Retroperitoneal fibrosis is a rare condition where a fibro-inflammatory mass envelops and potentially obstructs retroperitoneal structures like the ureters. It is idiopathic in most cases. Imaging shows a soft tissue mass surrounding the aorta and ureters, often causing hydronephrosis. Treatment involves stenting of the ureters to relieve obstruction and use of corticosteroids or immunosuppressants to reduce inflammation and fibrosis in active cases. Biopsy is needed to confirm diagnosis and rule out malignancy. The goal of management is to preserve renal function and prevent involvement of other organs.
genitourinary tb - contains radiological findings of genitourinary tuberculosis including ivp,, hsg, usg and ct findings in kidney, ureter, urinary bladder, uterus and prostate
genitourinary tb - contains radiological findings of genitourinary tuberculosis including ivp,, hsg, usg and ct findings in kidney, ureter, urinary bladder, uterus and prostate
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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
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Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
2. INTRODUCTION
Uncommon condition.
A fibro-inflammatory mass envelops and
potentially obstructs retroperitoneal structures,
including either or both ureters.
Fibrous, whitish plaque encases aorta, IVC &
their major branches, ureters, other
retroperitoneal structures, at times
intraperitoneal structures including GIT.
3. Centers around distal aorta at L4-L5 and wraps
around the ureters, leading to hydronephrosis via
extrinsic compression on the ureters or
interference with ureteral peristalsis.
Extent:
Longitudinal- from renal hilum to pelvic brim(Aotic
bifurcation); may extend into the pelvis,
mediastinum and optic orbit.
Transverse-laterally to outer edge of psoas
muscles.
AKA- Periureteritis fibrosa/plastica, Chronic
periureteritis, fibrous retroperitonitis, sclerosing
RP granuloma.
4. Ureteral obstruction in RPF appears minimal
despite severe renal failure. This suggests that
obstruction relates to impairment of normal
ureteric peristalsis by fibrotic tissue rather than
to mechanical obstruction.
5. EPIDEMIOLOGY
Peak age of incidence: 40-60 years.
Rarely in children.
Male predominance; M:F Ratio 2-3:1
Estimated annual incidence: 1 per 200,000-
500,000 population.
No racial predilection.
8. PATHOGENESIS
Exact pathogenesis- unclear.
Good evidence: an immunologic response to
antigens within atherosclerotic plaques.
Vasculitis of adventitial vessels of aorta &
perioaortic small vessels → release of antigens
from atheromatous plaque such as ceroid, a
complex lipoprotein → induces an autoimmune
antigenic response → local inflammation &
fibrosis.
Other immunologic events: CD3+ & CD20+
lymphocytes, IgG4-positive plasma cells
identified.
9. Immune reaction to an external agent:
Drugs/chemicals act as haptens-induce
hypersensitivity or immune reaction.
In Carcinoid tumor: result of circulating
serotonin or its metabolites.
Methysergide is a strong serotonin antagonist;
Rebound serotonin release after prolonged intake
may be an alternate mechanism.
Genetic influence- no major role, as no reports of
familial clustering.
11. CLINICAL FEATURES
Non-specific signs & symptoms.
Duration of symptoms prior to diagnosis: 4-6
months.
50% patients present with significant ureteric
obstruction & uremia.
SYMPTOMS:
M.C.symptom(92%)-dull, poorly localized,
noncolicky pain in flank, back, or lower abdomen.
Unrelated to posture; relieved by aspirin.
12. In children, pain may be referred to ipsilateral
hip or gluteal region, resulting in resistance to
hip extension.
Fever
Lower-extremity edema
Phlebitis
Deep venous thrombosis
Weight loss, nausea, vomiting, anorexia, and
malaise: Uncommon.
Raynaud phenomenon, ureteric colic, hematuria,
claudication, and urinary frequency: Rare.
13. SIGNS:
Hypertension: Present in 50%
Presence of an abdominal mass (occasionally)
Ureteric obstruction with varying degree of renal
insufficiency: Earliest and M.C.organ involved.
Uncommon physical findings due to late
complications:
Ascites
Peripheral edema or thrombosis
Hydrocele
Jaundice
Small- or large-bowel obstruction
Spinal cord compression
14. Hypertension: results from many factors.
An increase in renin release secondary to
obstructive uropathy.
In some patients, volume-dependent
hypertension may result from obstructive
nephropathy.
16. IMAGING STUDIES:
PLAIN RADIOGRAPHY:
Nonspecific findings.
Obliteration of psoas shadow & an enlarged
renal outline due to hydronephrosis.
INTRAVENOUS UROGRAPHY (IVU):
The classic triad (18-20%)
1. U/L(20%) or B/L(68%) hydronephrosis,
2. Medial deviation of middle third of ureters,
3. Tapering of ureter at L4/L5 level.
18. RETROGRADE PYELOGRAPHY:
Demonstrates poor distensibility of ureter.
Delineates PCS anatomy; performed prior to
stent insertion to decompress the kidneys.
Interestingly, very little resistance is
encountered during ureteric catheterization
despite extensive extrinsic fibrosis.
20. LYMPHANGIOGRAPHY:
Obstruction of lymphatic flow at L3/L4 level,
Opacification of collateral channels,
Nonvisualization of lymphatics above L4 vertebra,
Delay in passage of contrast through iliac and para-
aortic lymphatics.
Obsolete nowadays.
21. ULTRASONOGRAPHY:
Simple noninvasive modality used to assess
response to therapy.
RPF appears as a retroperitoneal, extensive, well-
defined, hypoechoic mass centered over the sacral
promontory.
Degree of hydronephrosis and hydroureter may
vary.
Doppler ultrasonography has no role in
differentiating benign from malignant RPF.
22. CT SCAN:
Most frequently used imaging method for
diagnosis & follow-up of RPF.
Unenhanced CT:
o RPF appears as a plaque that is isodense with
muscle
o envelops aorta & IVC b/w the renal hila & sacral
promontory
o usually extends laterally to incorporate ureters.
o Obliteration of the fat plane between the mass
and the psoas muscle may be observed.
23. CECT:
o Plaque may show a variable degree of
enhancement, depending on stage of the disease.
Significant enhancement in the early active
vascular stage, but poor in the late avascular
stage.
24. NCCT scan: periaortic fibrotic reaction associated
with an inflammatory aortic aneurysm &
bilateral ureteric stents
26. Unenhanced CT in RPF: Note hydronephrosis and
soft tissue mass indistinguishable from the great
vessels.
27. MAGNETIC RESONANCE IMAGING:
o T1-weighted images: Both benign and malignant
RPF have low-to-intermediate signal density
density.
o T2-weighted images vary based on disease stage.
Early stage- signal density is high because of
high fluid content & hypercellularity.
o Late-stage disease has low T2 signal intensity as
a result of avascular acellular fibrosis &
decreased fluid content.(majority of plaque is
composed of fibrosis)
28. WHY MRI IS SUPERIOR TO CT IN RPF:
Independent of patient’s renal functional status.
More accurately distinguishes the plaque from
the great vessels than unenhanced CT.
The disease can be followed without radiation
exposure of repeated CT.
Enhancement ratios can be calculated with
dynamic gadolinium enhancement; can be used
to assess disease activity & monitor treatment
responses.
29. 18-FDG PET SCAN:
o 18F-fluorodeoxyglucose positron emission
tomography (F-18 FDG PET) detects glucose
hypermetabolic activity.
o Degree of inflammation in the plaque, which may
predict response to immunosuppressive therapy
as well as its therapeutic response.
oCan also reveal other sites of disease (thyroid,
thorax) and may help to identify the most
appropriate sites for retroperitoneal biopsy.
30. Gallium-67 single photon emission–computed
tomography (SPECT) scintigraphy
In the acute phase, RPF may take up gallium-67,
due to binding of gallium-67 to lymphocytes.
Used for:
o Evaluating responses to medical therapy of RPF.
o Detection of recurrent disease.
o Demonstrates both the mass lesion and its
inflammatory component.
31. BIOPSY:
Open, Laparoscopic,
Percutaneous(USG/CT/MRI guided).
Core tissue biopsy (histologic confirmation) is
preferred over FNAC assessment.
RPF progresses through 2 clinical stages:
(1) Early inflammatory phase: an inflammatory
infiltrate(both perivascular and diffuse)
contains macrophages, lymphocytes, plasma
cells, and occasional eosinophils; highly
vascular & cellular.
(2) Late fibrotic phase: avascular & acellular with
scattered calcification and fibrous scarring.
consists of myofibroblasts and type-1 collagen.
32. Submucosal edema and lymphocytic infiltration
may be observed in the ureter.
Malignant RPF: scattered nests of malignant
cells within the inflammatory infiltrate.
33. TREATMENT
Goals of m/m:
1. to preserve renal function.
2. to prevent other organ involvement.
3. to exclude malignancy, and
4. to relieve symptoms.
Treatment of retroperitoneal fibrosis depends
on disease stage at diagnosis, & patient’s
clinical status.
35. Patients with hydronephrosis and uremia-
Emergency decompression by PCN or Indwelling
DJ stent.
Close monitoring for post-obstructive
diuresis(Urea diuresis, Sodium diuresis), renal
function status, & appropriate fluid & electrolyte
replacement.
Search for inciting cause; offending drugs
discontinued.
Imaging & Biopsy to rule out malignancy.
36. Medical Management:
Empirical therapy includes corticosteroids,
tamoxifen, and azathioprine;
Experimental therapy-azathioprine,
cyclophosphamide, mycophenolate-mofetil,
cyclosporin, medroxyprogesterone acetate, and
progesterone.
Glucocorticoids and azathioprine: most useful in
patients with signs of inflammation (eg, raised
ESR and WBC count and positive ANA results)
37. CORTICOSTEROIDS:
Beneficial effect: due to anti-inflammatory action & ability
to inhibit fibrotic tissue maturation.
A standard protocol is prednisolone at 40-60 mg/d tapered
to 10 mg/d within 2-3 months and discontinued after 12-24
months.
Prednisolone oral 60 mg on alternate days for 2 months,
tapered to 5 mg daily over next 2 months. The latter dose is
continued for a total of 2 years.
Methylprednisolone pulse therapy (MPPT) at 1 g/d IV for 3
days along with azathioprine or penicillamine.
Steroids can be used in combination with surgery.
38. Characteristic clinical response to steroid
therapy: resolution of pain and constitutional
symptoms within days after treatment, a rapid
fall of erythrocyte sedimentation rate, and
diuresis.
TAMOXIFEN:
Tamoxifen increases the synthesis and secretion
of transforming growth factor–beta (TGF-b), an
inhibitory growth factor, by human fetal
fibroblast in vitro.
Other possible mechanisms of action: inhibition
of protein kinase C, reduction of epidermal
growth factor production, inhibition of
calmodulin, and blockage of growth-promoting
histaminelike receptor.
39. Mycophenolate mofetil
Blocks the proliferation of T cells and B cells.
Surgical Management: Open Ureterolysis
Midline, transperitoneal abdominal incision.
Preoperative RGC placement to facilitate
identification & dissection.
Bilateral ureterolysis, even if single ureter
invloved.
40. After B/L ureterolysis, repositioning of ureters &
protection from fibrous entrapment.
Lateral retroperitonealisation: retract the
ureters laterally and secure the overlying
peritoneum medially to the psoas muscle to
maintain the ureters in this location.
Intra-peritonealisation: close the peritoneum
behind the ureters so that the ureters may be
displaced anteriorly into the peritoneal cavity.
Omental wrap: In extensive RPF cases,
surround the ureters with omentum and
reposition them within the peritoneal cavity.
Ureteral wrap in PTFE vascular graft/Gore-
tex graft.
42. POST-OP CARE:
Removal of ureteric stents 6-8 weeks after
surgery .
Postop Steroid therapy may be considered to
avoid recurrence.
43. OTHER OPTIONS:
High-risk & elderly patients- long term ureteral
stents.
Ureterolysis not possible d/t extensive fibrosis &
ureteric stricture:-
o Ileal substitution
o Appendix substitution
o Renal autotransplantation.
If lower ureter involved- Boari’s flap.
Poor Kidney function despite salvage
decompression & N contralateral kidney-
Nephrectomy.
44. Further Outpatient Care:
Biochemical markers (CRP, ESR, renal function)
monitored every 4-8 weeks to assess response.
Radiologic assessment (CT, MRI) performed
every 3 months; once disease stabilized, scanning
can be repeated at 6 months.
Recurrence reported as late as 10 years; thus,
long-term follow-up is necessary.
Renal failure patients- early Nephrology referral
& continued follow-up.