Obstructive uropathy refers to any obstruction in the urinary tract. It can cause changes including hydronephrosis (distension of the kidneys and ureters) and hydroureteronephrosis (distension of the kidneys, ureters and bladder). The document discusses the classification, causes, pathology, investigations and management of various types of obstructive uropathy including ureteric strictures and retroperitoneal fibrosis. Surgical intervention is often needed to relieve the obstruction and treat associated complications.
Please find the power point on Urinary Tract Injury (Kidney Injury). I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
POSTERIOR URETHRAL VALVES- Pediatric Surgery
• Dear viewers,
• Greetings from “ Surgical Educator”
• Today I have uploaded one more video in Pediatric Surgery/Pediatric Urology- “ Posterior Urethral Valves”
• Posterior Urethral Valves is the congenital cause for Bladder Outlet Obstruction, resulting in abnormal development of the kidneys as well as the bladder.
• In this video, I talked about the learning outcomes, introduction, etiopathogenesis, clinical features, investigations, differential diagnosis, treatment, follow-up and prognosis of “ Posterior Urethral Valves”
• I hope you will enjoy the video for its educational value.
• You can watch all my teaching videos in the following links
• surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
• Thank you for watching the video.
blockage or problem in the urinary tract can mean urine is unable to drain from the kidneys or is able to flow the wrong way up into the kidneys. This can lead to a build-up of urine in the kidneys, causing them to become stretched and swollen.
Dr Ho Siew Hong shared his experience on how to perform the ideal puncture for PCNL in a lecture to Asian urologists during the Advanced Urology Course 2008 in Singapore
genitourinary tb - contains radiological findings of genitourinary tuberculosis including ivp,, hsg, usg and ct findings in kidney, ureter, urinary bladder, uterus and prostate
Please find the power point on Urinary Tract Injury (Kidney Injury). I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
POSTERIOR URETHRAL VALVES- Pediatric Surgery
• Dear viewers,
• Greetings from “ Surgical Educator”
• Today I have uploaded one more video in Pediatric Surgery/Pediatric Urology- “ Posterior Urethral Valves”
• Posterior Urethral Valves is the congenital cause for Bladder Outlet Obstruction, resulting in abnormal development of the kidneys as well as the bladder.
• In this video, I talked about the learning outcomes, introduction, etiopathogenesis, clinical features, investigations, differential diagnosis, treatment, follow-up and prognosis of “ Posterior Urethral Valves”
• I hope you will enjoy the video for its educational value.
• You can watch all my teaching videos in the following links
• surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
• Thank you for watching the video.
blockage or problem in the urinary tract can mean urine is unable to drain from the kidneys or is able to flow the wrong way up into the kidneys. This can lead to a build-up of urine in the kidneys, causing them to become stretched and swollen.
Dr Ho Siew Hong shared his experience on how to perform the ideal puncture for PCNL in a lecture to Asian urologists during the Advanced Urology Course 2008 in Singapore
genitourinary tb - contains radiological findings of genitourinary tuberculosis including ivp,, hsg, usg and ct findings in kidney, ureter, urinary bladder, uterus and prostate
Presentation delivered at a paediatric clinical meeting of the Federal Medical Center, Lokoja. Nigeria
This presentation doesn't serve as a substitute for texts and/or journals.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
3. Classification
Obstruction can be divided according to:
Acute or chronic obstruction
Partial or complete obstruction
Unilateral or bilateral obstruction
Congenital or acquired obstruction
Extrinsic or intrinsic obstruction
Etiological (according to the cause of obstruction)
4. Etiological
(according to the level of obstruction)
Renal causes
1. Kidney stones
2. Congenital PUJO
3. Aberrant renal vessels
4. Renal pelvic tumors
5. Tuberculous stricture
Ureteric causes
1. In the lumen, e.g., stones and blood clots
2. In the wall
1. Congenital atresia and ureterocele
2. Ureteric stricture
3. Tumors (intrinsic or extrinsic)
3. Outside the lumen (compression)
1. Infiltration by carcinoma of the cervix, colon, or rectum
2. Idiopathic retroperitoneal fibrosis
(1)(2)
(3)
6. Pathology
Urethra
Increased hydrostatic pressure leads to urethral dilatation above
the obstruction
Urinary bladder
Early, (Compensated Phase): Hypertrophy of the detrusor
muscle --- bladder Trabeculation --- Saccules (mucosa
protrudes between muscle fibers) --- Diverticulae develop when
mucosa bulges outside bladder wall
Later, (Decompensated Phase): the bladder dilates more and
its wall thins out --- Atony of the bladder --- Urinary retention
Ureter
Early there is muscular hypertrophy of the wall, later atony occurs.
The ureter becomes dilated (hydroureter), elongated and tortuous
7. Kidney
• Morphological changes: Normally, the pressure within the
renal pelvis is close to zero. With obstruction this pressure
increases and pelvicalyceal system dilates leading to
hydronephrosis
1. In early stages, Renal pelvic musculature undergoes
compensatory hypertrophy. Later, muscles become stretched and
atonic (decompensated)
2. Calyces are the first to suffer from obstruction. The normal
concave appearance (cupping) of minor calyces , becomes flat
then rounded (clubbing) and lastly ballooned
3. Renal parenchyma starts to thin out as it suffers from ischaemic
atrophy as it is compressed between renal capsule externally, and
the centrally increasing intra-pelvic pressure
4. At a later stage, the kidney is completely destroyed and appears
as a thin-walled sac filled with clear fluid or, if infected, with pus
9. Functional changes
1. Intra-pelvic pressure continues to rise till it overcomes
the glomerular filtration pressure, where urine secretion
stops
2. Glomerular filtration rate and the renal plasma flow are
reduced and renal concentrating power is gradually lost
4. The contralateral normal kidney undergoes
compensatory hypertrophy in order to maintain an
overall normal renal function
5. In neglected bilateral obstruction, renal failure will occur
10. With relief of obstruction
Early treatment leads to remarkable improvement of morphology
and function
Delay in treatment results in some degree of irreversible renal
damage
Factors affecting morphological and functional changes
1. Level of obstruction (proximal or distal “uni or bilateral”)
2. Degree of obstruction (complete or incomplete)
3. Duration of obstruction. Long-standing partial or intermittent
obstruction tends to produce significant proximal dilatation. Acute
obstruction, on the other hand, tends to produce mild dilatation
but more rapid deterioration of function
4. Infection on top of obstruction
11. Complications
1. Stasis means infection --- faster deterioration of renal
function
2. Stone formation
3. Rupture of hydronephrotic kidney (rare, with trauma)
4. Renal failure in bilateral cases
Urgent Acute Obstructive Conditions
Acute Urinary Retention
Calcular Anuria
Bilateral ligation of both ureters
12. Hydronephrosis
Definition
Hydronephrosis is chronic aseptic distension of the renal pelvis
and calyces due to obstruction of the urinary tract
Aetiology
1. All causes of chronic obstructive uropathy
2. Pregnancy: especially on the right side. Dilatation occurs during
the first few weeks and reaches maximum between fifth and sixth
month. It is due to atony of ureteric musculature due to high
progesterone level. Also, the fetal head may compress both
ureters. Hydronephrosis of pregnancy subsides within 2-12 weeks
after delivery
3. Vesicoureteric reflux
17. Clinical features
1. Pain: There is usually slight dull aching pain or a
sense of discomfort in the loin
2. Swelling: In late stages a cystic swelling in renal angle
3. Polyuria of low specific gravity
4. Manifestations of renal failure, if present
Complications: As mentioned in general principles
Differential diagnosis:
Polycystic kidney
Hypernephroma
18. Investigations
1. Urine analysis for RBCs, WBCs, SG and crystals
2. Ultrasound examination to detect renal size, thickness of the
renal cortex (parenchyma) and possibly the cause, e.g., stones
3. IVU will show the following:
Dilatation of renal pelvis which becomes biconvex
Pelviureteric junction is distorted and is raised upwards
Loss of cupping, and clubbing and later ballooning of the minor calyces
Delayed excretion of contrast. In advanced cases no secretion occurs
4. Ascending (retrograde) pyelography. If IVU does not give
conclusive data, ascending pyelography is indicated to confirm
the diagnosis
5. Descending (antegrade) pyelography is sometimes done if a
nephrostomy tube is present
20. Treatment
Removing cause of obstruction
Nephrectomy in selected cases
The kidney is non functioning with infusion urography
Sonography showed very thin parenchyma
Renal scan shows zero function
The opposite kidney is normal
In compromised cases with bad other kidney, a
percutaneous nephrostomy may be left for long time till
obstruction is treated
In advanced cases of PUJO --- Pyeloplasty to provide
adequate drainage of the lowest part of the pelvis
21. Ureteric Stricture
Aetiology
1. Congenital: PUJO or UVJO (pin-hole meatus)
2. Traumatic: Following ureteric injuries e.g. Iatrogenic
3. Inflammatory
4. Bilharzial stricture: commonly affects the intramural and lower
part of the ureter. It may be bilateral
5. Tuberculous stricture: affects the whole ureter and is usually
multiple and bilateral
6. Long-standing stone may lead to stricture
7. Neoplastic: Carcinoma of the ureter (intrinsic) or more often,
invasion of ureter (extrinsic) by a malignant growth as carcinoma
of the uterus, colon, or rectum
22. Clinical features
1. Renal pain (dull aching) due to distension of the renal pelvis
2. Progressive hydronephrosis
3. Recurrent attacks of pyelonephritis
4. In Egypt, bilateral hydronephrosis is a common sequel of
bilateral Bilharzial ureteric stricture. These patients may present
by chronic renal failure
Investigations
1. Blood urea, serum creatinine and serum electrolytes
2. U/S will demonstrate hydronephrosis
3. IVU will determine site of the stricture and degree of functional
capacity of both kidneys
4. Retrograde and Antegrade pyelography
23. Treatment (mainly surgical)
Stricture of upper 2/3 (above the level of ischial spine)
Excision and end-to-end anastomosis: Both ends of the ureter
are trimmed obliquely, spatulated and then anastomosed by
interrupted sutures of 4-0 Vicryl over a ureteric stent which is
removed later by a cystoscopic forceps
Stricture of lower 1/3
Ureterovesical reimplantation: The ureter is divided above the
stricture and then a new ureterovesical anastomosis is established..
Bladder (Boari's) flap: for long stricture. A flap can be prepared
from the bladder wall, transformed into tube and anastomosed to
ureter
Stricture of long segment of ureter:
Ileal loop replacement
25. Retroperitoneal Fibrosis
Types
Primary (idiopathic) retroperitoneal fibrosis
Unknown aetiology but may be drug-induced, e.g., methysergide that is used for
prophylaxis against migraine
The patient may presents acutely with anuria. Ureteric catheterization is urgently
done to relieve obstruction. Unlike calcular anuria, the catheters pass up to the
kidneys easily.
ESR, urea and creatinine are usually elevated.
IVU and/or ascending pyelography demonstrates that both ureters are pulled
medially towards the mid line.
CT shows a retroperitoneal fibrous plaque in which both ureters and great
abdominal vessels (aorta an IVC) are embedded. Both kidneys show
hydronephrotic changes.
Definitive treatment is Surgical Ureterolysis i.e. release of ureters from fibrous
tissue, then wrapping them in pedicled omentum inside the peritoneal cavity to
avoid re-obstruction. Postoperative corticosteroid therapy is believed to reduce
the possibility of recurrence
Secondary retroperitoneal fibrosis
Diffuse infiltrating retroperitoneal malignancy
Previous leakage of an aortic aneurysm
This is Dr. Ayman Rashed, Urology department. and this is the first online narrated Urologic lecture for students of 6th Grade at faculty of medicine, October 6th University. today’s lecture “ Obstructive Urology” is the keynote of Urology by which you can understand most of Urology, that is why I prefer to start with
what is meant by Obstructive Uropathy? this is to signify any obstruction that occurs anywhere in the urinary tract from the kidneys above through ureters down to the urinary bladder and finally out of the body through the urethra.
It is associated with changes in the urinary system above the level of obstruction for example dilatation.
the picture in this slide denoting IVP of normal appearance of the urinary system. you can see obviously the collecting system with cupping, normal renal pelvis on both sides, normal caliber of ureters and normal filling of the bladder. by the way this is incomplete film because the urethra couldn’t be shown in this film
the obstruction can be classified according to the following
Is it Acute or chronic
Partial or complete
Unilateral or bilateral
Congenital or acquired
Extrinsic or intrinsic
Etiological (according to the cause of obstruction)
according to etiology will further subdivided according to the level of obstruction. so, at the renal level etiology may be due to: Renal stones, Congenital PUJO, Aberrant renal vessels, Renal pelvic tumors, Tuberculous stricture. at this level you will note dilatation of the collecting system what we call Hydronephrosis as appeared in IVP film No. (1) where the obstruction at the level of renal pelvis red arrow mostly due to congenital pelvi-ureteric junction obstruction (PUJ)
when the ureter is obstructed at any level it will cause dilatation including the ureter above the obstruction and the kidney or the collection system what we call hydrouretronephrosis. This may be due to causes inside the the ureteric lumen like stones as in film No. (2) red arrow or blood clots or causes in the wall of the ureter as ureteric stricture as in film No. (3) showing bilateral hydrouretronephrosis due to bilateral ureteric strictures (red arrows, atresia, uretrocele
at the urinary bladder level the causes of obstruction may include : Impacted stone at bladder neck, Tumors involving ureterovesical junction or Neurogenic bladder dysfunction. at the level of the prostate: BPH Cancer prostate or even Acute prostatitis can cause obstruction. as you see in the picture this an IVP film denoting a filling defect due to enlarged prostate (red arrows) note the smooth edge of the filling defect of the prostate that elevating the bladder upward causing outlet obstruction and the diverticulum on the left side of the bladder (yellow arrow) due to increased pressure inside the bladder. finally at the level of the urethra the obstruction may be due to Congenital: e.g. meatal stenosis and posterior urethral valves or due to Stricture of the urethra
Now what are the pathologies resulted as a consequence of the obstruction
as regard to the urethra it is just a dilatation above the level of obstruction.
As regard to the urinary bladder: the pathology occurred subdivided to Early (Compensated Phase): where Hypertrophy of the detrusor muscle --- bladder Trabeculation --- Saccules (mucosa protrudes between muscle fibers) --- Diverticulae develop when mucosa bulges outside bladder wall as we just have seen in the previous slide IVP film. then Later (Decompensated Phase): when the bladder couldn’t contract anymore against the obstruction the bladder dilates more and its wall thins out --- Atony of the bladder --- Urinary retention
As regard to the Ureters. they take the same way as the Bladder
The renal pathology will suffer from obstruction Morphologically and functionally
the morphologic changes will occur due to elevated hydrostatic pressure inside the collecting system (from normally zero) leading to hydronephrosis. the severity of the changes depends upon many factors that we will discuss later. So, in early stages the renal pelvis musculature undergoes compensatory hypertrophy. Later, muscles become stretched and atonic (decompensated)
The Calyces are the first to suffer from obstruction. The normal concave appearance (cupping) of minor calyces , becomes flat then rounded (clubbing) and lastly ballooned
Renal parenchyma starts to thin out as it suffers from ischaemic atrophy as it is compressed between renal capsule externally, and the centrally increasing intra-pelvic pressure
At a later stage, the kidney is completely destroyed and appears as a thin-walled sac filled with clear fluid or, if infected, with pus
this is an IVP film: an example for hydrouerteronephrosis due to bilateral lower ureteric stricture (red arrows). Note the clubbing of the calyces more evident on Lt side (yellow arrows)
the functional changes include stopping of urine secretion due to increased intra-pelvic pressure which at some point will overcome the glomular filtration pressure this will subsequently reduce the filtration rate and reduce the concentrating power of the kidney. the contralateral normal kidney undergoes compensatory hypertrophy in order to maintain an overall normal renal function. In neglected bilateral obstruction, renal failure will occur
Early treatment leads to remarkable improvement of morphology and function, while Delay in treatment results in some degree of irreversible renal damage.
the factors affecting the degree of renal changes include
1. Level of obstruction (proximal or distal “uni or bilateral”)
2. Degree of obstruction
3. Duration of obstruction. Long-standing partial or intermittent obstruction tends to produce significant proximal dilatation. Acute obstruction, on the other hand, tends to produce mild dilatation but more rapid deterioration of function
4. Infection on top of obstruction
the complications of urinary obstruction include
1. Stasis means infection --- faster deterioration of renal function
2. Stone formation
3. Rupture of hydronephrotic kidney (rare, with trauma)
4. Renal failure in bilateral cases
and the emergency conditions are
Acute Urinary Retention where the urine couldn’t expelled out of the bladder
Calcular Anuria where the obstruction above the level of the bladder and the urine cannot reach down to the bladder
Bilateral ligation of both ureters is another example of anuria
Hydronephrosis as a separate entity. means chronic aseptic distension of the renal pelvis and calyces due to obstruction of the urinary tract, so it is a manifestation of a hidden disease and a diagnosis
Aetiology
1. All causes of chronic obstructive uropathy commonly due to stones within the urinary tract
2. Pregnancy: especially on the right side. Dilatation occurs during the first few weeks and reaches maximum between fifth and sixth month. It is due to atony of ureteric musculature due to high progesterone level. Also, the fetal head may compress both ureters. Hydronephrosis of pregnancy subsides within 2-12 weeks after delivery
3. Vesicoureteric reflux
This is again normal IVP showing normal urinary system
this is an IVP done by mistake elsewhere for a pregnant woman near full term. the fetal sac shadow appeared to bilaterally obstructing the urinary system (compression from outside) resulting in bilateral Hydroureteronephrosis. of course it is a temporary condition which relieved after labor.
this is an antegrade pyelography study showing the nephrostomy tube (red arrows) inside the kidney and the contrast media was injected through this tube to assess the morphology of the Rt. kidney which is obstructed by cancer colon invading the ureter. in such cases we try to maintain the kidney function and patency of the tract by inserting a ureteric stent (yellow arrows) or by directing the urine directly outside by nephrostomy tube (red arrow)
here in you can see normal Renal U/S above and hydronephrosis in the below picture. Note the difference between normal calyces (yellow arrows) and dilated calyces (red arrows). Also note, renal capsule (black arrows) and Renal parenchyma (green arrows)
clinical features include: dull aching pain due to stretch of renal capsule, swelling can be palpated in late stages as a cystic swelling in renal angle. lab investigations may reveal polyuria with low specific gravity due to loss of concentration power and elevated serum urea and creatinine in bilateral renal hydronephrosis cases denoting renal failure
Dx include polycystic kidney and hypernephroma both can be investigated using U/S and CT
these are the investigations that should be done to reveal the etiology of Hydronephrosis
this a Retrograde or ascending pyelography study showing the cystoscope (red arrows) introduced through the urethra inside the bladder and two ureteric catheters (yellow arrows) advanced in both ureters though which contrast media is injected to delineate the urinary tract. this is a morphologic study by which you can study the anatomy of urinary tract but not functional study as you inject the contrast media not secreted by the kidney unlike in IVP which assess morphologic and functional parameters of the urinary tract
of course treatment will depend on treatment of the cause for example removing obstructing stones. however in some cases with end stage non functioning kidney the nephrectomy may be the treatment of choice. In compromised cases with bad other kidney, a percutaneous nephrostomy may be left for long time till obstruction is treated
In advanced cases of PUJO --- Pyeloplasty to provide adequate drainage of the lowest part of the pelvis
Stricture is also another separate entity and also is a manifestation for hidden etiology which may be one of the following
Congenital: PUJO or UVJO (pin-hole meatus)
Traumatic: Following ureteric injuries e.g. Iatrogenic
Inflammatory
Bilharzial stricture: commonly affects the intramural and lower part of the ureter. It may be bilateral
Tuberculous stricture: affects the whole ureter and is usually multiple and bilateral
Long-standing stone may lead to stricture
Neoplastic: Carcinoma of the ureter (intrinsic) or more often, invasion of ureter (extrinsic) by a malignant growth as carcinoma of the uterus, colon, or rectum
this is an example for PUJ obstruction on Lt picture and after excision of the strictured part of the ureter (red arrow) and repair on the rt picture
here in you can see ascending pyelography showing straightening of the Lt ureter and its shifting toward spinal column also hydronephrosis is noted these features denoting retroperitoneal fibrosis