Genitourinary 1 Flashcards
vitamin D
absorption of Calcium
renal activation of vit D
secondary to hyperparathyroidism and bone disease (renal osteodystrophy) w/out kidney
renal osteodystrophy
bone mineralization deficiency
nephrotic syndrome
- glomerular filtration increases
- abnormality in GBM/mesangium
- glomerulus loses capacity for selective retention of proteins in blood
nephrotic syndrome leads to
1 proteinemia (mostly albumin)
2 hypoalbuminemia causing generalized edema by decreasing plasma colloid pressure or oncotic pressure
3 hyperlipidemia bc of reduced serum apolipoproteins (proteins that bind lipids)
nephritic syndrome
- disturbance of glomerular structure that involves reactive cellular proliferation
- reduced glomerular flow
- oliguria, hematuria, proteinuria, uremia (retention of waste prdts)
- activation of renin-angeiotensin system w/ fluid retension and mild hypertension
- mild edema, not as prevalent as nephrotic syndrome
glomerular perfusion failure
nephritic syndrome
3 signs of nephrotic syndrome
1 massive proteinuria
2 hypoalbuminemia
3 generalized edema
Interruption of the capillary walls of the glomeruli which leads to increase permeability of plasma proteins leads to
nephrotic syndrome
structural or physiochemical alteration of the GBM allows protein to escape from blood…this occurs in
nephrotic syndrome
edema
extension of salt and water in kidneys
Good pasture syndrome
a rare autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys, leading to bleeding from lungs and to kidney failure
primary causes of nephrotic syndrome
1 minimal change nephropathy - everything looks normal under a microscope but in an electron microscope, there’s a problem with the nephrons
2. membranous neuropathy- slowly progressive disease of the kidney affecting adults 30-50 yrs
membranous nephropathy
- slowly progressive
- 30-60 yrs
- subepithelial Ig deposits along GBM, -thickening capillary wall
- 85% idiopathic
- antibodies reacting to endogenous or implanted glomerular antigens
minimal change nephropathy (lipid nephropathy)
1 pathology is detected only w/ electron microscope
2 T cells produce a cytokine that attacks foot processes and nephrins so proteins can seep through
Nephritic syndrome**
1 hematuria= elevation of blood urea
2 azotemia= high creatine or N-compds in blood
3 oliguria= little urine
4 crescent shaped
what has an acute onset, hypertension, and proteinuria, but not like nephrotic
nephritic syndrome!
chronic glomerulonephritis**
develops insidiously, discovered late in its course after onset of renal insufficiency, compensatory metabolic regulation hides the disease until late
nephritic vs. nephrotic
nephritic= acute diffuse proliferative glomerulonephritis, crescent glomerulonephritis nephrotic= membranous glomerulopathy and minimal change glomerulopathy
Glomerular diseases
- structural changes in GBM
- damage to both basement membrane and cell proliferation (mixed nephritic and nephrotic syndrome)
benign nephrosclerosis
- hyaline thickening of small arteries and arterioles
- leads to decreased blood flow
- ischemia + diffuse tubular atrophy
malignant nephrosclerosis
- leads to malignant hypertension
- rapid increase in BP
- the glomerular capillary netowrk–> segmental tufts necrosis
fibrinoid necrosis
looks like onion skin, malignant hypertension or malignant nephrosclerosis
most common cause of renal infarction
1 emboli going down renal arterial branches like emboli from a mural thrombus (recent MI)
2 thrombotic vegetations on mitral/aortic valves /prosthesis
3 thrombus from left atrium of patients with atrial fibrillation
wedge shaped subscapular areas of necrosis with broad base at capsular surface
renal infarction
wedges of renal infarction
- first, wedge intially red and slightly raised
- 4-5 days later, wedge is yellow white center with rim of hyperemia
- old infarcts are narrow, wedge shaped, depressed sacs
**what is the most common cause of end stage renal disease?
diabetusssss!
complications of diabetic vascular disease
1 increase severity of small, med, large arteries (general renal ischemia)
2 hyaline atherosclerosis in afferent arterioles (ischemic glomerular damage)
diabetic glomerular damage
red stained coagulated fibrin protein (“protein cap”) on the surface of glomerulus
kimmelstiel-wilson nodules only seen in
Diabetes!!!
kimmelstiel wilson nodules description
excess mesangial matrix formation first as an even pattern throughout the glomerulus, but later as laminated spheres or nodules
diabetic renal disease
- BM thickens
- exudative lesions as fibrin like material (fibrin caps
- fibrin caps over tips of glomerular capillary loops
adult polycystic disease
autosomal dom, manifestation in adults, 2 genes on chrom #2 and #16, kidneys enlarged bilaterally, partial parenchyma replaced w/ cysts
In what disease do cysts enlarge over the years but are asymptomatic until # and size become so great that abdominal mass is observed
adult polycystic disease
Wilm’s tumor
nephroblastoma, tumor of kidney in children (1-4 yrs)
renal adenocarcinoma symptoms
hematuria (blood in urine)
flank pain (dull pain in lower part of body)
after 50 years; men
-palpable mass
renal adenocarcinoma
- 90% of primary malignant renal tumors in adults
- from tubular epithelium
- majority are sporadic
- molecular classification advances help us understand etiology, often in poles (especially upper)
gross renal adenocarcinoma
round, yellow cut surface w/ hemorrhage + necorsis
histiology of renal adenocarcinoma (SEEN IN ADULTS)
polygonal clear cell
Wilms tumor description
from primitive metanephros w/ at least 3 diff genetic alterations
- less frequently hematuria
- abdominal palpable, often huge mass
reflux nephropathy
- chronic reflux- associated pyelonephritis
- scarring and atrophy results from superimposition of a UTI on congenital vesiculouretal reflux
- unilateral or bilateral
vesiculouretal reflux
constant UTI b/c valves stop functioning
**What is the most comomn cause of acute renal failure?
acute tubular necrosis
*How old is the peak incidence of Wilm’s tumor?
peaks incidence 1-4 yrs (children!)
glomerular damage associated with proliferation of endothelial or mesangial cells is associated with
microhematuria or nephritic syndrome
deposition of excessive mesangial matrix leads to
abnormal loss of protein in urine or to nephrotic syndrome
If glomerular damage is RAPID, what develops?
acute renal failure
diverticula of urethra
outpouching of bladder mucosa
megaureter
enlarged ureter, dilated, dilation of pelvicalyceal system (dydronephrosis)
end stage hydronephrosis
- unilateral obstruction of ureter
- renal fxn maintained by nonobstructed kidney
bilateral obstruction
usually w/ lesions of bladder base or retroperitonial tissues
What occurs before severe atrophy of both kidneys?
renal failure
bilateral kidney obstruction also predisposes to
infection and stone formation
urinary calculi
kidney stones
predisposing factors of urolithiasis
- increase solute in urine
- metabolite or low fluid
- reduced solubility bc abnormal PH
- stony concentrations in bladde or urinary tract
What is the second most common type of urinary calculi made of ?
struvite ( Mg, NH4+, Calcium Phosphate)
What is the most common symptom of transitional cell carcinoma of the bladder ?
hematuria
transitional cell carcinoma of the bladder
- most common tumor of urinary collecting system (calyces, pelvis, ureter, bladder)
- often multifocal
What causes transitional cell carcinoma of the bladder?
environmental agents excreted in high concentration in urine like aniline dye, cigarettes, cyclophosphamide
are multiple tumors common in transitional cell carcinoma of the bladder
yes, field change in all of urothelium so multiple tumors are common
what is the men:female of transitional cell carcinoma of the bladder
3:1
what is the growth pattern of transitional cell carcinoma of the bladder
papillary growth pattern with cauliflower appearance
Susceptibilities of nephrotic syndrome
1 susceptibility of infection b/c low Ig and complement
2 susceptibility to thrombosis bc increased fibrinogen in blood
most frequent cause of nephrotic syndrome in children
minimal change nephropathy (lipid nephropathy)
What does malignant nephrosclerosis do to large muscular vessels?
large muscular vessels w/ loose fibroelastic proliferation of the intima- the afferent arterioles exposed to sudden high prressure frequently undergo necrosis, w/ fibrin in damaged walls (fibrinoid necrosis)
acute renal failure- when sufficient nephrons are destroyed (damage to tufts and afferent arterioles) leads to
malignant nephrosclerosis
What nodules are seen in diabetic renal disease?
kimmelstiel wilson nodules
infarction
is tissue death (necrosis) caused by a local lack of oxygen, due to an obstruction of the tissue’s blood supply
