urinary

Question 1

how many nephrons

Answer 1

2 million

Question 2

what are the 2 developmental abnormailities

Answer 2

: Renal agenesis (only 1 kidney)or solitary horse shoe kidney:- both kidneys are fused together

Polycystic Kidney disease:

Question 3

adult polysystic

Answer 3

Adult Polycystic
1. 8-10% of all ESRD
2. Mode of Inheritance
Autosomal dominant

3. Pathology:
Gross (huge 2-3 Kg):
	Bilateral
	Markedly enlarged
	Numerous cysts Associated With: 
	liver cysts (full of whole- tubules)
	Berry aneurysm of circle of 	willis (10-30%)
Clinical:
	4th decade
	sense of heaviness
	bilateral flank masses
	hematuria
	Azotemia
	CRF
	gene is called polysystic (senses that cell is damage and keeps repairing (proliferating) where there is no damage- dont need to know)
Rx:	Dialysis and Transplant

Question 4

glomerulus deseases affect

Answer 4

filtration

Question 5

immune mediated

Answer 5

antibodies get deposited or antibody complexes get deposited and interfere with filtration and attract inflamatory cells :
acute renal failure, nephritic(i for inflamation) syndrome, nephrotic (o for edema fluid leaks out ) syndrom, isolated hematuria (blood in urine)

Question 6

metabolic mediated

Answer 6

diabetes (so much sugar in blood), amyloidosis (abnormal protein get deposited )

Question 7

circulatory mediated

Answer 7

hypertension, atherosclorosis DIC (not enough blood or nutrients so starts to die)

Question 8

Acute Renal Failure

Answer 8

Sudden onset – renal failure (anuria or oliguria) when urine output is less then 300 ml
#Pre-Renal
Shock or heart failure
#Renal
Glomerular or tubular disease
#Post-Renal
Urinary obstruction (due to stones, prostatic enlargement)

mesured by mesuring createnin tells us its not functioning

Question 9

Nephrotic Syndrome

Answer 9

Dx by clinical findings
Edema more than3g/day
Proteinuria
Hypoalbuminemia
Hyperlipidemia (when losing so much protein so the liver starts making lots of proteins and lipids at the same time) more creatinin means not filtering properly

Question 10

Nephritic syndrome

Answer 10

Dx by clinical findings
Edema (not as much)
Hypertension (increase BP)(na and cl are retained so pulls more water in)
Hematuria
Proteinuria
Hypoalbuminemia

Question 11

Lipoid Nephrosis

Answer 11

Also known
“Minimal change disease”
“Nil lesion disease”
Unknown etiology
Most common cause of Nephrotic syndrome in children

Question 12

filtratrion barrier

Answer 12

1: endothelial cell (
2: glomerular basement membrane
3: podocytes and slit diafragms

Question 13

what is the ultimate filtration barrier

Answer 13

SD outside the gbm- in nephrotic this is where the damage is

Question 14

in nephritic what is damaged

Answer 14

damage the GBM AND BLOOD GOES OUT (HEMATURIA)

Question 15

nephrotic syndrome

Answer 15

Minimal Change disease most common in children( under microscope we dont see any lesions or abnormality becasue too small witha tiny slit )
Focal segmental glomerulosclerosis
Membranous nephropathy

Question 16

lipoid nephrosis

Answer 16

Histology
Light – nil (cant see any change)
Immuno – nil
EM – fusion of foot processes (cytoscleton cannot maintain erectile stature  because of slit) of podocytes
Clinical
Responds to steroids

Question 17

Membranous nephropathy (changes in the membrane)

Answer 17

Immune mediated glomerulopathy
Diffuse thickening of glomerular basement membrane
Massive deposition of immune complexes (gbm tries to eat all the imunoglobulin so grows and grows to sufficates

Question 18

Nephrotic syndrome

of membranous nephropathy

Answer 18

Nephrotic syndrome
No signs of inflammation
Most common cause of nephrotic syndrome in adults
Etiology unknown in 85%

Question 19

what is the histology of Membranous Nephropathy

Answer 19

Histology
Thickened basement membrane
No cellular changes
Immuno-fluorescence
Granular immune complexes

Question 20

Nephritic Syndrome

Answer 20

Dx by clinical findings
Edema
Hypertension ( BP)
Hematuria
Proteinuria
Increased serum creatinine

Question 21

Acute Post-Infectious Glomerulonephritis

Answer 21

Immune mediated inflammatory glomerulopathy
1 – 2 weeks after acute infection (strep throat
Anti-strep antibodies are formed
Ag-Ab complexes are trapped in glomerular basement membrane
Complexes activate complement
Attract inflammatory cells to glomerulus
- blodd cannot go through

Question 22

what is th histology of Acute Post-Infectious Glomerulonephritis

Answer 22

Histology
Glomeruli are hypercellular
increase Inflammatory cells within capillary lumen- block blood flow

Question 23

clinical Acute Post-infectious Glomerulonephritis

Answer 23

Clinical
Damaged basement membranes “leak”
Proteinuria & hematuria
Urine is murky brown
Decreased blood flow and retention of sodium—Hypertension
decrease Blood flow in glomeruli —increase Renin= High blood pressure
Loss of albumin :decrease serum albumin = edema

Question 24

prognosis of Acute Glomerulonephritis

Answer 24

Prognosis
Short lived illness
Most recover completely 1 – 2% lead acute renal failure <10 %  end stage renal failure

Question 25

Crescentic Glomerulonephritis

Answer 25

Exudate in glomerular space (mainly macrophages)
Occurs after focal necrosis of capillaries from Goodpasture’s Syndrome (renal and lung disease)- (ANCA (neutrophase cytoplasmic antibodies) associated vasculitis)
Antibodies to basement membrane collagen
Crescents compress capillary loops
decrease Blood flow decrease glomerular filtration increase Anuria
Recovery rare  dialysis

Question 26

anti gbm anti body vs anca anti body

Answer 26

anti- agaisnt one of the types of collagen in the gbm goes stright for it and destroys it and going to make a whole and can see it blood leaks out the body sees this and cleans up and send all the macrophages to eat all the blood and this compresses to glomerulus- acute renal failure
2 ANCA: not agasint gbm, are agaisnt cytoplasmic proteins in the neutrophils some antibody get attached to endothelial - make whole in capilary loop, macrophages come in and crescent is formed again-acute reanl failure

Question 27

what is the most common cause of adult nephrotic syndrome

Answer 27

Membranous Nephropathy