in a similar sequence. If the left kidney cannot be seen (usually due to excess bowl gas), try the right decubitus position
Bowl gas can also be displaced by drinking 3-4 glasses of water
The left kidney can then be visualized through the fluid-filled stomach with the patient in the supine position
If the kidneys have not been imaged adequately, scan through the lower intercostal spaces : Turn the patient prone and apply enough gel to the left and right renal areas and perform longitudinal and transverse scans
Both kidneys can be also examined with the patient sitting or standing erect
When examining any part of renal area, compare both kidneys in different projections. Variations in size, contour and internal echogenicity may indicate an abnormality

For adults use a 3.5MHz transducer, for children and thin adults use a 5.0 MHz transducer. Start by placing the transducer over the right upper abdomen, then angle the beam as necessary and adjust the time gain compensation (TGC) with adequate sensitivity settings to allow uniform acoustic pattern, thus obtaining the best image of renal parenchyma
Gain is the amplification of the reflected U/S waves by the U/S unit. The “ near gain” control amplifies echoes returning from tissues above the focal point of the beam, while the “far gain” control amplifies echoes returning from beyond the focal point of the beam i.e. echoes coming from deeper tissues need more amplification. These controls can be adjusted to allow proper comparison of echogenicity at different levels
Renal detail may be obscured if there is a significant amount of perirenal fat, hepatocellular disease, gall stones, rib interference or other abdominal masses or collections between the liver and kidney. When scanning it is better to identify : the renal capsule, the cortex, macula, sinus, ureters, renal arteries and veins
The kidneys are imaged by U/S as organs with smooth outer contours surrounded by highly echogenic peri-renal fat. The renal capsule appears as a bright, Smooth, echogenic line surrounding the renal cortex which is homogeneous with smooth contour. Its echogenicity is moderate (mid to low-level echoes) in an even texture that is less echogenic than normal liver or spleen but more echogenic than the adjacent renal medullary pyramids. The renal medulla contains the pyramids which appear as triangular or blunted hypo-echoic to anechoic areas (it should not be mistaken for renal cysts or tumors ).
(Fig 9)
صورة
the normal left kidney in longitudinal axis

صورة
the normal
left kidney in transverse axis
صورة

مشاركات: 11468
اشترك في: الخميس إبريل 04, 2013 10:28 pm

Re: رسالة الماجستير فى الموجات فوق الصوتية

مشاركةبواسطة دكتور كمال سيد » الخميس يوليو 31, 2014 6:23 pm

C 11)
contd


The renal columns(septal cortex or the columns of Bertin) are projections of cortex that extend between the pyramids. They are sonographically identical to the peripheral cortex. It is easier to visualize the pyramids in children and young adults
The central echo complex (the renal sinus) is imaged as a very highly hyperechoic(very echogenic) area normally occupying about one third of the kidney and includes the collecting system (pelvis and calyces), fat, and vessels. It is the innermost part of the kidney and has the greatest echogenicity due to the fat deposition. The sinus is surrounded by the renal parenchyma (the area from renal sinus to outer renal surface whose thickness is 11-18 mm in males and 11-16 mm in the female

The pelvis is not visualized unless urine filled when it appears unechoic. It is scanned through the renal sinus in an anterior transverse view

The renal arteries and veins are best seen at the hilus. They enter the kidney at different levels and may be multiple
The right renal vein extends from the central renal sinus directly into the IVC. Both vessels appear as tubular structures in the transverse plane

The arcuate vessels are demonstrated as intense specular echoes in cross section or oblique section at the corticomedullary junction

The renal arteries are best seen in supine and lateral decubitus views. The right renal artery can be seen in a longitudinal scan as a circular structure posterior to the inferior vena cava
The renal arteries have an echo –free central lumen with highly echogenic borders that consist of the vessel wall and the surrounding retroperitoneal fat and connective tissue. They lie posterior to the veins and can be demonstrated with certainty if their junction with the aorta is seen. The left renal artery flows from the posterolateral wall of the aorta to the central renal sinus

An extra-renal pelvis may be seen as a fluid-filled structure medial to the kidney on transverse scans. Differentiation of the normal variant from obstruction is made by noting the absence of intra-sinus distension of the renal pelvis and infundibula

Dilatation of the collecting system has also been noted in pregnancy (the right kidney is generally involved with mild degree of hydronephrosis which reverts to normal after delivery
Normally in the non-hydrated subject, the renal pelvis is collapsed and therefore not demonstrated on the scan, the renal pelvis is influenced by bladder distension, diuretics and the state of hydration. Distension of the renal pelvis is seen in 50% of non hydrated and in 90% of hydrated subjects examined with a full bladder
The normal renal pelvis in the hydrated patients is between 2-14 mm. If two separate collections of renal sinus fat are identified, a double collecting system should be suspected
Ability to visualize the kidney does not mean that it is functioning. To assess renal function, use contrast urography, a radionuclide study or laboratory tests..

Injury to a kidney may result in temporary loss of function
صورة

مشاركات: 11468
اشترك في: الخميس إبريل 04, 2013 10:28 pm

Re: رسالة الماجستير فى الموجات فوق الصوتية

مشاركةبواسطة دكتور كمال سيد » الخميس يوليو 31, 2014 6:37 pm

C11 )
contd


Normal ureters are not always seen. They should be sought where they leave the kidney at the hilus. They may be multiple and are often seen in the coronal projection

Generally, echogenicity from higher to decreasing order is : renal sinus, spleen, liver
renal cortex, renal medulla.

In adult, the thickness of the renal parenchyma decrease at about 10% per decade after 20 years of age
The corticomedullary ratio is 1:1.6 up to 30 years old ; 1:1.2 up to 50 years old ; I:1 above 50 years old with thinning of cortex with age. The overall size decreases with age and only apparent in the elderly

The fetal kidney size in cm equals the gestational age in weeks plus or minus 3 mm. Infantile kidneys are large compared to overall body size (typically 4- 5 cm long at
birth) and may be imaged from 12- 14 weeks onwards but clearly seen after 16 weeks
In transverse section they appear hypoechogenic, circular structures on either side of the spine
; Within them can be seen the strongly echogenic renal pelvis
the capsule is also echogenic
The renal papillae are hypoechogenic and can appear large. Some dilatation of the renal pelvis (less than 5mm) may sometimes be seen but is a normal finding

It is important to assess renal size by comparing the renal circumference with the abdominal circumference, the normal ratio being 0.27- 0.3
The fetal urinary bladder can be recognized as a small ovoid cystic structure within the fetal pelvis as early as 14- 15 weeks. The normal urinary production at 22 weeks is 2 ml per hour, whereas at full term it is 26 ml per hour. Until the age of 6 month
neonatal kidneys differ acoustically from adult kidneys in that : the difference between cortex and medulla is less marked in the infant; pyramids are relatively hypoechogenic and may resemble cysts; cortex is less echogenic than liver parenchyma
for the first 3 years of life Its pyramids appear large because the cortex is relatively thin and hyperechoic. During the first year of life the cortex gradually develops to assume the adult corticomedullary proportions
The pediatric renal sinus is poorly echogenic because it contains little fat

Fat deposition and accumulation occurs gradually to achieve adult proportions by about age 10 years. The majority of infants have a slight separation of the central echo complex, reflecting the presence of a small amount of urine of unknown cause

There is no absolute measurement to separate normal distension from hydronephrosis; 10 mm separation is considered the upper limit of normal
Unlike in adult practice, detection of children with vesicoureteric reflux is important and may only be reflected by minor separation of the central sinus echoes without renal scarring

: Normal renal length of the pediatric kidney is determined using this guide
; (Renal length (over one year) in cm = 6.79 + (0.22 x age in years)
(in those less than one year = 4.98 + (0.155 x age in months
Asymmetry in renal lengths exceeding 5mm in infants and 10 mm in older children should raise the suspicion of an underlying problem even if both kidneys are within the normal range
صورة

السابقالتالي

العودة إلى ULTRASOUND الموجات فوق الصوتية

الموجودون الآن

المستخدمون المتصفحون لهذا المنتدى: لا يوجد أعضاء مسجلين متصلين و 2 زائر/زوار

cron