Urogenital - renal patho Flashcards
1
Q
causes of chronic renal failure
A
- Diabetic nephropathy
- Glomerulonephritis
- Hypertensive nephrosclerosis
- Interstitial nephritis
- Chronic urinary outflow tract obstruction
- Pyelonephritis (kidney inflammation)
- Polycystic kidney disease
- congenital kidney diseases / malformations
- tumours
2
Q
complications of end-stage renal disease (ESRD) (7)
A
- dehydration, anemia, hyperkalemia, metabolic acidosis
- hyperphosphataemia, hypocalcemia, hyperparathyroidism, renal osteodystrophy
Systems:
- cardiopulmonary: HTN, HF, Cardiomyopathy, Pulmonary oedema, uraemic pericarditis
- GIT: Nausea and vomiting, bleeding, esophagitis, gastritis, colitis
- neuromuscular: myopathy, peripheral neuropathy, encephalopathy
- skin: dermatitis, pruritus (itch)
3
Q
treatment for chronic renal failure (3)
A
- Hemodialysis: removal of solutes across a semi-permeable membrane within a dialysis machine
3x a week, requires pt to go down to NKF - peritoneal dialysis: removal of solutes across the peritoneal membrane into peritoneal dialysate fluid
- renal transplant
pt needs to be on immunosuppressive therapy for rest of life to prevent organ rejection
4
Q
chronic renal failure
- gross and micro appearance
- clinical presentation
A
- BILATERAL small contracted kidneys
- Widespread glomerulosclerosis, tubular atrophy and interstitial fibrosis
- polyuria - cause tubules cannot concentrate the filtrate
5
Q
acute renal failure
- clinical presentation
A
- oliguria/ anuria = decrease/ absence of urine production
- azotaemia = rise in serum creatinine
6
Q
acute renal failure causes
- pre-renal, renal, post-renal
A
- pre-renal (blood supply TO kidney is poor)
HTN, hemorrhage, dehydration, shock, heart disease, liver failure - renal (kidney disease)
- Glomerulonephritis
- Acute tubular necrosis (due to drugs, toxins, pigment)
- Acute interstitial nephritis
- Haemolytic uraemic syndrome (HUS)
- vasculitis
- severe infections (pyelonephritis)
- post-renal (exit renal system)
Acute urinary tract outlet obstruction (due to blood clots, stones, tumour)
Acute atonia, hypotonia (loss of muscle tone) of the bladder to the nerve damage (neurogenic bladder) -> lack of bladder control
7
Q
renal failure investigations (4)
A
- Blood tests: Urea, Creatinine, Electrolytes
- Urine tests: Protein, RBCs, WBCs, Haemoglobin, Myoglobin
- Imaging studies: IVU, Ultrasound of the Kidneys, CT urogram, CT / MRI
- kidney biopsy: light/electron microscopy, IF
8
Q
clinical presentation of glomerular disease
A
glomerulus becomes leaky/ cannot filter through
presentations:
- Nephrotic syndrome: leaky filters
- Nephritic syndrome: some glomeruli leaky, some unable to filter
- Microscopic haematuria: mild leak
- ARF: sudden development of inability to filter
- CRF: slow development of inability to filter
9
Q
nephrotic syndrome**
- pathology + causes (5)
- clinical manifestations (4)
A
- leaky filter, w/o inflammation
causes
- Minimal change disease
- Idiopathic focal segmental glomerulosclerosis (FSGS)
- Membranous glomerulonephritis
- Membranoproliferative glomerulonephritis
- IgA nephropathy
- heavy proteinuria: 3.5g of protein loss/ day
- hypoalbunemia: liver cannot produce enough albumin to maintain normal serum levels
- Anasarca: generalized edema due to decrease in serum oncotic pressure -> starling’s forces
- lipiduria
10
Q
nephrotic syndrome
- clinical symptoms (2)
A
- generalised edema: face (eyelids), abdomen (ascites), ankle
- Large urine volumes with frothy urine
cause of high protein levels in urine -> decrease surface tension of liquid -> bubbling
11
Q
clinical consequence of nephrotic syndrome affecting diff age groups
A
- differential diagnosis
- affects response to steroidal therapy
children usually more sensitive to steroids
12
Q
nephritic syndrome
- pathology
- clinical manifestations (6)
A
- damaged glomeruli: some cannot filter, some leaky
- Oliguria: decrease in urine volume, because of poor filtration
- Azotaemia: elevation of serum creatinine level
- Oedema: due to fluid retention (but not as prominent as in nephrotic syndrome)
- HTN: due to fluid retention
- Gross hematuria: presence of RBCs in the urine, often with red cells found in urine microscopy
- Proteinuria
largely caused by IVDA
13
Q
glomerulonephritis
definition
A
includes diseases characterized by increased glomerular cellularity caused by proliferation of indigenous cells and/or leucocyte infiltration
14
Q
glomerular injury caused by antibodies
A
- In situ formation of Ag-Ab Complexes
against native antigen (Anti-GBM = Goodpasture’s disease - autoimmune against lungs/kidneys)
against planted antigen that localises in glomerulus (HBV) - Circulating immune complexes (lupus nephritis)
- Antineutrophil Cytoplasmic Antibodies (ANCA)
stimulate inflammatory response in the glomeruli -> glomerular injury
15
Q
diagnosis of immune complexes (3 methods)
A
- Immunofluorescence: Granular staining seen when immune complex is present
Allows determination of what types of antibody and complement involved
-> C3 = proteinuria, hematuria
-> IgM/ IgG - Electron microscopy:
Allows more precise localisation of immune complexes
identification of ultrastructural pathology (GBM abnormalities) - light microscopy
16
Q
other factors causing glomerular injury (2)
A
- Activation of alternative complement pathway
- platelets?
- Coagulation system: leakage of fibrin into Bowman space stimulates parietal cell proliferation and crescent formation
17
Q
minimal change disease
- causes what syndrome
- affects who
- clinical manifestation
A
- causes nephrotic syndrome
- esp in childhood
- selective proteinuria
- EM: fusion of foot processes and occasionally detachment from basement membrane
18
Q
Idiopathic focal segmental glomerulosclerosis (FSGS)
- causes what syndrome
- caused by
- clinical manifestation
A
- nephrotic syndrome, steroid resistant
- Due to podocyte injury with loss of podocytes
- light micro: some glomeruli show segmental sclerosis
- IF: sclerotic lesions stain with IgM and C3
19
Q
Membranous Glomerulopathy
- causes what syndrome
- affects who
- clinical manifestation
A
- causes nephrotic syndrome
- esp in adults (most common cause of nephrotic syndrome)
- LM: basement membrane thickening
- IF: IgG and C3
(“spikes” or “string of pearl appearance)
20
Q
post-infectious glomerulonephritis
(what happens after glomerulus infection)
- clinical manifestation
A
- IF: IgG and C3 in large granular deposits
- EM: sub-epithelial humps of large electron dense deposits
- most gets resolved - even w/o biopsy
21
Q
Membranoproliferative Glomerulonephritis
- causes what syndromes
- clinical manifestation
A
- nephrotic or nephritic syndrome
- LM: proliferative changes involving thickening of basement membrane
- decreased serum C3
22
Q
IgA nephropathy
- pathogenesis
- manifestation
- common cause
A
- Mesangial proliferation with mesangial deposits of immune complexes containing IgA
- microscopic proteinuria w/ hematuria
- could be caused by URTI
23
Q
glomerular damage caused by antibodies: lupus nephritis
- manifestation
A
- majority of SLE pts develop lupus nephritis - major cause of morbidity and mortality in lupus pts
- IF: IgG, IgA, IgM, C1q and C3 all present - strong immune complex deposits
24
Q
Rapidly Progressive Glomerulonephritis (RPGN)
- attention
- manifestation
A
- requires immunosuppressive treatment!! if not will progress to renal failure
- IF-pos: severe immune complex proliferative glomerulonephritis
- IF-neg: systemic vasculitis caused by ANCA antibodies
25
Q
Goodpasture’s Syndrome
- what is it
- consequence
A
- Anti-glomerular basement membrane disease Crescentic glomerulonephritis (anti-GBM antibodies)
- basement membrane of alveoli also attacked -> pulmonary hemorrhage
26
Q
Amyloidosis in kidney
- what is it
- diagnosis
A
- Extracellular accumulation of fibrillary proteins
- positive staining with the Congo red stain - cause of beta-pleated sheets
- apple green birefringence under polarised light examination
27
Q
Amyloidosis in kidney
- affects pts w/ what disease
- consequence
A
occurs in pts w/
- Plasma cell dyscrasia (AL amyloid)
- Chronic inflammatory diseases or neoplasms (AA amyloid)
- amyloid deposition in glomeruli, interstitium and blood vessels walls.
- > proteinuria
28
Q
Hypertensive nephrosclerosis
- clinical presentation
A
- proteinuria and/or impaired renal function
- Arterioles show hyalinosis w/ muscular thickening.
- Arteries show arteriosclerosis
29
Q
diabetic nephropathy
- pathogenesis
- complications
A
- Hyperglycaemia leads to the non-enzymatic glycosylation of collagen and other glomerluar matrix and GBM proteins
- > advanced glycation end-products (AGEs)
complications:
- ESRD (end stage renal disease)
- proteinuria
30
Q
diabetic nephropathy effects (5)
A
- glomeruli:
GBM thickening (seen on EM)
Mesangial widening (increase in matrix and cells) -> becomes nodular
Hyalinosis lesions
Microaneurysms of glomerular capillary loops.
glomerular sclerosis - tubules:
Thickened tubular basement membranes
Tubular atrophy - interstitium: Interstitial fibrosis
- vessels:
Arteriolar hyalinosis
Arteriosclerosis (often associated with hypertension). - pyelonephritis
