BIOM3002 Lecture Notes - Lecture 6: Hypertensive Kidney Disease, Benign Prostatic Hyperplasia, Uterine Fibroid
26 May 2018
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HISTOPATHOLOGY
HISTOPATHOLOGY LECTURE SIX
TOPICS:
1. Vascular plexus problems: hypertensive kidney disease and
renal ischemia due to renal artery occlusion
2. Obstructive conditions lower urinary tract using benign
prostatic hyperplasia as an example [zones of prostate and
prostate adenocarcinoma]
3. Kidney infections/urinary tract infections e.g.
pyelonephritis
4. Features uterine fibroids e.g. benign neoplasms
Urinary system:
o Kidney [cortex, medulla, glomeruli, calyx and renal pelvis]
o Ureters
o Urinary bladder
o Urethra and prostate
Note: kidney = biggest energy user; lots of mitochondria in
different segments nephron
Proximal tubular epithelial cells: have large active
mitochondria, therefore nephron segment is particularly prone
to oxidant injury
Acute/chronic kidney disease: localised to 4 basic anatomical
compartments [glomeruli, tubules, interstitium and BVs]
1. Blood not cleansed; toxic contents build up
2. Fluid balance no longer automatic – need to watch what you
eat and drink
3. Hypertension common in people with kidney failure [cause and
complication]
4. Anaemia [without healthy BVs]
5. Calcium and phosphate imbalance; kidney disease-associated
bone disease
Describe vascular problems of the kidney including
hypertensive kidney disease and renal ischaemia due to renal
artery occlusion:
o Hypertension = outcome and contributing factor to CKD
o Significant atrophy
o Iman pathology starts as vascular disease
o Glomerulosclerosis – spot the glomerulus [attached nephron
has atrophied]
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HISTOPATHOLOGY
o Glomerular hypertrophy occurs, but with some sclerosis. Note
nephron atrophy with thick basement membranes [arrowed].
Normal nephrons
o Kidney ischemia from kidney artery occlusion
Acute kidney injury [AKI]:
o Sudden deterioration of renal function due to destruction of
tubules of nephron
o Usually due to an acute ischaemic or toxic event [causes an
acute tubular necrosis or AKI]
o Stenosis, trauma, nephrotoxic antibiotics
[cyclosporin, amphoterian], multiple myeloma, heavy metals,
myoglobinuria, x-ray contrast disc, aminoglycosides
o Kidney is highly vascularised
o Renal artery stenosis may restrict blood flow
o Acute ischaemic stress to the kidney causes acute renal
failure that may, or may not, resolve 'acute ischaemic
tubular necrosis' - glomerulus is reasonably healthy
o Apoptosis
Importance of tubulointerstitium: characterising AKI
o Kidney is highly vascularised
o Renal artery stenosis may restrict blood flow
o Acute ischaemic stress to the kidney causes acute renal
failure that may, or may not, resolve 'acute ischaemic
tubular necrosis' - glomerulus is reasonably health -
apoptosis
Functionally:
o Fall in glomerular filtration rate [GFR]
o Low or little urine
o Increased levels nitrogenous wastes in blood, primarily urea
and creatine
Structurally:
o Cell death [apoptosis and necrosis]
o Loss cell adhesion in intrinsic renal cell populations, in
particular renal tubular epithelium
Structurally, why do we get decreased glomerular filtration
rate [hallmark of acute renal failure]?
Vascular:
o Endothelial dysfunction
o Increased vasoconstriction
o Deceased vasodilation
o Increased adhesion acute inflammatory cells
Tubular:
o Cytoskeletal injury
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Urinary system: kidney [cortex, medulla, glomeruli, calyx and renal pelvis, ureters, urinary bladder, urethra and prostate. Note: kidney = biggest energy user; lots of mitochondria in different segments nephron. Proximal tubular epithelial cells: have large active mitochondria, therefore nephron segment is particularly prone to oxidant injury. Histopathology: glomerular hypertrophy occurs, but with some sclerosis. Note nephron atrophy with thick basement membranes [arrowed]. Normal nephrons: kidney ischemia from kidney artery occlusion. Acute kidney injury [aki]: sudden deterioration of renal function due to destruction of tubules of nephron, usually due to an acute ischaemic or toxic event [causes an acute tubular necrosis or aki, stenosis, trauma, nephrotoxic antibiotics. Functionally: fall in glomerular filtration rate [gfr, low or little urine, increased levels nitrogenous wastes in blood, primarily urea and creatine. Structurally: cell death [apoptosis and necrosis, loss cell adhesion in intrinsic renal cell populations, in particular renal tubular epithelium. Vascular: endothelial dysfunction, increased vasoconstriction, deceased vasodilation, increased adhesion acute inflammatory cells.
