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Ureter Anatomy
Gross Anatomy
Abdominal ureter
The ureter is roughly 25 - 30 cm long in adults and courses down the
retroperitoneum in an S curve. At the proximal end of the ureter is the renal
pelvis at the distal end is the bladder. The ureter begins at the level of the renal
artery and vein posterior to these structures. This uretero-pelvic junction
usually coincides with the second lumbar vertebra on the left, with the right
being marginally lower.
The ureter then continues anteriorly on the psoas major muscle, crossing under the
gonadal vein at the level of the inferior pole of the kidney. . Here, the ureter lies
anteriorly and slightly medial to the tips of the L2-L5 transverse processes.
It enters the pelvis anteriorly to the sacroiliac joint at the bifurcation of the
common iliac vessels (at the pelvic brim) and then courses anteriorly to
the internal iliac artery down the lateral pelvic sidewall. The colon and its
mesentery are associated anterior to the ureters. Specifically, the cecum,
appendix, and ascending colon lie over the right ureter, and the descending and
sigmoid colon lie over the left ureter.
Pelvic ureter The ureter enters the pelvis, where it crosses anteriorly to the iliac
vessels, which usually occurs at the bifurcation of the common iliac artery into the
internal and external iliac arteries. Here, the ureters are within 5 cm of one
another before they diverge laterally.
The ovarian vessels travel in the suspensory ligament of the ovary
(infundibulopelvic ligament) and cross the ureter anteriorly and lateral to the iliac
vessels. The ureters then course out to the ischial spines before coursing medially
to penetrate the base of the bladder. The anteromedial surface of the ureter is
covered by peritoneum, and the ductus deferens runs anteriorly. It travels with the
inferior vesical neurovascular pedicle into the bladder. In females, the ureter runs
posterior to the ovary and then deep to the broad ligament and through the
cardinal ligament. The uterine artery crosses anteriorly in the rectouterine fold of
peritoneum.
At the level of the ischial spine it
turns forward and medially to enter the posterolateral wall of the bladder, where it
runs an oblique 1-2cm course, before opening into the bladder at the internal
ureteric orifice 1-2.
ureter joins the renal lymphatics to the lumbar nodes. The middle ureter drains to
the common and internal iliac
nodes. The lymphatic vessels of the pelvic ureter drain to the internal iliac and
vesical nodes.
Innervation
The ureter has an intrinsic pacemaker that governs peristalsis but also has
autonomic inputs. Thoracolumbar
preganglionic inputs synapse with aorticorenal and inferior and superior
hypogastric sympathetic plexuses before
innervating the ureter. Parasympathetic inputs derive from the S2-S4
segments. Mucosal irritation and luminal distention stimulate nociceptors whose
afferents travel with sympathetic nerves and confer the visceraltype referred pain
that results in the manifestations of ureteral colic. Pain or hyperesthesia may be
sensed from the region of the ipsilateral ribs down to the scrotum or labia.
Clinical corollaries
Close association of the abdominopelvic viscera places the ureter at risk for
inflammatory, infectious, or malignant
processes of the colon, appendix, oviducts, or ovaries. This may manifest as
hematuria, pyuria, fistula, or
obstruction. The mass effect of constipation, gravid uterus, or ovarian cysts may
obstruct the ureter. The aorta and iliac vessels may exert deleterious effects on the
ureter by mass effect or fibrotic reaction from the vasculopathy itself or by
complications of the surgical management of aortoiliac disease.
The ureter has 3 physiologic narrowings: (1) the ureteropelvic junction, (2) the
crossing over the iliac vessels, and (3)the ureterovesical junction. This is crucial in
the manifestations of calculus disease. These narrowings may result in ureteral
stones becoming trapped and obstructing at these specific levels. These
narrowings may also limit retrograde instrumentation performed for diagnostic or
therapeutic purposes.
The close association of the ovarian vessels at the level of the pelvic brim and the
uterine artery in the rectouterine fold render the ureter subject to injury during
oophorectomy or hysterectomy, as they are just deep to the crucial vasculature
(see the following image).
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Relations
The relations of the ureter are somewhat complex due to the differences between the left and
right sides of the abdominal cavity and differences between male and female pelvic viscera.
Abdominal ureter
Following the course of the ureter from superior to inferior
1-
posteriorly: psoas
muscle; genitofemoral nerve; common
iliac vessels; tips of L2-L5 transverse
processes
anteriorly
laterally
right ureter: IVC
Pelvic ureter
inferiorly
anteriorly
laterally
o
female: cervix
Constrictions
The ureter has a diameter of 3mm 1 but there are three constrictions, which are the most
common sites of renal calculus obstruction:
at the pelvi-ureteric junction (PUJ) of the renal pelvis and the ureter
as the ureter enters the pelvis and cross over the common iliac arterybifurcation
at the vesicoureteric junction (VUJ) as the ureter enters the bladder wall
Blood supply
arterial supply: from branches of the renal artery, abdominal aorta, superior and
inferior vesical arteries
o
some texts also include supply from the gonadal, middle rectal and uterine
arteries 1-2
1-2
Lymphatic supply
Nerve supply
Histology
The ureteric wall is composed of three layers (from outside to inside): adventitia, smooth
muscle and transitional cell epithelium 1.
Variant anatomy
bifid ureter
ectopic ureter
ureterocoele
Persistent albuminuria (>300 mg/d or >200 g/min) that is confirmed on at least 2 occasions 3-6 months apart
Progressive decline in the glomerular filtration rate (GFR)
Elevated arterial blood pressure
Three major histologic changes occur in the glomeruli of persons with diabetic nephropathy. First, mesangial expansion
is directly induced by hyperglycemia, perhaps via increased matrix production or glycosylation of matrix proteins.
Second, thickening of the glomerular basement membrane (GBM) occurs. Third, glomerular sclerosis is caused
by intraglomerular hypertension (induced by dilatation of the afferent renal artery or from ischemic injury induced by
hyaline narrowing of the vessels supplying the glomeruli). These different histologic patterns appear to have similar
prognostic significance.
The key change in diabetic glomerulopathy is augmentation of extracellular matrix. The earliest morphologic abnormality in
diabetic nephropathy is the thickening of the GBM and expansion of the mesangium due to accumulation of extracellular
matrix.
pH. The kidneys monitor and regulate the levels of hydrogen ions (H+) and bicarbonate
ions in the blood to control blood pH. H+ ions are produced as a natural byproduct of the
metabolism of dietary proteins and accumulate in the blood over time. The kidneys excrete excess
H+ ions into urine for elimination from the body. The kidneys also conserve bicarbonate ions,
which act as important pH buffers in the blood.
Osmolarity. The cells of the body need to grow in an isotonic environment in order to
maintain their fluid and electrolyte balance. The kidneys maintain the bodys osmotic balance by
controlling the amount of water that is filtered out of the blood and excreted into urine. When a
person consumes a large amount of water, the kidneys reduce their reabsorption of water to allow
the excess water to be excreted in urine. This results in the production of dilute, watery urine. In
the case of the body being dehydrated, the kidneys reabsorb as much water as possible back into
the blood to produce highly concentrated urine full of excreted ions and wastes. The changes in
excretion of water are controlled by antidiuretic hormone (ADH). ADH is produced in
the hypothalamus and released by the posterior pituitary gland to help the body retain water.
Blood Pressure. The kidneys monitor the bodys blood pressure to help maintain
homeostasis. When blood pressure is elevated, the kidneys can help to reduce blood pressure by
reducing the volume of blood in the body. The kidneys are able to reduce blood volume by
reducing the reabsorption of water into the blood and producing watery, dilute urine. When blood
pressure becomes too low, the kidneys can produce the enzyme renin to constrict blood vessels
and produce concentrated urine, which allows more water to remain in the blood.
Filtration
Inside each kidney are around a million tiny structures called nephrons. The nephron is the
functional unit of the kidney that filters blood to produce urine. Arterioles in the kidneys deliver
blood to a bundle of capillaries surrounded by a capsule called aglomerulus. As blood flows
through the glomerulus, much of the bloods plasma is pushed out of the capillaries and into the
capsule, leaving the blood cells and a small amount of plasma to continue flowing through the
capillaries. The liquid filtrate in the capsule flows through a series of tubules lined with filtering
cells and surrounded by capillaries. The cells surrounding the tubules selectively absorb water and
substances from the filtrate in the tubule and return it to the blood in the capillaries. At the same
time, waste products present in the blood are secreted into the filtrate. By the end of this process,
the filtrate in the tubule has become urine containing only water, waste products, and excess ions.
The blood exiting the capillaries has reabsorbed all of the nutrients along with most of the water
and ions that the body needs to function.
Production of Hormones
The kidneys produce and interact with several hormones that are involved in the control of
systems outside of the urinary system.
Calcitriol. Calcitriol is the active form of vitamin D in the human body. It is produced by the
kidneys from precursor molecules produced by UV radiation striking the skin. Calcitriol works
together with parathyroid hormone (PTH) to raise the level of calcium ions in the bloodstream.
When the level of calcium ions in the blood drops below a threshold level, the parathyroid
glands release PTH, which in turn stimulates the kidneys to release calcitriol. Calcitriol promotes
the small intestineto absorb calcium from food and deposit it into the bloodstream. It also
stimulates the osteoclasts of the skeletal system to break down bone matrix to release calcium
ions into the blood.
Renin. Renin is not a hormone itself, but an enzyme that the kidneys produce to start the
renin-angiotensin system (RAS). The RAS increases blood volume and blood pressure in response
to low blood pressure, blood loss, or dehydration. Renin is released into the blood where it
catalyzes angiotensinogen from the liver into angiotensin I. Angiotensin I is further catalyzed by
another enzyme into Angiotensin II.
Angiotensin II stimulates several processes, including stimulating the adrenal cortex to produce
the hormone aldosterone. Aldosterone then changes the function of the kidneys to increase the
reabsorption of water and sodium ions into the blood, increasing blood volume and raising blood
pressure. Negative feedback from increased blood pressure finally turns off the RAS to maintain
healthy blood pressure levels.