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33 Cards in this Set

  • Front
  • Back


Arteriovenous malformation


Histopathological


- Totuous blood vessels


- Evidence of hemorrhage


- Gliotic scar tisue (evidence of hemorrhage) separating vessels


- Hyalanised blood vessles




Clinical


- AVM most common type of clinically significant vascular malformation


- Males affected 2x more


- Recognised b/w 10-30 yoa.


- Presenting as a seizure disorder, an intracerebral hemorrhage or subarachnoid hemorrhage.


- Mot common site are posterior branches of MCA




DDx


Cavernous malformations: Distended, loosely organised vascular channels with thin collagenous walls devoid of nervous tissue


Capillary talengiectasias: Microscopic foci of dilated, tin-walled vascular channels, separated by normal brain parenchyma




Treatment


- Microsurgical resection


- Endovascular embolisation





Meningioma


- Predominately benign tumor in adults, usually attached to the dura, arising from meningothelial cells of the arachnoid.


- A very vascular lesion


- Found along the external surfaces of the brain as well as in the ventricular system




Clinical features


- Slow growinglesions, varying from vague non-specific symptoms to focal findings due to underlying compression


- 3:2 female occurence


- Has progesterone receptors, therefore may be exacerbated in pregnancy




Morphology


- Rounded mass with well defined dural base that can compress the brain but is easily separated from it


- Surface of the mass is usually encapsulated within a thin, fibrous tissue


- Presence of syncitial 'whorled' pattern that sit in tight clusters


- 'Psamomma' bodies, calcification of these syncitial masses.


- Elongated cells, eosinophillic cytoplasm, round, uniform nuclei




DDx


- stress


- Migraine


- Drug/ alcohol abuse


- Other space occupying lesion (cyst, glioma etc.)




Treatment


- surgical removal

Glioblastoma multiformae


- This is a 'high grade' astrocytoma




Clincial features


- Depend on the location and growth rate


- Well- differentiated may remain static or progress only slowly


- However, clinical deterioration occurs, usually with appearance of more rapidly growing tumor of high histological grade.


- In class, it as a 69 year-old man becoming more forgetful, difficulty concentration, morning headaches w nausea + some weakness in his left arm




Macroscopic


- Intraparenchymal, variable size, poorly delineated


- Some areas are firm and white, others are soft and yellow (necrosis), other areas show cystic degeneration and hemorrhage




Microscopic


- Necrosis is a key among other DDx


- Pleiomorphic, hyperceullular, mitotic figures w' enlarged and hyperchromatic nuclei. Cells pseudo-palliasaide around areas of necrosis.


- Vascular/ endothelial cell proliferation forms 'tufts' of piled up cells, 'glumeruloid bodies'


- Areas of hemorrhage may be present




- Believed to arise from lower grades, with a genetic involvement of P53 knock out/ PDGF-A overexpression




DDx


- lower grade astrocytomas; diffuse astrocytoma, anaplastic astrocytoma (no necrosis)



Oligodendroglioma


- 5-15% of glioma


- Mostcommonly occurs in the 4-5th decades


- Patients may have had several years of neurological complaints, often including seizures.


- Lesions often occur in the hemispheres, witha predilection for white matter




Macroscopic


- Well circumscribed, gelatinous, grey mass.


- Often present with macroscopic cysts, hemorrhage and calcification




Microscopic


- Sheets of regular clls w' spherical nuclei containing fine granular chromatin, surrounded by clear cytoplasm 'fried egg'


- Delicate network of anastamosingcapillaries


- Calcification in 90%, from microscopic foci to massive depositions


- Microcystic degeneration


- Perineuronal stellatosis (branching of lesion to local neurons)


- Mitotic activity DIFFICULT to observe


Astrocytotic tumor cells may also be present




Notes


-Better prognosis that glioblastoma/ other astrocytomas


-Tx by surgery, chemo, radio,


-Avg survival of 5-10 years



Spinal Scwannoma


- Benign tumors that arise from neural-crest derived schwaan cells


Cause symptoms by local compression of the involved nerve


- In the cranial vault, commonly affect CN8 (termed 'acoustic neuroma'), as well as sensory trigeminal


- Infrequent occurence after initial Tx.


Morphology


- Well circumscribed, encapsulated masses that are attached to the nerve but can be separated


- Firm grey masses w' areas of cystic and xanthomatous change




Microscopically


- 2 growth patterns


- Antoni A: Elongated cells w' cytoplasmic processes


- arranged in fasicles


- Moderate to high cellularity


- Scant stromal matrix


- Verochay bodies




-Antoni B- Less dense in cells, consists of loose mesh work of cells w' micro cysts and mixoid stroma




Cells in both changes are elongated shape w' regular oval nuclei.

Prostatic adenocarcinoma to bone


- Note that the most common primary bone cancers are Osteosarcoma (highly anaplastic, pleiomorphic tumor that produces osteoid) and lymphoma


- Common secondary tumors arise from prostate, lung, kidney, thyroid, testes




Histologcial features


- Neoplastic cells arranged in a glandular pattern


- Surrounedd by desmoplastic stroma


- Round hyperchromatic nuclei w' distinct nucleoli


- Invasion into local tissue


- Positive PSA immunostain on the mass




- also note the multinucleated osteoclast-like cells.

Rheumatoid arthritis


- A chronic, systemic, inflammatory disorder that principally affects the joints, producing a non-supporative, proliferative and inflammatory synovitis that often progresses to destruction of the articular cartilage and ankylosis of the joint




Morphology


- Odematous, thickened and hyperplastic synovium (normally only 2-3 cell layers thick) (can produce villous projections)


- Infiltration of synovial stroma by inflammatory cells (T-cells, B-cells, Plasma cells, macrophages) (sometime lymphoid follicles may develop)


- Increase in vascularity due to vasodilation and angiogenesis


- Superficial hemosiderin deposits


- Aggregation of fibrin covering portions of the synovium and floating in the joint space as rice bodies


- Accumulation of neutrophils in synovial fluid and alongside the surface of the synovium


- Pannus formation (mass of synovium with inflammatory cells, granulation tissue and synovial fibroblasts)




Pathogenesis


- Believed to be due to exposure to a genetically susceptible host to an arthritic antigen resulting in breakdown of immunological self-tolerance. HLA-DRB1 allele identified, EBV, retrovirus, mycobacteria, borellia, mycoplasma have all been implicated. Autoimmune T-cell reaction.




Clinical features


- Swan neck deformity


- Boutonniere deformity


- Bouchards nodes


- Rheumatoid nodules


- Worse in morning >1 hr



Reactive synovitis (detritic synovitis)


- Can occur due to a failing implant, which could be loose, infected, damaged the underlying bone, have instability as well as other patient factors (age, activity level, surgical history, weight etc.)




Morphological features


- Synovial thickening


- Chronic inflammatory infiltrate (macrophages, giant cells)


Exogenous pigment, from the metallic debris from the joint implant

Synovial chondromatosis (reichels syndrome)


- Usually affects a single joint


- Pain does not ease with exercise, steroid injection or heat treatment.


- Affects males twice as much as females




- This is a benign lesion


- Shows nodules of hyaline cartilage with clusters of chrondrocytes


- The clusters show atypical features and nuclear enlargement


- Pyknotic nuclei (condensation of chromatin)


- Very difficult to identify mitotic features




Diagnosis


- MRI can detect loose bodies as the disease progresses


- These will not appear on x-ray




Treatment


- Non-operative if mild symptoms and not affecting ROM


- Operative: Open or arthroscopic synovectomy and loose body resection if limiting ROM and ADL's




DDx


- Tentinopathy


- Arthritis



Adrenal cortical adenoma



Clinical presentation


Depends on if it is a functionaing or non-functionaing adenoma. Also depends if the cells implicated are the glomerulosa, fasiculata or reticularis cells.




Key histological features


- Well defined capsule


- Hyperplasia of cortical cells (type of cell could indicate the S&S if it is functional). In our case, we have zona fasiculata hyperplasia, attributed to the lipid-laden cells with vacuolations. (could also produce mineralocorticoid and sex hormones if functional)


- There is only mild atypia, with some pleipomorphic and enlarged nuclei


- No mitotic activity.


- No areas of necrosis




- Other types of cushing disease include


- Pituitary causes


- Small cell cell carcinoma


- iatrogenic

Pheochromocytoma


- These are neoplasms composed of chromaffin cells that synthesize and secrete catecholamines and in some instances, peptide hormones.




- They are a rare cause of surgically treatable hypertension


- Rule of 10's


- 10% are extraadrenal


- 10% are bilateral


- 10% are malignant


- 10% are not associated with HTN




Morphology


- They range from small circumscribed lesions confined to the adrenal gland, to large hemorrhagic masses weighing kilograms


- AVG weight is 100gm


- Smaller lesions are yellow-tan colour, larger ones are hemorrhagic, necrotic, cystic


Polygonal- spindle shaped neoplastic chromaffin cells that form nests (nests of Zellballen)


- Accompanied by a rich vascularised network of fibrous trabeculae, owing to its lobule appearance


- Cytoplasm of cells are granular, and the nuclei have a stifled appearance.




- There is no histologcal feature that reliably predicts clinical behavior




Clinical features


- Triad of sweating attacks, tachycardia and headaches is relatively specific for pheochromocytoma


- Related to catecholamine hypersecretion (usually norepinephrine > epinephrine)


- Usually hypertension (abrupt; with tachycardia, palpitations, headaches, tremor, sense of apprehension and weight loss; unresponsive to treatment; isolated paroxysmal episodes of hypertension in < 50%)

Parathyroid adenoma


- One of the main causes of primary hyperparathyroidism (85-95%)


- other causes include primary hyperplasia (5-10%)


- PT carcinoma: 1%


- Primary hyperparathyroidism is a disease of adults


- Women: Men = 4:1




Clinical presentation


- Reflects increase PTH secretion- Bone disease (osteomalacia, osteoporosis)


- Renal stones


- GI disturbances (constipation, nausea, peptic ulcers, pancreatitis, gallstones)


- CNS alterations (depression, lethargy, seizures)- Neuromuscular (weakness and fatigue)


- Cardiac (aortic and mitral valve calcifications)




Normal histology


- Normal histology of parathyroid has an abundance of fat (approx half), as well as oxyphil (reddish cytoplasm) and chief cells (bluish cytoplasm)




Morphology


- In the disease state, there is an increased number of cells (could be either oxyphil, chief or both; but most commonly chief cells)


- There cells are fairly uniform, with centrally placed nuclei.


- There is minimal adipocytes


- There is presence of residual normal tissue in the periphery


- Well-circumscribed mass, .5-5gm


- Soft-tan -> reddish brown colour


- Encapsulated lesion




DDx


Note that these features are similar to parathyroid hyperplasia, therefore all 4 PT glands should be assessed for changes.


Parathyroid carcinoma is also another DDx, diagnosed by metastases and local invasion alone, and not cytologic details.

Pituitary adenoma


Morphology


- Typically a soft, well-circumscribes lesion


- May be confined to the sella turcica, or extend into supra-sellar region, where the optic chiasm can be compressed




Histologically


1. Monomorphic cells arranged in sheets or cords


2. Supporting tissue (reticulin), is sparse, which account for the soft consistency


3. Minimal mitotic activity


- The cytoplasm could be acidophilic, basophilic or chromophobic (owing back to the clinical signs and symptoms)




- It is the monomorphism (similarity of cells), and the absence of significant reticulin network that differentiated it from non-neoplastic anterior pituitary parenchyma




- Prolactinomas are the most common hyperfunctioning pituitary adenoma, accounting for 30% of all recognised cases.


- Sx and Sx of prlactinemia include amenorrhea, galactorrhea, loss of libido, inertility


- Diagnosis made more readily in females that males, age range is typically 20-40 years of age.




Other types include


- GH adenomas (Gigantism or acromegly like signs and symptoms)


- ACTH adenoma (hypercortisolism -> cushings syndrome)





Graves disease


Morphology


- Usually the thyroid is symmetrically enlarged due to diffuse hypertrophy and hyperplasia


- The follicular epithelial cells are tall and crowded, owing to a papillary-like structuring of the follicle (these papillary structure LACK vascularture, compared to those of papillary carcinoma)


- The colloid is sparse and pale, with scalloped margins


- Lymphoid infiltrates, predominately T cells, with fewer B cells and plasma cells are found in the interstitium




Clinical features


- Thyrotoxicotc symptoms (thyroid stare, lid lag, exopthalmos, tachycardia, tremor, fatigue, restlessness/agitation, oligomenorrhea, irritability, sweating, proximal myopathy)



Hashimotos thyroiditis


- The most common cause of hypothyroidism in regions where iodine intake is normal


- Gradual thyroid failure because of autoimmune destruction of the thyroid gland.


- Most prevalent in 45-65 yoa.




Morphology


- Often diffuse enlarge thyroid


- Capsule is intact, and is well demarcated from surrounding structures


1. Extensive lymphoid infiltration with germinal centres.


2. Atrophy of residual thyroid follicles


3. Presence of Hurthle cells


4. Fibrosis in late stage.



Nodular hyperplasia/ goitres (simple or multinodular)


Morpholohy


- Diffuse simple goitres will show enlargement of the entire gland without producing nodularity.


- The vast majority of people with simple goitres are clinically euthyroid


- As well, people with mulitnodular goitres are also euthyroid or subclinical hyperthyroid.


- As such, signs and symptoms generally relate to the mass effect of the enlarges thyroid (dysphagia, hoarseness, dyspnea, throacic outlet syndrome, cosmetic effects)




Microscopically


1. Nodular enlargement of follicles


2. Rich abundant colloid follicles


3. Inactive flattened follicle epithelium


4. Areas of follicular hyperplasia


5. Degenerative changes: hemorrhage, fibrosis, calcification, cysts




Investigations


- TFT


- minimal uptake of radioactive iodine


- USS


- Fine needle biopsy




Other


- Papillary thyroid carcinomas spread via lymphatics


- Whereas follicular carcinomas metastases via vascular spread



Papillary thyroid carcinoma


Morphology


- Solitary or multifocal lesion.


- They can be well circumscirbed or even encapsulated, whilst other may invade local parenchyma with ill-defined margins.


- Lesions may have fibrotic, calcified or cystic areas


- Contain branching papilae that have CONTAIN a fibrovascular stalk (covered by single or multiple layers of cuboidal epithelium)




1. The nuclei of papillary carcinoma contain finely dispersed chromatin, giving an empty or 'Orphan annie', frosted glass, coffee bean (all synonyms)


2. Psamomma bodies may also be present (absent in follicular and medullary carcinoma, therefore highly indicative of papillary carcinoma)


3. Invasion into local lymph node or skeletal muscle (invasion into vasculature is rare)


4. Reactive fibrosis




Clincial course


- Most present with asymptomatic thyroid nodules


- However, hoarseness, dysphagia, cough or dyspnea suggest advanced disease


- Excellent prognosis, with 10 year survival in excess of 95%




Investigations


- TFT- Clinically euthyroid or subclinical hypothyroid


- USS


- Radioiodine uptake --> cold areas


- Fine needle biopsy.



Breast Cancer- Ductal carcinoma.




DCIS= Populations of cells limited to ducts and lobules by the basement membrane.




Morphology


- On gross examination, most tumors are firm to hard and have an irregular border


- Microscopically can be variable


- Well- differentiated can have prominent tubule formation, small round nuclei and no mitosis.




Poorly differentiated can have infiltrating nests composed of atypical epithelial cells.


- Pleiomorphic, hyperchromatic nuclei.


- Mitosis may be present


- Necrotising, cystic changes, hemorrhage


- Microcalcifications (plus hemosiderin laden bodies)


- Desmoplastic stroma (collagen tissue proliferation)











Breast fibroadenoma


- Most common benign tumor of the female breast


- Most occur in women who are in their 20's and 30's


- They are frequently multiple and bilateral


- Young women usually present with palpable masses, older women usually present with mammographic changes.




- Fairly uniform, with a rubbery texture, greyish, freely movable


- Well circumscribed and encapsulated


- majority of this tumor is fibrous tissue (arising from the intralobular stroma in this case. Note the colour difference b/w intra and interlobular stroma)


- Impacts on the ductal epithelium, distorting it into slit-like shapes


- No invasion into interlobular stroma


- Other than that, the epithelium does not show any atypia

-Vulvar intraepithelial neoplasia (VIN)


Carcinoma of the vulva is an uncommon malignant neoplasm, representing about 3% of all genital cancers in the female..




Carcinomas are divided into basiloid and wart carcinomas related to HPV (30%), and keratinizing squamous cell carcinoas, not related to HPV infection (70%)




Invasive basaloid and warty carcinomas develop from VIN.




Morphology


- Normal histology is stratified squamous epithelium that is keratinised.


- In this lesion, there is evidence of hyperkeratosis


- Hyperplasia of the epithelium


- Dysplastic changes of the epithelium


- Delayed maturity of the middle squamous cells (they should have become more flat, however they still resemble basal epithelium)


- Hyperchromatic, increased nuclear:cytoplasm, crowded nuclei


- No invasion through the basement membrane




Risk factors


- Are the same for cervical squamous intra-epithelial lesions


- Young age at first intercourse


- Male partner with multiple sexual partners


- HPV infection


- Note that 10-30% of people with this lesion will also have vaginal or cervical related HPV lesions, so must check for these as well



Normal skin histology

Endometriosis


- Endometriosis can occur anywhere along the ovaries, pelvic peritoneum, uterine ligaments, bowel, bladder, umbilicus, lungs or extremitites. If it occurs in the myometrium it is adenomyosis, and is a DDx for AUB.




Morphology


- The key give away is the histological presence of endometrium outside of the endometrium.


1. Endometrial stroma


2. Endometrial grands


3. Hemosidering laden deposits


4. In an area other than the endometrium




- There may also be evidence of current hemorrhage (RBC's) and past hemorrage (Hemosidering-laden macrophages)

Normal uterus


Layers


Perimetrium


Myometrium


Endometrium- stratum basalis (undergoes little change), stratum spongiosum, stratum compacta (latter 2 form stratum functiosum; containing surface epithelium, glands and lamina propria)




Menstrual phase- loss of progesterone leads to constriction of spiral arteries in the stratum funtiosum, with the sloughing and leakage of blood. The glands collapse and stromal cells disaggregate showing features of necrosis. There is also presence of apoptotic bodies from epithelium. By the end of the menstrual period the stratum basalis starts proliferating again




Proliferative phase


Endometrium thickens and has acquired microvilli/cillia by day 5/6, with presence of stagith tubular glands




Secretory phase


Occur from ovulation onwards. The glands a coiled in appearance and are their maximal thickness. progesterone leads to glycogen synthesis by the glandular epithelium and this forms vacuoles at the base of the cells.




The last secretory endometrium is marked by the saw-toothed appearance of glands with copius glycogen secretion.

Uterine fibroids- Leiomyoma


Perhaps the most common tumor in women


Leiomyomas, even when extensive, may be asymptomatic. The most important abormal symptoms are zbnormal bleeding, urinary frequency, sudden pain if disruption of blood supply occurs, impaired fertility




Morphology


- Appears as a well-circumscribes mass composed of interlacing bundles of uniform spindle cells resembling smooth muscle.


- Smooth muscle bundles in a whorled pattern resembling the surrounding myometrium.


- Spindles are regular in shape with elongated nuclei.


- High mitotic activity, cellular atypia and necrosis are NOT noted in this lesion


- Sometimes are so well differentiated it is difficult to distinguish from myometrium, so better to distinguish at a lower power view







Ectopic pregnancy


- Refers to implantation of the fetus in any site other than its normal intrauterine location.


- Most common site is the fallopian tubes (90%)


- Other sites include the ovary, abdominal cavity, intrauterine portion of the fallopian tube


- Occur once in every 150 pregnancies


- Most important predisposing condition is pelvic inflammatory disease resulting in fallopian tube scarring.


- Other include appendicitis, endometriosis and previous surgeries.




Clinical features


- Severe onset of severe abdominal pain, normally about 6 weeks after a normal menstrual period. Rupture of the tube leads to pelvic hemorrhage.




Investigations


- HCG assay, pelvic U/S and laproscopy may be helpful




Morphology


- initially, the embryonic sac surrounded by placental tissue (composed of immature chorionic villi) implants on the lumen of the fallopian tube


- With time, trophoblastic cells and chorionic villi start to invade the fallopian tube


- Also look for presence of blood clots




- Syncitiotrophoblasts secrete HCG


Molar pregnancy- Hydatidiform mole


- The most important reason for identifying this is the associated risk of persistent trophoblastic disease; invasive mole or choriocarcinoma


- Molar pregnancy can develop in any age, but more commonly at the far ends of the reproductive life




Clinical features


- Most women present with spontaneous pregnancy loss or undergo cutterage b/c of abnormalities in U/S showing diffuse villous enlargement


- HCG far exceed those of a normal pregnancy




Morphology


- Gross appearance is of a delicate, friable mass of thin-walled, translucent, cystic grape-like structures


- Increased trophoblastic proliferation


- Cystic degeneration/ swelling of chorionic villi, leading to a scalloped pattern


- Absence of fetal blood vessels

Normal fallopian tube

Seminoma


This is the most common germ cell tumor, making up around 50%.


Peak incidence is in third decade




Morphology


- Bulky mass


- Homogenous, grey-white, lobulated surface usually devoid of hemorrhage or necrosis.


- It does not breach the tunica albuginea


- Sheets of uniform cells divided into poorly demarcated lobules by a delicate septa of fibrous tissue; that contains a moderate amount of lymphocytes.


- The classic cell is large, round, has a distinct cell-membrane, a clear cytoplasm, and a large central nucleus


- Mitoses will vary in frequency


- Serum is positive for c-KIT, placental alkaline hosphate (PLAP)


- Approx 15% contain syncitiotrophoblasts, therefore may have positive HCG


-Also may have elevated AFP




DDx


- Embryonal carcinoma


- Yolk sac tumor- Will have elevated AFP


- Spermatocytic seminoma


- choriocarcinoma- Will have elevated HCG


- teratoma




Clinical presentation


- Painless mass in 3-4th decades of life




Treatment


- Generally for all testicle masses, it is considered maligant until proven otherwise. Biops can increase risk of spillage of cancerous cells, therefore rapid orchiectomy is usually reccommended.


- Otherwise, seminomas are extremely sensitive to radiotherapy

Transitional cell carcinoma


Urothelial tumors represent 90% of all bladder tumors




Clincal presentaiton


- Painless hematuria w increased frequency


- Hx of smoking




Morphology


- Hemorrhage visible


- Interrupted and thickened urothelial lining


- Dysplastic epithelial cells (loss of polarity, poorly differentiated, hyperchromiatic, mitotic)


- Poor neovascularisation


- May reveal a papillary growth pattern


- Local invasion into detrusor muscle.




- Precurser lesions are non-invasive papillary tumors, and flat non-invasive urothelial cell carcinoma




Treatment


- Radiotherapy or chemotherapy




DDx


- Cystits


- Squamous cell carcinoma


- Small cell carcinoma


- Uretitis


- Pyeloephritis

Renal cell carcinoma


Clinical features


- Triad of costovertebral pain, palpable mass, and hematuria (however only seen in 10%of cases)


- Most reliable of the three is hematuria


- Generalised constitutional symptoms


- Polycythemia (EPO), HTN (renin), hypercalcemia (PTH




Morphology


- Can affect any portion of the kidneys, but generally affects the poles


- Generally area of necrosis and hemorrhage are present.


- Look for poor localisation


- Clear cells with pin-point nuclei


- Generally well-differentiated (not what you'd expect)


- Cells are in nests around a vascular stromal network


- Absence of normal histology (however look for it in periphery of slides)




DDx


- Renal calculus


- Pyelopnephritis


- renal papillary adenoma




RF's


- Smoking


- Familial variants


- 5-year survival 45-70%




Treated by nephroectomy



- Normal Histology


- Note that the glands will always be separated by a thin layer of connective tissue


- The glands will normally grow in varying directions, and can have papillary-like structuring.


- The glands have 2 cell-layers, a peripheral cuboidal layer and a central columnar (secretory layer)


- These cells do not have obvious nucleoli in them


- There may be presence of concretions in the lumen of the glands


-




Prostatic adenocarcinoma


- The most common form of cancer in men, accounting for around 30%


- 1 in 6 lifetime probability of being diagnosed with prostate cancer


- Typically a disease in men over 50


- Age, family history, race, hormone levels, environmental influences all thought to play a role.




Morphology


- May involve local extension into periprostatic tissue, seminal vesicles, and the base of the urinary bladder


- Lymph spread is generally to para-aortic lymph nodes.


- Hematogenous spread to lumbar spine, proximal femur, pelvis, thoracic spine and ribs.




- Microscopically, glands are crowded with limtited stroma dividing.


- However, glands are still uniform albeit smaller than normal


- Atypical and pleiomorphic.


- Large nuclei with prominent nucleoli




- Grading is done by the Gleason scale


- <6 suggests low grade


- >8 suggests advanced tumor




- PSA is the most important marker when diagnosing and doing follow-up of the cancer




Treatment


- Depends on the Gleason score



BPH- Nodular hyperplasia


- Extremely common in men over 50


- Can be seen in 20% of men over 40, rses to 70% by age 60 and 90% by age 80.




Clinical features


- Nocturia, urinary urgency, incomplete voiding, poor stream, overflow dribbling


-Increased risk of UTI




Morphology


- Nodular hyperplasia originates almost exclusively in the transitional zone


- Early nodules are comprised almost entirely of stromal cells, where later lesions are prodominately epithelial




- Miscroscopic hallmark is nodularity.


- The composition ranges from purely stromal fibromuscular nodules to fibro-epithlial nodules.


- Presence of glandular hyperplasia, which are well differentiated cells, with stromal network in between the glands


- Can have papillary infolding in the glands


- Presence of corpora amylacea in the center of the gland (small hyaline masses of unknown significance)




Treatment


- 5 alpha reductase inhibitors


- TURP (trans-urethra resection of the prostate)


- Radiotherapy 'seeding'


- Follow-up with annual PSA



Thyroid scans