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Pathology of urinary system - Coggle Diagram
Pathology of urinary system
Introduction
Functions of
the kidney
Excretion of waste products
Regulation of water/salt
Maintenance of acid/base balance
Secretion of hormones
Diseases of the kidney
– Glomeruli
– Tubules
– Interstitium
– Vessels
Nephrotic syndrome
• Massive proteinuria
• Hypoalbuminemia
• Generalized edema
• Hyperlipidemia/-uria
Nephritic syndrome
• Hematuria
• Oliguria
• Azotemia
• Hypertension
RENAL FAILURE
Acute or chronic
Result from any of the glomerular or tubulointerstitial lesions
Azotemia of renal origin is always associated
In advanced stages, renal failure results in uremia
Biochemical and clinical syndrome
characteristic of symptomatic renal disease
Gromerlar diseases
Nephrotic syndrome
Minimal change disease
Light microscopy
Normal glomeruli
Lipid accumulation in proximal tubule cells
Immunofluorescence: negative; no immune complexes
Diagnosis of exclusion
Electron microscopy
– Effacement of epithelial (podocyte) foot processes
– No immune complex deposits
Peak incidence: ages 2-6 years
Most common cause of nephrotic syndrome in children
Lipoid nephrosis, nil disease
Treatment: corticosteroids
Prognosis
Excellent
– Dramatic response to steroids in children
– Majority have a complete recovery
Membranous nephropathy
Drugs, Tumors, SLE, Infections
Deposition of Ag-Ab complexes: subepithelium
Indolent, but >60% persistent proteinuria
MC cause of nephrotic syndrome in adults
Microscopic: uniform, diffuse thickening of the glomerular capillary wall.
Basement membrane material is laid down between these deposits, appearing as irregular spikes protruding from the GBM.
Nephritic syndrome
Postinfectious GN
IgA nephropathy
Acute Diffuse Proliferative Glomerulonephritis
This produces the nephritic syndrome (hematuria, red cell casts, moderate proteinuria and edema) in children
Two weeks following a respiratory or skin infection with a "nephritogenic strain" of group A, beta-hemolytic streptococci.
Acute post-streptococcal glomerulonephritis
The cause is deposition of circulating immune complexes which fix complement and attract PMN's.
There is swelling and proliferation of glomerular endothelial cells.
Deposits of circulating immune complexes fix complement and attract neutrophils.
This chokes off their blood supply, making the glomeruli hypercellular and bloodless.
Immunofluorescence
coarse granular deposits containing immunoglobulin and complement.
This explains the oliguria, edema, and hypertension.
Electron microscopy
granules are large, dense, hump-shaped deposits located subepithelially (i.e., on the epithelial side of the GBM).
Goodpasture syndrome (antiglomerular
basement membrane disease)
Fluorescent antibody studies for IgG
demonstrate linear immunofluorescence
Clinical manifestations include
Pneumonitis with hemoptysis (hemorrhagic pneumonitis)
Peak incidence in men in their mid-20s
Nephritic syndrome
RPGN crescentic morphology with linear
immunofluorescence
Antiglomerular basement membrane antibodies directed against antigens in glomerular and pulmonary alveolar basement membranes
Urinary tract infection
นิยาม
• Infection of urethra, bladder, or kidney
• Most commonly arises clue to ascending infection; increased incidence in females
• Risk factors include sexual intercourse,urinary stasis, and catheters
Acute cystitis
Presents as dysuria, urinary frequency, urgency,
and suprapubic pain
Etiology
E.coli (80%)
– Staphylococcus saprophyticus —increased incidence in young, sexually active women
– Proteus mirabilis —alkaline urine with ammonia scent
– Enterococcus faecalis
Infection of the bladder
Acute
Pyelonephritis
Causes:
Ascending infection
Hematogenous seeding
Patchy process, pinpoint microabscesses on cortical surface.
Common in patients
Incompetent ureteral valves.
Diabetes.
Immunocompromise.
Mechanical obstruction
This obstruction may occur anywhere in the urinary system.
In children, the condition is
most often congenital.
In adults, the condition is most often acquired, usually occurring as a consequence of renal stones or benign prostatic hyperplasia.
Clinical manifestations include
Renal colic
Hydronephrosis
Infection
Renal lithiasis
Calcium stones (80%–85%)
Calcium oxalate or calcium phosphate, or both
Radiopaque
Associated with hypercalciuria
Ammonium magnesium phosphate stones
Second most common form of urinary stones.
Alkaline urine
Ammonia-producing (urease-positive) organisms
Radiolucent
Form large staghorn (struvite) calculi (casts of renal pelvis and calyces)
Uric acid stones
Hyperuricemia
Secondary to gout or to increased cellular turnover, as in the leukemias or myeloproliferative syndromes
Cystine stones
Cystinuria or genetically determined aminoaciduria
Acute Tubular Necrosis
Acute renal failure associated with dysfunction and necrosis of tubular epithelial cells.
Classification
Ischemic
Toxic
Pathology: variable, focal to
extensive epithelial necrosis
Pathogenesis
vasoconstriction, obstruction, tubular leakage of filtrate.
Drug-Induced interstitial Nephritis
Drug-induced hypersensitivity involving the interstitium and tubules
Acute renal failure (intrarenal azotemia)
NSAIDs, penicillin, and diuretics.
Oliguria, fever, and rash days
to weeks after starting a drug
Eosinophils may be seen in urine.
Resolves with cessation of drug
May progress to renal papillary necrosis
Adult Polycystic kidney Disease
Manifests clinically between 15 and 30 years of age
• Genetic defect is present at birth
• Autosomal dominant inheritance
• Replacement of renal parenchyma by cysts
• Occurs bilaterally; the kidneys are greatly enlarged
• Associated with berry aneurysm of the circle of Willis
Frequently associated with cystic disease of the liver or other organs
Clinical manifestations
Hypertension
–Hematuria
– Palpable renal masses
– Progression to renal failure
Childhood Polycystic kidney Disease
Autosomal recessive
inheritance
Bilateral cystic disease; cysts in
the cortex and medulla
Cysts also occur in the liver; association with congenital hepatic fibrosis leading to portal hypertension
Enlarged kidneys at birth; most serious types are incompatible with life
Maternal oligohydramnios
Renal Cell Cercinoma
85% of renal cancers in adults.
• M>F; 50-60’s.
• VHL gene
Spherical, yellow-gray-white mass with necrosis and hemorrhage.
Invasion of renal vein is common.
Prognosis depends on size and
extent of spread.
25% show metastasis at time of
diagnosis
Clear cell variant
(70-80%)
solid sheets, cords and tubules.
– round to polygonal cells with clear to granular cytoplasm.
– They can be familial, associated with VHL disease, or in most cases (95%) sporadic.
Papillary carcinoma accounts for
10% to 15%.
Classic triad
hematuria, costovertebral pain,
palpable mass
May produce systemic symptoms
Polycythemia
– Hypercalcemia
– Hypertension
– Hepatic dysfunction
– Feminization, masculinization
– Cushing’s syndrome
– Eosinophilia, amyloidosis
Wilm's tumor
Macro
Large solitary wellcircumscribed mass,
• Soft, homogenous, tan-to-gray cut surface
• +/- necrosis, cyst,hemorrhage
Micro
Blastemal component : primitive small blue cells
Stromal component : spindle-shape cells
Epithelial component : immature tubules immature glomeruli
Urinary Bladder tumors; common in
Increase incidence of bladder tumor
M:F=3:1
Industrialized than developing nations
Urban than rural
Older patients; between 50-80 yrs
Most are sporadic (not familial)
Risk factors
Cigarette smoking (increase threefold to sevenfold)
Industrial exposure to arylamines
Schistosoma haematobium infections
Long-term use of analgesics
Heavy long-term exposure to cyclophosphaminede
Prior exposure of the bladder to radiation
Genetic alteration
Urinary bladder CA
Epithelial origins (95%)
Transitional cell (Urothelial) CA (90%)
Squamous cell CA
Adenocarcinoma
Clinical course
Painless hematuria* dominant
Frequency, urgency & dysuria occasionally accompay the hematuria
After excision; tendency to develop new tumors and recurrences
Early detection ; Urine cytologic study
Prostate
Inflammation
Acute bacterial prostatitis
Similar organisms that cause urinary tract infection;Escherichia coli, etc
Intraprostatic reflux of urine from the posterior urethra or from the urinary bladder
Occasionally: lymphohematogenous routes from distantfoci of infection
Fever, chills, and dysuria Rectal examination: prostate is tender and boggy
Diagnosis: Urine culture and clinical features
Chronic bacterial prostatitis
Asymptomatic or low back pain, dysuria, and
perineal and suprapubic discomfort
Often have a history of recurrent urinary tract infections, same organisms as acute prostatitis
Diagnosis: demonstration of leukocytosis in the expressed prostatic secretions, along with positive bacterial cultures
Chronic abacterial prostatitis
Most common form
Signs and symptoms: indistinguishable from chronic bacterial
prostatitis, but no history of recurrent urinary tract infection
Granulomatous prostatitis
Benign enlargement
Benign prostatic hyperplasia (BPH)
Most common benign prostatic disease in men older than age 50 years
Proliferation of benign stromal and glandular elements
Unknown ultimate cause of BPH, it is believed that
Dihydrotestosterone (DHT) is the major hormonal stimulus
Medical therapy
alpha blockers, inhibitors of 5-α-reductase
Tumor
Adenocarcinoma
Definitive risks factors
Age
Family history
Race/geography
Probable risk factors
Diet
Hormone levels