pediagenosis: Urinary
Article Update
Loading...
Showing posts with label Urinary. Show all posts
Showing posts with label Urinary. Show all posts

Tuesday, April 27, 2021

POSTERIOR URETHRAL VALVES

POSTERIOR URETHRAL VALVES


POSTERIOR URETHRAL VALVES
Posterior urethral valves (PUVs) are abnormal mucosal folds in the distal urethra that arise during fetal development and interfere with the normal outflow of urine. They are the most common cause of congenital urinary tract obstruction, occurring in 1 in 8000 to 1 in 25,000 live births, and are seen only in males. Even if treated early on, the obstruction associated with PUVs frequently causes severe, often permanent urinary tract abnormalities.
The traditional classification system describes two major types of valves, which vary both in morphology and relative frequency. Type I valves, said to account for more than 95% of cases, begin as a mucosal ridge from the seminal colliculus, which extends distally and divides into two flaps that fuse with the walls of the membranous urethra. There is typically incomplete fusion of the flaps with the anterior wall of the urethra, and there is a small opening in the membrane near the posterior wall of the urethra, adjacent to the seminal colliculus. Type III valves, in contrast, are said to account for about 5% of cases and resemble disklike membranes that span the entire circumference of the membranous urethra and contain a small central opening. (Type II valves, extending from the seminal colliculus toward the bladder neck, are no longer thought to be actual valves but rather bladder neck hypertrophy, which accompanies any distal urethral obstruction.) More recent work, however, suggests that in fact all PUVs are membranous, originally resembling type III valves, and that type I valves are actually an artifact of urethral instrumentation, which divides the single membrane into two flaps.

GROSS APPEARANCE OF POSTERIOR URETHRAL VALVES

Pathogenesis
The male urethra is divided into four portions, the precursors of which become evident early in development. The segments include the prostatic urethra, which extends from the bladder neck to the urogenital diaphragm; the membranous urethra, which traverses the diaphragm; the bulbous urethra, which extends from the urogenital diaphragm to the penoscrotal junction; and the spongy (penile) urethra, which continues through the penile shaft until the urethral meatus.
BASIC FUNCTIONS AND HOMEOSTASIS

BASIC FUNCTIONS AND HOMEOSTASIS


BASIC FUNCTIONS AND HOMEOSTASIS
Blood enters the kidneys in a series of branching vessels that give rise to afferent arterioles. Each afferent arteriole leads to a tuft of glomerular capillaries. Plasma and small, non–protein bound solutes are filtered across the walls of the glomerular capillaries into Bowman’s space, the initial portion of the nephron. From there, the filtrate is conveyed through the remaining segments of the nephron which include the proximal tubule, thin limb, distal tubule, and collecting duct before being excreted in the final urine.
In the various segments of the renal tubules, there is extensive exchange of material with the surrounding capillaries. Such exchange is known as “reabsorption” if materials are transferred from the tubular lumen to the capillaries and/or interstitium, and as “secretion” if they are transferred in the opposite direction.
By continuously adjusting the contents of blood, the kidneys make critical contributions to the maintenance of fluid and salt homeostasis, as well as to the excretion of unwanted chemicals and waste products. In addition, the kidneys contribute to the regulation of arterial pressure, acid-base status, erythropoiesis, and vitamin D synthesis.

BASIC FUNCTIONS AND HOMEOSTASIS


Mechanisms Of Homeostasis
To maintain homeostasis, the kidneys must adjust their retention or excretion of fluid and filtered solutes so that, in cooperation with other excretory organs (lungs, skin, bowel), overall output equals intake.
RENAL HANDLING OF SODIUM AND CHLORIDE

RENAL HANDLING OF SODIUM AND CHLORIDE


RENAL HANDLING OF SODIUM AND CHLORIDE
Sodium and chloride are both predominantly extracellular ions. In plasma, the sodium concentration is maintained between 135 to 145 mmol/L, whereas the chloride concentration is maintained between 98 to 108 mmol/L.
Both sodium and chloride are freely filtered at the glomerulus and almost completely (approximately 99%) reabsorbed. 60% of the filtered load is reabsorbed in the proximal tubule; 30% is reabsorbed in the thick ascending limb; 7% is reabsorbed in the distal convoluted tubule; and 2% to 3% is reabsorbed in the connecting tubule and collecting duct.
 
NEPHRON SITES OF SODIUM REABSORPTION
NEPHRON SITES OF SODIUM REABSORPTION

Mechanisms Of Transport
In all portions of the nephron, basolateral Na+/K+ ATPases pump sodium from the tubular epithelial cells into the interstitium. As a result, intracellular sodium concentrations remain low, establishing a gradient for transcellular reabsorption.

Tuesday, April 13, 2021

RENAL HANDLING OF POTASSIUM

RENAL HANDLING OF POTASSIUM


RENAL HANDLING OF POTASSIUM
Potassium is a primarily intracellular ion, with skeletal muscle alone containing more than 75% of the body’s total load. Less than 2% of this load is found in the extracellular fluid. The normal plasma concentration is between 3.5 and 5.0 mmol/L.
Extracellular potassium is freely filtered at the glomerulus. A large fraction of the filtered load is consistently reabsorbed along the proximal tubule (66%) and loop of Henle (25%). In the distal tubule, however, there is a variable degree of reabsorption or secretion that depends on input from homeostatic feedback mechanisms. In this manner, the kidneys make a crucial contribution to plasma potassium concentration.
RENAL HANDLING OF POTASSIUM

Transport Mechanisms
Proximal Tubule. In the proximal tubule, potassium is reabsorbed along a paracellular route. A chemical gradient is established as the reabsorption of sodium and water concentrates potassium in the tubular fluid. An electrical gradient is established as chloride is reabsorbed, which leaves a positive charge in the late part of the proximal tubule. There is some evidence that potassium also undergoes some transcellular reabsorption in this segment, but the details and relative importance of this pathway remain unknown.

Monday, April 12, 2021

RENAL HANDLING OF CALCIUM, PHOSPHATE, AND MAGNESIUM

RENAL HANDLING OF CALCIUM, PHOSPHATE, AND MAGNESIUM


RENAL HANDLING OF CALCIUM, PHOSPHATE, AND MAGNESIUM
Calcium
More than 98% of total body calcium is in bones, whereas the remainder is located in intracellular and extracellular fluid. Normal plasma concentrations, which range from 8.8 to 10.3 mg/dL, are maintained by the actions of PTH, 1,25-hydroxy vitamin D, and calcitonin on bones, the gastrointestinal tract, and the kidneys.
About half of the extracellular calcium load is in an active, ionized form, whereas the remainder complexes with albumin and other anions. The ionized calcium is freely filtered at the glomerulus, and normally almost all of it is reabsorbed.
In the proximal tubule, 50% to 60% of the filtered load is reabsorbed along a paracellular route. A chemical gradient is established as sodium and water are reabsorbed, concentrating calcium in the tubular fluid. Meanwhile, an electrical gradient is established by the paracellular reabsorption of chloride, which leaves a positive charge in the lumen. Specialized tight junction proteins, such as claudin-2, may form a cation-specific paracellular pathway.
In the thick ascending limb, 15% of the filtered load is reabsorbed along a paracellular route. An electrical gradient, formed secondary to K+ recycling, drives this process. Claudin-16, another tight junction protein, is an important component of this paracellular pathway, and mutations are associated with familial hypomagnesemia with hypocalciuria.
In the distal convoluted and connecting tubules, 10% to 15% of the filtered load is reabsorbed along a transcellular route. Calcium crosses the apical membrane through TRPV5 channels, binds to calbindin, then exits the basolateral membrane on the NCX1 Na+/Ca2+ exchanger and, to a lesser degree, a Ca2+ ATPase (PMCA).
The collecting duct makes an unknown, but likely minor, contribution to calcium reabsorption.
Hypocalcemia triggers release of PTH, which has numerous effects on renal function. In the proximal tubule, it inhibits the NHE-3 Na+/H+ exchanger, reducing the gradient for paracellular calcium reabsorption. (This seemingly paradoxical effect allows PTH to increase phosphate excretion, as discussed later.) In the distal nephron, however, it up-regulates the apical TRPV5 calcium channel, causing a net increase in calcium reabsorption. Meanwhile, hypercalcemia both suppresses PTH release and directly inhibits calcium reabsorption. In the thick ascending limb, for example, the increased load of reabsorbed calcium activates a basolateral calcium-sensing receptor (CaSR), which then inhibits NKCC2 transporters and ROM-K channels, reducing the electrical gradient for calcium reabsorption.
Finally, acidosis inhibits the TRPV5 calcium channel, whereas alkalosis has the opposite effect.
RENAL HANDLING OF CALCIUM AND PHOSPHATE
RENAL HANDLING OF CALCIUM AND PHOSPHATE

Phosphate
About 85% of total body phosphate is stored in bones, 14% in soft tissues, and 1% in extracellular fluid. Normal plasma concentrations, which range from 3 to 4.5 mg/dL, are maintained by the actions of PTH, 1,25-hydroxyvitamin D, and phosphatonins on the parathyroid glands, bones, gastrointestinal tract, and kidneys.
COUNTERCURRENT MULTIPLICATION

COUNTERCURRENT MULTIPLICATION


COUNTERCURRENT MULTIPLICATION
The countercurrent multiplier system is a sophisticated apparatus that evolved in mammals and birds to con-serve water. It forms a longitudinal concentration gradient in the medullary interstitium that increases in strength toward the papilla. This gradient is crucial for water reabsorption from the renal tubules, which is a passive process that depends on osmotic pressure from the interstitium.

MODEL OF THE COUNTERCURRENT MULTIPLIER: PART I
MODEL OF THE COUNTERCURRENT MULTIPLIER: PART I

The creation and maintenance of this gradient is best understood by first considering a simplified model of the loop of Henle. In this model, a tube of fluid is divided by a membrane in all but its most inferior aspect. The left side represents the entire descending limb, whereas the right side represents the entire ascending limb. Fluid enters at the top of the left-sided column, travels beneath the membrane, and then exits at the top of the right-sided column. The dividing membrane is impermeable to water but contains active transporters, which pump solute from the ascending limb to the descending limb. These transporters are powerful enough to establish a transmembrane gradient of about 200 milliosmoles (mOsm).
URINE CONCENTRATION AND DILUTION AND OVERVIEW OF WATER HANDLING

URINE CONCENTRATION AND DILUTION AND OVERVIEW OF WATER HANDLING


URINE CONCENTRATION AND DILUTION AND OVERVIEW OF WATER HANDLING
In normal kidneys more than 180 liters of fluid are filtered into the nephrons each day, but nearly all of it is reabsorbed into the peritubular circulation.
Tight junctions form a watertight seal between tubular epithelial cells throughout most of the nephron. Thus, water reabsorption occurs primarily through a transcellular route, requiring specialized channels known as aquaporins (AQPs) in both the apical and basolateral compartments of the plasma membrane.
URINE CONCENTRATION AND DILUTION AND OVERVIEW OF WATER HANDLING

Because aquaporins are channels, and not pumps, the reabsorption of water is a passive process, dependent on osmotic pressure from solutes concentrated in the sur-rounding interstitium.
ANTIDIURETIC HORMONE

ANTIDIURETIC HORMONE


ANTIDIURETIC HORMONE
ADH, also known as vasopressin, plays a crucial role in maintaining the normal osmolality of extracellular fluid, which depends primarily on the extracellular sodium concentration. ADH exerts its effect by altering the osmolality of excreted urine, which can range from 50 to 1200 mOsm/kg H2O.
When plasma osmolality increases, ADH release causes extensive water reabsorption in the distal nephron. As a result, the urine becomes highly concentrated, and the plasma consequently becomes more dilute. In contrast, when plasma osmolality decreases, inhibition of ADH release prevents water reabsorption in the distal nephron, leading to dilution of urine and concentration of plasma.
 
MECHANISM OF ANTIDIURETIC HORMONE IN REGULATING URINE VOLUME AND CONCENTRATION
MECHANISM OF ANTIDIURETIC HORMONE IN REGULATING URINE VOLUME AND CONCENTRATION
MECHANISMS OF RELEASE
ADH is produced in the supraoptic and paraventricular nuclei of the hypothalamus. It is then conveyed along axons to the posterior pituitary for storage and release. ADH release occurs primarily in response to activation of osmoreceptors in the anterior hypothalamus. These receptors, located outside of the blood-brain barrier, are extremely sensitive to changes in plasma osmolality. Their activation has been hypothesized to occur when there is a loss of intracellular fluid secondary to increased extracellular osmotic pressure. In support of this hypothesis, the osmoreceptors are not equally sensitive to all solutes. Sodium, for example, reliably activates osmoreceptors at high concentrations because, as a predominantly extracellular ion, it establishes a transmembrane osmotic gradient. In contrast, urea and glucose generally do not activate osmoreceptors even at high concentrations because they freely enter cells, thus failing to establish an osmotic gradient. When patients experience extreme insulin depletion, however, osmoreceptors may become sensitive to high concentrations of glucose, presumably because of its increased restriction to the extracellular space.

Anatomy Physiology

[AnatomyPhysiology][recentbylabel2]

Featured

[Featured][recentbylabel2]
Notification
This is just an example, you can fill it later with your own note.
Done