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Histopathology 1

Alexander Wolff English 5.0Average rating 5.0 out of 5 (1 rating) 200 cards

briefly revise the anatomy of the kidney, including blood supply

Cards in this deck (200)

  1. 1briefly revise the anatomy of the kidney, including blood supplybriefly revise the anatomy of the kidney, including blood supply
  2. 2Briefly revise the anatomy of the nephronBriefly revise the anatomy of the nephron
  3. 3revise the function of the various parts of the nephronrevise the function of the various parts of the nephron
  4. 4familiarise yourself with the histology of the nephron- remember to also look in the book.familiarise yourself with the histology of the nephron- remember to also look in the book.
  5. 5name the three layers of the glomerulus-Endothelial cells
    - basement membrane (basal)
    - podocytes.
  6. 6name the charge of the basal membrane in the glomerulus, and give an example of its usefulness- negatively charged
    - this is the charge of albumin, preventing its filtration into the nephron.
  7. 7why are podocytes necessary?-their foot processes limit the removal of useful materials from the blood
  8. 8what is the purpose of tubules in the nephron?-primarily reabsorption
  9. 9disease of the nephron starts where? why is this important?- can start anywhere of: glomeruli, tubules, interstitium, and blood vessels.
    - dependent on the type of disease so can give away what the cause is by knowing where it has started.
  10. 10name the two types of glomerular disease- nephrotic and nephritic syndromes
  11. 11list the features of nephrotic syndrome- chronic
    - massive proteinuria- selective for albumin.
    - hypoalbuminemia
    -edema- due to proteinuria/loss of hydrostatic pressure
    -hyperlipidemia, seen as frothy urine
  12. 12in general, how does glomerular damage occur (autoimmune wise)-cross- reactions occur
    -Leads to local deposition of immune complexes/complement
    -become irregularly activated
  13. 13give the main features of nephrotic syndrome- Chronic
    -massive proteinuria (selective- albumin)
    -hypoalbuminemia
    -oedema- as a function of proteinuria (loss of hydrostatic pressure)
    - hyperlipidemia/uria- causing frothy urine
  14. 14describe the main features of nephritic syndrome- Acute
    - variable proteinuria- non-selective
    - haematuria
    - mild oedema
    - oliguria
    -azotemia
    - hypertension- loss of RAAS control
    -nephritic syndrome is much more easy to identify
  15. 15which of nephrotic and nephritic syndrome is the worst?- neither
    -both as bad as each other
  16. 16describe the pathophysiology of nephrotic syndrome on the kidney- initially loss of glomerular basal lamina sialoprotein
    - loss of normal negative charge
    - leads to increased vascular permeability
    - causes massive proteinuria/albuminuria
  17. 17describe how these effects of nephrotic syndrome effect the whole body- decrease in proteinemia
    - leads to decreased plasma oncotic pressure
    -fluid therefore shifts from the vascular to interstitial compartments- oedema
    - contraction of plasma volume occurs
  18. 18why is nephrotic syndrome important haematologically?- can cause loss of platelets and coagulation factors
    - leads to hypothrombotic status
  19. 19what damage actually occurs to the glomerulus in nephrotic syndrome?- - loss of foot processes from podocytes
    - remember that this is not followed by inflammation or proliferative response
  20. 20approximately what level of proteinuria is seen in nephrotic syndrome?- >3.5g/day
    -massive
  21. 21how does nephrotic syndrome manifest itself in children?- minimal change disease
    -focal segmental glomerularnephritis
    - membranous glomerularnephritis
  22. 22how does nephrotic syndrome manifest itself in adults?- from systemic disease (such as diabetes)
  23. 23what is the commonest cause of nephrotic syndrome in childhood?-minimal change disease/glomerulopathy
  24. 24what is the basis of minimal change disease?- immune
    - however has no detectable immune deposits
  25. 25what associations to minimal change disease are there?- resp. infection, and immunisation
  26. 26give some clinical features of minimal change disease in children- very important: periorbital oedema
    - look for any increased weight
    - responds well to corticosteroids
  27. 27analyse the H and E stained glomerulus from someone with minimal change - notice the lack of difference between this and normal -no difference in basement membrane thickness/cellularity -damage only visible on electron microscopyanalyse the H and E stained glomerulus from someone with minimal change - notice the lack of difference between this and normal -no diffe...
  28. 28analyse the electron microscopy for minimal change disease -can see diffuse effacement of the foot processes (fusing) compared to normal -remember that this is not visible in light microscopyanalyse the electron microscopy for minimal change disease -can see diffuse effacement of the foot processes (fusing) compared to normal ...
  29. 29describe focal segmental glomerulosclerosis- can be primary or secondary
    - some (focal-not kidney-wide) glomeruli show partial (segmental) hyalinisation
    -of unknown pathogenesis
    -has a poor prognosis
  30. 30what problem occurs in FSGS biopsies?-the need to take many samples to find the focal segments- otherwise could think the problem is not present
  31. 31name a problem in treating FSGS- doesn't respond well to corticosteroids
  32. 32what is the main pathophysiological reason for membranous glomerulonephritis?- a deposition of anti-glomerular basal membrane antibodies occurs
  33. 33how does this lead to disease?-causes a thickened glomerular basal membrane
    -leads to subepithelial deposits/spikes
  34. 34in what group of individuals in membranous glomerulonephritis most common?- adults
  35. 35what are the causes of MGN?- 85% of the time- idiopathic
    - 15% secondary to malignancy (tumours), SLE, drugs, chronic infection
  36. 36look at the histopathology image overleaf of MGN -see how capillaries are much thicker due to immune complexes within the basal membrane - also note the lack of increased cellularitylook at the histopathology image overleaf of MGN -see how capillaries are much thicker due to immune complexes within the basal membrane ...
  37. 37give the general changes seen in an acute nephritic syndrome- inflammation, vascular and epithelial damage
    - +/- proliferation of glomerular cells
  38. 38give some signs/symptoms of nephritic syndrome- haematuria
    - azotemia (increased level of nitrogenous compounds in blood such as urea)
    - oliguria
    - mild oedema (facial puffiness)
    - variable proteinuria
    -mild to moderate hypertension
  39. 39what key feature shown in microscopy could give away a proliferative glomerulonephritis?- increased number of cells (increased cellularity)
  40. 40name three forms of membranoproliferative (mesangiocapillary) glomerulonephritis- diffuse membranoproliferative glomerulonephritis
    -crescentic glomerulonephritis
    - lupus nephritis
  41. 41describe the glomerulonephritis'- primary or secondary to systemic disease
    - immunological aetiology AND shows immune complex deposition in capillaries and glomerulus
  42. 42what three types of immunological substances are found in glomerulonephritis?- immune complexes- complement deposited from the local circulation
    - anti-glomerular basal membrane antibodies
    - antibodies against glomerular components
  43. 43what difference in outcome is seen between adults and children with glomerulonephritis?-normally a benign in children (occurs most commonly post-infection)
    - permanent compromise of renal function in adults
  44. 44name an example of a glomerulonephritis condition involving local deposition of circulating immune complexes- acute proliferative glomerulonephritis
    - this is the major cause of acute nephritis in childhood
  45. 45when is acute proliferative glomerulonephritis most likely to occur?- in children
    - arising from a group A-hemolytic streptococcal infection
  46. 46study image overleaf demonstrating acute proliferative glomerulonephritis -shows marked increase in glomerular cellularity - "endocapillary hypercelluarity" - numerous neutrophils can be seen - closure of glomerular vessels -increased cell sizestudy image overleaf demonstrating acute proliferative glomerulonephritis -shows marked increase in glomerular cellularity - "endocapilla...
  47. 47name a glomerulonephritis that shows antibodies against glomerular components- membranoproliferative glomerulonephritis (MPGN)
  48. 48give features of MPGN- presents with a combined nephritic/nephrotic picture
    - crescentic or rapidly progressing glomerulonephritis ("can cause renal failure within weeks")
  49. 49picture overleaf for MPGN -note the increase in mesangial substance (proliferation of mesangial cells) - localised capillary wall thickening - increased cellularity -pronounced lobulationpicture overleaf for MPGN -note the increase in mesangial substance (proliferation of mesangial cells) - localised capillary wall thicken...
  50. 50how is acute tubular necrosis (ATN) caused?- by ischaemic or toxic tubular injury
    - toxic injury by drugs, radio contrast dyes, haemoglobin, myoglobin
    - disseminated intravascular coagulation
    - urinary obstruction
  51. 51how might disseminated intravascular coagulation cause ATN?- by up regulating clotting cascade
    - lots of mini clots
    -ischaemia
  52. 52what is the prognosis for most patients who suffer acute tubular necrosis?- most recover
    - most of the time is reversible
  53. 53why does lack of perfusion effect the tubules mainly?- they are the area with the highest metabolic rate and therefore require most perfusion for exchangers etc
  54. 54what clinical sign might be an indication of a more advanced acute tubular necrosis (ATN)?- polyuria
  55. 55image overleaf showing ATN - notice the focal necrosis - desquamation of the cells into the tubular lumenimage overleaf showing ATN - notice the focal necrosis - desquamation of the cells into the tubular lumen
  56. 56what is the basis of a tubulointerstitial nephritis (TIN)?- an inflammatory reaction of the tubules and interstitium
  57. 57name three causes of this TIN- acute pyelonephritis
    - chronic pyelonephritis and reflux nephropathy
    - drugs and toxins- analgesic nephropathy
  58. 58what nephropathy is commonly caused by UTI?-reflux nephropathy
  59. 59name two groups at risk of reflux nephropathy- women (smaller urethra), elderly
    - patients with catheters/ malformations
  60. 60give two common signs/symptoms of UTI/reflux nephropathy- dysuria
    -frequency
  61. 61what are the two most common bacteria found in UTI?- E-coli
    -proteus
  62. 62image overleaf of acute pyelonephrisis specimen - shows whiter abscess's in cortex -remember this is usually unilateral and effects multiple parts of the kidneyimage overleaf of acute pyelonephrisis specimen - shows whiter abscess's in cortex -remember this is usually unilateral and effects multi...
  63. 63what might someone with acute pyelonephritis present like?- fever
    -escalated creatinine
  64. 64acute pyelonephritis histology -note the acute inflammatory infiltrate in the interstitium and tubular laminaacute pyelonephritis histology -note the acute inflammatory infiltrate in the interstitium and tubular lamina
  65. 65describe chronic pyelonephritis- causes a devastated renal structure with multiple scars
    - much more aggressive than acute phase
    - can lead to chronic renal failure
    -can affect both kidneys simultaneously- however scaring is asymmetrical
  66. 66image of chronic pyelonephritis on a kidney specimen - kidney is irregularly depressed with pseudo bulging of the intact parenchyma -cut surface would reveal dilated, blunted or deformedimage of chronic pyelonephritis on a kidney specimen - kidney is irregularly depressed with pseudo bulging of the intact parenchyma -cut ...
  67. 67image to show histology of chronic pyelonephritis -remember to understand that this shows colloid filled tubules - this is known as THYROIDISATION of the kidney- a key feature of chronic pyelonephritisimage to show histology of chronic pyelonephritis -remember to understand that this shows colloid filled tubules - this is known as THYRO...
  68. 68just for reference- an image of thyroid tissue to show you why the colloid structure seen in chronic pyelonephritis is named thyroidisationjust for reference- an image of thyroid tissue to show you why the colloid structure seen in chronic pyelonephritis is named thyroidisation
  69. 69describe the pathogenesis of benign nephrosclerosis- focal sclerosis of renal arterioles and smaller arteries
    -leads to focal ischaemia
    - cortical scarring occurs
  70. 70when does this exist/who does this exist in?- some degree of nephrosclerosis is found in most autopsies- old age
    - hypertension and diabetes
    -both of these increase the severity of the lesions
  71. 71what can accelerate nephroscelrosis?- malignant hypertension
    -may be rapid in onset and is much more severe with this aetiology
  72. 72slide to show histology of nephrosclerosis - notice the granular surfaces - also has fibrous intimal thickeningslide to show histology of nephrosclerosis - notice the granular surfaces - also has fibrous intimal thickening
  73. 73give two broad reasons for cystic disease of the kidney- congenital/malformative
    - acquired
  74. 74give two examples of congenital cystic diseases of the kidney-multicystic renal dysplasia- most common cause of abdominal mass in a newborn
    - medullary sponge kidney
  75. 75image and labels to demonstrate medullary sponge kidney -doesn't involve the corteximage and labels to demonstrate medullary sponge kidney -doesn't involve the cortex
  76. 76give two acquired causes of cystic kidney disease and give a brief line of how they are caused- acquired renal cystic disease- mainly post-dialysis
    - simple cysts - most common abnormality of the kindey
  77. 77give three causes of cystic kidney disease- autosomal dominant (ADULT) polycystic kidney disease
    - autosomal recessive (INFANTILE) polycystic kidney disease
    -Nephronophthis-medullary cystic kidney disease complex
  78. 78what is the prevalence of adult polycystic disease?- 1 in 500
  79. 79describe adult polycystic disease (APD)- autosomal dominant
    - bilateral
    -presents in middle age
  80. 80how does APD present clinically?- Haematuria
    - UTI
    - abdominal mass
    - hypertension
    - associated with cerebral aneurysms, subarachnoid haemorrhage
    - also associated with other organ cystic disease (45% have liver cysts/lung cysts/splenic and pancreatic cysts)
    -increased stone probability
  81. 81why do symptoms of APD take years to show, despite it being genetic?- due to renal reserve
    -make sure you view scans of PCKD
    -familiarise yourself with the gross anatomy of a PCKD kidney
  82. 82what is the biggest complication of PCKD?- chronic renal failure
  83. 83what is involved in the management of PCKD?- supportive care
    - treat the hypertension
    - some will need dialysis
    - some will need a transplant
  84. 84how common is infantile polycystic kidney (IPCK) disease?- 1 in 20,000
    -remember this is autosomal recessive
  85. 85what is the most common sign of IPCKD?- large abdo masses bilaterally
    -also commonly associated with liver abnormalities (hepatic fibrosis, biliary dysgenic, bile duct ectasia)
  86. 86What is a Potter phenotype?- a prevention of the development of the lungs
    - is found in IPCKD
    - due to reduced amniotic fluid (oligohydramnios) and associated with cranial abnormalities also
  87. 87what does IPCKD mean for an infant?in SEVERE cases- death
    - renal failure
    - hypertension
    - portal hypertension
  88. 88what cystic disease of the kidney is found routinely in biopsies?-simple renal cystswhat cystic disease of the kidney is found routinely in biopsies?
  89. 89essentially, what is the cause of chronic renal failure?- abnormal kidney function/ structure
  90. 90chronic renal failure is the end result of which diseases?- glomerulornephritis- 40%
    - chronic pyelonephritis-20%
    -polycystic disease- 9%
    - vascular- 8%
    - multi system diseases- 9%
    - drugs- 3%
    -is commonly unrecognised
  91. 91why might chronic renal failure be easy to miss?- can be asymptomatic until it progresses into end stage renal disease
    -mainly due to reserve
  92. 92what are the two main causes of chronic renal failure to look out for?-DIABETES
    -HYPERTENSION
  93. 93view table overleaf demonstrating the stages of chronic kidney disease -refer to the histopathology handbook page 12 first slideview table overleaf demonstrating the stages of chronic kidney disease -refer to the histopathology handbook page 12 first slide
  94. 94gross specimen of benign glomerulosclerosis kidney -note the granular appearance -but also note the relatively similar morphology to normal kidney (maintains most structure)gross specimen of benign glomerulosclerosis kidney -note the granular appearance -but also note the relatively similar morphology to norm...
  95. 95what is the most common cause of acute renal failure? (ARF) -how can we define ARF?- acute kidney injury
    -a rapid reduction in renal excretory function (within 48 hours)
  96. 96what occurs in ARF?- absolute increase in serum creatinine >= 0.3 mg/dl
    -serum urea, Cr, K with anuria/oliguria (<15ml/hr)
    -reduction in urine output (oliguria) less than 0.5ml/kg per hour for more than 6 hours
  97. 97broadly speaking, what are the two phases of acute renal failure? -explain each- oliguric phase- creating a metabolic acidosis due to increased urea production
    -recovery phase- polyuria
  98. 98ARF is often uni or bilateral?- bilateral
  99. 99broadly, there are three causes of ARF - what are they?- pre-renal
    -renal-parenchymatous
    -post-renal/obstructive
    -all three reduce GFR
  100. 100name some pre-renal causes of ARF- anything effecting renal perfusion
    - shock
    - renal artery stenosis
  101. 101give some renal/parenchymal causes of ARF- ATN
    -acute interstitial nephritis
    -CRF
  102. 102give some post renal causes of ARF- obstructive lesions
    -stones
    -tumours
    -effects urine output
  103. 103define nephrolithiasis- stone formation either in the kidney or renal tract
  104. 104who is effected by nephrolithiasis? -what are the recurrence rates?- 20-30 year olds
    -M>F
    - 5% of the population
    -recurrence stands at 40-70%
    - symptomatic- 50% will cause some problem within 5 years of discovery
  105. 105what are stones made of?- calcium oxalate- hypercalcemia/idiopathic hypercalciruria (75%)
    - triple phosphate (magnesium ammonium calcium phosphate)- this can be caused by a proteus infection which splits urea into ammonium (Staghorn calculus)- 15%
    -urate (hyperuricaemia-GOUT)-6%
    -Cystine- in born error of metabolism-1%
  106. 106have in the back of your mind that proteus can cause or at least help to create nephrolithiasisok
  107. 107image to demonstrate stone types and formations -uric acid crystals can become lodged/stuckimage to demonstrate stone types and formations -uric acid crystals can become lodged/stuck
  108. 108list of predisposing conditions for nephrolithiasislist of predisposing conditions for nephrolithiasis
  109. 109name a childhood renal tumour- Wilm's tumour
  110. 110name two types of benign renal tumours- papillary adenoma- often found at autopsy (<5mm)
    -Fibroma
  111. 111name two forms of malignant renal tumours- and how common they are- renal cell carcinoma- 80%
    - transitional cell carcinoma- 20%
    -epithelial tumours
  112. 112why is mortality lower for renal cancer?- techniques such as dialysis exist
  113. 113what risk factors exist for renal cell carcinoma?- hypertension, obesity, heavy metals
    -Von Hippel Lindau syndrome
  114. 114what is Von Hippel Lindau syndrome?- collectively made up of:
    -haemangioblastoma of the cerebellum, retinal detachment
    - renal cysts
    -bilateral renal cell carcinoma
  115. 115how might RCC present?- polycythaemia, hypercalcaemia, liver dysfunction, Cushing syndrome, amyloidosis
    -palpable mass
    - haematuria
    - back pain
  116. 116what three histotypes exist for RCC?- clear cell
    - papillary
    -chromophobe- has complicated genetics
  117. 117what is the prognosis like for RCC?- 5 years is 70% IF no mets
    - 45% IF mets
  118. 118image to show gross anatomy of kidney with RCCimage to show gross anatomy of kidney with RCC
  119. 119image to show histology of a clear renal cell carcinoma -demonstrates a clear cytoplasm - and a sharply outlined membraneimage to show histology of a clear renal cell carcinoma -demonstrates a clear cytoplasm - and a sharply outlined membrane
  120. 120image to show renal pelvis carcinoma -familiarise yourself with this image -normally found in the renal pelvis- transitional cell carcinoma (remember that the only part of the kidney that is transitional cell is the pelvis)image to show renal pelvis carcinoma -familiarise yourself with this image -normally found in the renal pelvis- transitional cell carcino...
  121. 121-Low-grade transitional cell carcinoma of renal pelvis growing in a pushing fashion around the medullary renal tubules-Low-grade transitional cell carcinoma of renal pelvis growing in a pushing fashion around the medullary renal tubules
  122. 122how common are tumours of the urinary bladder?Represent 7% of cancer in USA with 3% cancer mortality and in 90% of the cases they arise from the urothelium
  123. 123what percentage of tumours of the urinary bladder are benign?- 1%
    -Papilloma
  124. 124what is the problem with these benign papilloma's?- they have malignant potential
    - e.g. papillary urothelial neoplasm with low malignant potential (PUNLMP)
  125. 125what two malignancies are there in the bladder?- low grade papillary urothelial carcinoma
    - high grade urothelial carcinoma
  126. 126slide showing papilloma of urinary bladder - just a reminder- make sure you observe the normal histology of the bladder/ any structure on google -be able to distinguish different tumoursslide showing papilloma of urinary bladder - just a reminder- make sure you observe the normal histology of the bladder/ any structure on...
  127. 127give some risk factors for bladder carcinoma- smoking
    -industrial exposure to arylamines
    - previous irradiation
    -long term use of analgesics
    cyclophosphamide
    - Schistosoma Haematobium- causes squamous cell carcinoma
  128. 128image to demonstrate histology of infected bladder-  Schistosoma Haematobium-- shows eggs of Schistosoma haematobium surrounded by intense infiltrates of eosinophils -chistosoma haematobium is a diagenetic trematodeimage to demonstrate histology of infected bladder-  Schistosoma Haematobium-- shows eggs of Schistosoma haematobium surrounded by inten...
  129. 129name the most useful symptom to diagnose epithelial tumours of the bladder- painless haematuria
  130. 130give some facts about epithelial tumours of the bladderRecurrence
    Papillomas, PUNLMP and LG Pa Carcinomas 98% of survival at 10 years with 10% progressing toward high grade.
    HG Pa Carcioma 75% of survival at 10 years
    Rare variants (squamous and adenocarcinoma have a worse prognosis)
  131. 131give some general information about the the anatomy of the testis- normally paired, lying within the scrotum suspended by the spermatic cord
    -covered by capsule with three layers: 1) outer serosa/tunica vaginalis. 2) tunica albuginea and 3) tunica vasculosa
    -the posterior part of the capsule is named the mediastinum, containing blood and lymph nodes, nerved and the mediastinal portion of the reti-testis (anastomosis of lobules- sperm from seminiferous tubules to efferent ducts
  132. 132image for the anatomy of testisimage for the anatomy of testis
  133. 133describe the histology of the testis- the parenchyma (the functional part of the organ), is divided into 250 different lobules
    -each lobule contains up to four seminiferous tubules
  134. 134what do these tubules contain?- Sertoli cells
    -germ cells
    -in various stages of their development- spermatogonium, primary, secondary spermatocyte, spermatid, spermatozoon (mature)
  135. 135who histology of testiswho histology of testis
  136. 136histology of lobules within testishistology of lobules within testis
  137. 1371) what is the function of Sertoli cells? 2) what is the function of leydig cells?1) keeps germ cells nourished and healthy
    absorb extra cytoplasm in order to create new spermatazoa
    2) produce testosterone for germ cell development in the presence of LH
  138. 138another testis histology imageanother testis histology image
  139. 139a basic description as to the function of the various histologically identifiable components of the testis- the intersitium contains stromal (connective) cells and leydig cells
    - rete testis- hilum of the testis- receives the luminal contents of the seminiferous tubules
    - empties this contents into the ductuli efferentis, which consists of 12-15 aggregated tubules in the head of the epididymis
  140. 140describe the structure of the epididymis- tubular structure
    -connects the ductili efferentis to the vas deferens
    - vas deferens- 30-40 cm tubular structure, empties into the prostatic urethra at the level of the velumontanum
    -the distal portion of this joins the excretory duct of the seminal vesicle to form the ejaculatory duct
  141. 141how common are testicular tumours?- most common tumour of males in the age group 15-34 (peak incidence)
    -accounts for less than 1% of all cancer deaths in the UK- treatment is good!
  142. 142how can we classify testicular tumours?- germ-cell tumours- 90%
    - sex-cord stromal tumour
    - mixed germ cell/sex-cord stromal tumours
    - primary tumours not specific to the testis
    -metastatic tumours
  143. 143describe germ cell tumours of the testis (GCT)- if present, tend to be malignant
    - derived from germ cells
    -therefore can divide into any embryonic or extra embryonic tissue
  144. 144how can GCT of the testis presents clinically?- painless unilateral enlargement of testis
    - secondary hydrocele
    - symptoms from metastases (ask history)
    - retroperitoneal mass
    - gyneacomastia (enlargement of male breast tissue)
  145. 145table to show types of germ cell tumours of the testis and their precursorstable to show types of germ cell tumours of the testis and their precursors
  146. 146give some risk factors for GCT of the testis- Cryptorchidism (undescended testis) - higher the location, greater the risk
    - genetic predisposition- siblings have 10-fold high risk
    -africans (black pop) have low incidence
    - testicular dysgenesis e.g. testicular feminisation/klinefelter syndrome
  147. 147what genetic change is associated with a higher risk of GCT of the testis?- isochromosome of the short arm of 12- in 90% cases
    -sometime involve chromosome 1
  148. 148briefly define an in-situ tumour- in which the tumour has not infiltrated the BM
  149. 149what broad classifications are there for GCT of the testis?- in- situ
    - invasive
  150. 150name an in-situ tumour of the testis- intratubular germ cell neoplasia
  151. 151name some invasive GCT of the testis- seminoma
    - non- seminomatous germ cell tumours such as:
    1) embryonal carcinoma
    2) yolk sac tumour
    3) choriocarcinoma
    4) teratoma
    -can also be a mixture
  152. 152describe an intra-tubular germ cell neoplasia of the testis (ITGCN)- in situ
    - proliferation of neoplastic germ cells within seminiferous tubules
    -up to 80% pf GCT show ITGCN
    - sometimes seen in the biopsy performed for the study of infertility or cryptorchidism
  153. 153histology of ITGCN -note the thick basement membrane - ITGCN cells present (whitish)histology of ITGCN -note the thick basement membrane - ITGCN cells present (whitish)
  154. 154another ITGCN imageanother ITGCN image
  155. 155describe seminoma- commonest type of testicular tumour (infiltrative)
    -main subtypes:
    1) classical- most common
    2) spermatocytic
  156. 156describe classical seminoma- peak incidence in the 4th decade of life
    - histologically- sheets of rounded cells with a clear cytoplasm
    - has variable lymphocytic infiltrate in the stroma
  157. 157histology of classical seminoma -look at the infiltrative lymphocyte -also white cytoplasmic cellshistology of classical seminoma -look at the infiltrative lymphocyte -also white cytoplasmic cells
  158. 158describe spermatocytic seminoma- 3-5% of all seminoma
    - older age affected more
    - mixed population of small, intermediate and giant cells with increased mitotic rates (histology)
    - prognosis is excellent
  159. 159histology of spermatocytic seminoma -note the varying sizes of the cells - due to the rapid proliferation/mitotic ratehistology of spermatocytic seminoma -note the varying sizes of the cells - due to the rapid proliferation/mitotic rate
  160. 160describe embryonal carcinoma - malignant teratoma, undifferentiated- occurs mostly in 20-30 years age group
    - more aggressive than seminoma
    - M/S the cells are anaplastic and arranged in glandular, alveolar, solid or papillary growth
    -usually associated with other germ cell tumour- pure form only accounts for 3% of GCT
  161. 161histology of teratoma (MTU)histology of teratoma (MTU)
  162. 162describe a yolk sac tumour- "pure form" occurs in children- most common GCT in infants and children up to the age of 3- good prognosis
    - in adults this is associated with embryonal carcinoma
    -serum levels of AFP are raised and the neoplastic cells are positive for AFP
  163. 163what is AFP?- alpha-fetoprotein
  164. 164what does the histology look like for yolk sac tumours?- has variable morphology
    - Schiller-Duval bodies- formed by perivascular layer of tumour cells
  165. 165characteristic Schiller-Duval bodies shown in 50% of yolk sac tumourscharacteristic Schiller-Duval bodies shown in 50% of yolk sac tumours
  166. 166another image of yolk sac tumouranother image of yolk sac tumour
  167. 167describe choriocarcinoma (also called a malignant transformation of a testicular teratoma- MTT)-occurs on its own in only 0.3% cases
    -however is found in 1.5% of NSGCT- these have choriocarcinomatous components
    -highly malignant
  168. 168choriocarcinoma- MTT, is composed of what two types of cells?- cytotrophoblasts
    -syncitiotrophoblasts
    -these have embryonic origins
  169. 169what serum component is raised in choriocarcinoma?-HCG
  170. 170histology of choriocarcinoma -note the abundant syncitiotrophoblasts -in some cases these might be less conspicuous/non-existenthistology of choriocarcinoma -note the abundant syncitiotrophoblasts -in some cases these might be less conspicuous/non-existent
  171. 171describe a teratoma- these tumours can differentiate into any of the three germ cell layers
    -PURE teratoma (TD) 2nd most common in children-has a good prognosis
    -in adults, pure form is rare- only 2-3%- treated as malignant due to metastatic potential
  172. 172what two tissue types exist in teratoma's?- mature- adult form- TD
    -immature - fetal type
  173. 173teratoma hiology -important to note the different cell lines/tissue types - cartilage, respiratory epithelium, thyroid tissue in this slideteratoma hiology -important to note the different cell lines/tissue types - cartilage, respiratory epithelium, thyroid tissue in this slide
  174. 174how common are mixed testicular germ cell tumours?- 14% of all testicular GCT
    - can be in various combinations- e.g. semioma and NSGCT
    - treated as NSGCT
  175. 175how do GCT disseminate/move/metastasise?- directly to rete testis and epididymis
    - via lymphatics and then to mediastinal lymph nodes
    - via blood to the lungs, liver and bone- teratoma
  176. 176what factors determine the prognosis of a GCT?- type of the tumour
    - stage of disease
    - size of the tumour
    - involvement of rete testis
    - vascular invasion
  177. 177describe stage 1 of the GCT staging system- earliest stage of invasive testicular cancer
    - contained in the testicle
    - hasn't spread to nearby lymph nodes or other organs
    - e.g. stage 1S= raised markers after surgery
  178. 178describe stage 2 of the GCT staging system- cancer cells have spread into the nearby lymph nodes in abdomen or pelvis
    -marker level may be normal - S0, or raised slightly- S1
    - split into 2a, b and c
  179. 179describe stages: 2A 2B 2C of the GCT staging system- 2A= lymph nodes smaller than 2cm
    - 2B lymph nodes between 2cm and 5cm
    - 2C means at least one lymph node bigger than 5cm
  180. 180describe stage 3 of the GCT staging system -describe stage 3A- split into A,B,C
    - 3A- cancer has spread to distant lymph nodes- for example collarbone or lungs. Marker level may be S0 or S1
    -
  181. 181describe stage 3B of the GCT staging system- 3B cancer has spread to nearby nodes- moderately high marker levels- S2
    - OR cancer has spread to lungs or distant lymph nodes and have a moderately high marker level- S2
  182. 182describe stage 3C of the GCT staging system- same as stage 3B, but very high marker level- S3
    - OR cancer spread to another organ- such as liver or brain
    -used to be called stage 4
  183. 183slide discussing anatomy of the prostateslide discussing anatomy of the prostate
  184. 184anatomy and orientation of prostateanatomy and orientation of prostate
  185. 185glandular prostate tissue -overlead-whole prostateglandular prostate tissue -overlead-whole prostateglandular prostate tissue -overlead-whole prostate
  186. 186describe nodular hyperplasia (BPH)-very common in men over age of 50 years (70% by the age of 60)
    - involves periurethral region of the prostate
    - results in urinary retention
    - caused by androgen release- dihydrotestosterone (DHT)
    - increased weight 60-100 grams
  187. 187- histology of BPH - note that both the glandular and stromal components are subject to hyperplasia- histology of BPH - note that both the glandular and stromal components are subject to hyperplasia- histology of BPH - note that both the glandular and stromal components are subject to hyperplasia
  188. 188describe carcinoma of the prostate- most common form of cancer in males
    -second commonest cause of death
    - increased incidence after the age of 50
    -Blacks>whites>asian
  189. 189table showing incidence of carcinoma of the prostate broken down into age groupstable showing incidence of carcinoma of the prostate broken down into age groups
  190. 190what is the aetiology of carcinoma of the prostate?- multifactorial
    -hormones- androgen receptor
    - genetic susceptibility genes- 1q24-25, 1st degree relatives
    -fat consumption
    - lycopene in tomatoes reduces risk
  191. 191a premalignant lesion, such as PIN, is associated with what percentage of prostatic Adenocarcinomas?- 59-100%
  192. 192describe the grading system for grading carcinomas of the prostate- Gleason's score- dependent on growth patterns
  193. 193describe staging of carcinomas of the prostate- stage A- not palpable
    -stage B- palpable, confined to prostate
    -stage C- extracapsular extension
    - stage D- metastatic
  194. 194histology of adenocarcinoma -The single most important diagnostic morphologic feature is the complete absence of basal cell layer normally present around benign prostate glands. Thus, normal prostate glands have a double cell layer, the inner glandular cells and an outer basal layer whereas in prostate cancer the outer basal cell layer is absent.histology of adenocarcinoma -The single most important diagnostic morphologic feature is the complete absence of basal cell layer normall...
  195. 195histology of adenocarcinoma of the prostate -Additional histological features supporting a diagnosis of carcinoma are the presence of intraluminal crystals (arrow) and intraluminal mucin.histology of adenocarcinoma of the prostate -Additional histological features supporting a diagnosis of carcinoma are the presence of int...
  196. 196how do we diagnose carcinoma of the prostate?- looking at raised PSA levels- range according to age: 50-59 >3mg/ml, 60-69 > 4mg/ml, 70 yrs and older >50mg/ml
    - digital PR exam
    -imaging
    -biopsies
  197. 197quickly remind yourself: -anatomy of the respiratory system- extends from nasal cavity orifices to the periphery of the lung and surrounding pleuraquickly remind yourself: -anatomy of the respiratory system
  198. 198describe the histology to the respiratory tract- nose-> distal bronchus= pseudo stratified ciliated columnar epithelium with mucus secreting goblet cells
    - portion of larynx and nasal vestibules = stratified squamous
  199. 199what are the anatomical constituents of the lower resp tract?- trachea
    -bronchi
    - bronchioles
    - alveolar ducts
    -alveoli
  200. 200describe the path of bronchioles- branch until they form terminal bronchioles
    -<2mm diameter
    - distal to the terminal bronchiole- acinus Or terminal respiratory unit
    -gas exchange occurs at these units

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Flashcards on Histopathology 1, created by Alexander Wolff on 07/09/2017.
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Alexander Wolff
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