2023 S2 Renal Practical CSB520
2023 S2 Renal Practical CSB520
2023 S2 Renal Practical CSB520
Evolution and inheritance: Genetic mutations can propagate within a population only if they do not interfere
with our ability to replicate, for example if I have a novel mutation, it disappears with me if I do not pass it on
to the next generation. In the case of many disorders, genetic screening can ensure the birth of a child that is
neither affected with or a carrier of the disorder and yet many conditions prevail.
Autosomal recessive inheritance: Diseases that show autosomal recessive inheritance will continue even if
they impair fertility. This is due to the fact that to have these diseases you must inherit 2 mutated alleles, one
from each parent, if you only have one then you are an asymptomatic carrier of the condition.
Autosomal dominate inheritance: The ability of diseases with autosomal dominant inheritance to prevail
within a population is dependent upon their ability to interfere with fertility, however, many autosomal
dominant diseases only exhibit clinical symptoms in the 3rd to 5th decade of life, after a person has
propagated and thus potentially passed on the gene.
a. What has happened to the normal renal parenchyma in response to the formation and growth of the
cysts?
B. Neoplasms
2.0 Nephroblastoma (Wilms’ tumor)
Nephroblastoma excised surgically from a boy aged 5 and half years of age. This type of malignant tumour occurs in children, usually
before their fifth year of life. Hypertension, pain and haematuria are common symptoms associated with this tumour.
Question 2
b. The cancers in 2.2 and 2.3 are named papillary as they are growing in a papillary structure, what would
be the appropriate name based on their cell of origin?
c. Why are the names of the cancers in 2.0, 2.1 and 2.2 not the same?
d. Why are cancers of the kidney, ureter and bladder generally diagnosed late, what signs and symptoms
do patients present with?
a. Routes of entry for microbes infecting the kidney include haematogenous (descending) and urinary
(ascending) spread, what are the most significant differences between these?
3.4 Chronic glomerulonephritis (end stage kidney) (H&E) Note the massive reduction in both the number and size of
tubules (tubular atrophy) and progressive hyalinisation and loss of glomeruli. Hyaline is a complex of trapped plasma proteins,
increased mesangial matrix, basement membrane material and collagen.
a. What are the risk factors for atherosclerosis that are prioritized in the cardiovascular risk charts?
5.1 Urolithiasis
Impacted stone (urolith) in the ureter - note the chronic inflammatory response leading to thickened ureteric walls. Contraction of
the chronic proliferative inflammatory tissue (scar) in the wall of the ureter has produced a ureteral stricture. Hydronephrosis: back
pressure of urine has caused extensive loss of renal tissue, enlargement of the renal outline and accumulation of fluid in the dilated
spaces.
5.3 Hydronephrosis
Kinking of the pelvic-ureteric junction has produced a unilateral obstruction and hydronephrosis.
Question 5