Female Genital System Vulva Vulvitis

Non-neoplastic Epithelial Ds

1) Lichen Sclerosus

2) Lichen Simplex Chronicus

Vulvar Tumours

1) VIN I

2) VIN II or III or carcinoma of vulva

-more inflammatory than life threatening ds -Pruritus -5 most impt infxns: -HPV – condylomata acuminate and vulvar intraepithelial neoplasia -HSV 1 or 2 -gonococcal suppurative infxn of vulvovaginal glands -syphilis with primary chancre -candidal vultitis -atrophic thinning or hyperplastic thickening -2 forms: -1) lichen sclerosus -2) lichen simplex chronicus -can co-exist -may look like leukoplakia (also see in vitiligo, benign dermatoses like psoriasis and lichen planus, carcinoma in situ, Paget dx, and invasive carcinoma) -rete pegs -thin epidermis -superficial hyperkeratosis and dermal fibrosis -white plaques, parchment-like -labia atrophic, vaginal constriction -m/c postmenopausal -a/i? -epithelial thickening w/ significant hyperkeratosis -looks like leukoplakia -more mitotic activity and leukocyte infiltration -epithlium no atypia -at margins of cancer but does not increase risk of CA -1) condylomas and low-grade vulvar intraepithelial neoplasia (VIN I) -2) high grade vulvar intraepithelial neoplasia (VIN II or III) and carcinoma of the vulva -3) extramammary Paget Disease -4) melanoma of vulva -condylomas – anogenital warts -two categories -1) condylomata lata (uncommon or in secondary syphilis – flat moist lesions) -2) condylomata acuminate – m/c (papillary and elevated or flat and rugose) -red to pink to brown -HPV 6 and 11 -low malignant potential -m/c > 60yoa -90% squamous cell carcinomas -2 biological forms: -1) HPV – younger, smokers -2) not HPV – older, preceded by non-neoplastic epithelial changes (more lichen sclerosus)

Vagina Vaginitis

Vaginal Intraepithelial Neoplasia and Squamous Cell Carcinoma Cervix Cervicitis

Tumours of Cervix Cervical Intraepithelial Neoplasia and Squamous Cell Carcinoma CIN

Invasive carcinoma of the cervix Endocervical Polyp

Body of Uterus Endometritis


-less than 2cm, 75% survival after surgery -seldom site of primary disease -congenital anomalies uncommon -leukorrhea -usually Candida albicans and Trichomonas vaginalis -C albicans – curdy white d/c -T vaginalis – water gray-green d/c -very uncommon -concurrence of neoplasms in other sites – probably viral -vaginal clear cell adenocarcinoma – teenage girls with mothers who took Diethylstilbestrol during preg -barrier -usually banal inflammations (Cervicitis) -squamous cell carcinoma -inflammations extremely common -mucopurulent to purulent vaginal d/c -either non-infxs or infxs -Chlamydia trachomatis, T. vaginalis, Candida, N gonorrhoeaea, HSV II and HPV -STD -C trachomatis m/c by far -dysplastic change can increase CA risk (HPV) -cervical carcinoma – CA related deaths -endocervical polyp -incidence of precursor CIN has increased -squamous cell carcinoma arises from CIN -PAP test (pre CA can be seen as long as 20 yrs prior) -CIN I – mild dysplasia -CIN II – moderate dysplasia -CIN III – severe dysplasia and carcinoma in situ -not always progress to CA -risk factors: early 1st intercourse, multiple partners, male partner with multiple previous partners, HPV infxn, other -HPV 16 and 18 -m/c squamous cell carcinoma, from CIN -rest are adenocarcinoma or adenosquamous carcinomas, small cell neuroendocrine carcinomas -1-3 grade on cellular differentiation and stage 1-4 on spread -m/b inflammatory -soft, smooth glistening surface with dilated spaces with mucinous secretion -lesions on top may bleed, but no malignant potential -many disorders, common, chronic, recurrent -relatively resistant to infections -acute rxns – bacterial after parturition or miscarriage -chronic endometritis – follows chronic gonorrheal pelvic ds, TB, endometrial cavities after preg, IUDs, idiopathic -endometrial tissue in pelvis -3 possibilities: -1) regurgitation theory: menstrual backflow

Dysfunctional Uterine Bleeding

Endometrial Hyperplasia Tumours of Endometrium and Myometrium Endometrial Polyps

-2) metaplastic theory: endometrial or coelomic -3) vascular or lymphatic dissemination theory: extrapelvic or intranodal -abnormal bleeding in absences of well-defined organic lesion in uterus -4 functional groups -1) failure of ovulation: proliferative but no secretory -2) inadequate luteal phase: corpus luteum problem with decreased progesterone -3) contraceptive-induced bleeding: usually BCP -4) endomyometrial ds: chronic endometritis, polyps, submucosal leiomyomas -xs estrogen to progestin -simple, complex, atypical -may rise to carcinoma of endometrium -m/c polyps leiomymoas, carcinomas -all get bleeding as earliest manifestation -hemispherical -may project into uterine cavity -usually at menopause -abnormal uterine bleeding, may lead to CA -fibroids – benign tumours from smooth muscle cells -related to estrogen and BCP -menorrhagia w/ or w/o metrorrhagia -leiomyosarcoma – mesenchymal cells or myometrium -usually solitary (unlike leiomyoma) -recurrence common with removal -m/c CA of female genital tract -55-65yoa -risk: obesity (increase estrogen), DM, HTN, infertility -usu late-metastasizing neoplasms -increase estrogen is a risk -some that aren’t associated with estrogen have poorer prog -seldom site of primary disease -usually inflammation – PID - ectopic pregnancy, endometriosis, rare primary tumours -usually inflammation of the tubes with bacteria -now usu – strep and staph -nongonococcal now more invasive, bloodborne infections (HT, BR, joints) -salpingitis sxs: fever, lower pelvic pain, pelvic masses, obstruction of tubal lumina -primary adenocarcinomas – if start here, not usually found until spread -infrequently primary site of disease except neoplasms -CA of ovary more deaths -very common -in unruptured graafian follicles or in follicles that rupture and immediately sealed

Leiomyoma and Leiomyosarcoma

Endometrial Carcinoma

Fallopian Tubes

Ovaries Follicle and Luteal Cysts

Polycystic ovaries

Tumours of Ovaries

Surface epithelialstromal tumours Serous Tumours Mucinous Tumours

Endometrioid Tumours

Other Ovarian Tumours Teratomas 1) Benign (mature) cystic teratomas

-multiple, under ovarian serosal covering -small, filled with clear serous fluid -rupture  intraperitoneal bleeding and acute abd sxs -oligomenorrhea, hirsutism, infertility, obesity -secondary to excessive estrogens and androgens -aka stein-leventhal syndrome -big ovaries, gray-white smooth outer cortex, with subcortical cysts -xs androgens, xs LH, low FSH -3 cell types normally: multipotential surface (coelomic) covering epithelium, totipotential germ cells, multipotential sex cells -usually neoplasms of surface epithelial origin -risk: nulliparity and family history -BCP reduce risk -BRCA genes often there -from coelomic epithelium -have intermediate borderline category – tumours of low malignant potential -most frequent ovarian tumours -aka cystadenomas or cystadenocarcinomas -usually borderline and malignant lesions -epithelium has mucin-secreting cells like those in endocervical mucosa -less malignant -cystadenocarcinomas – malignant, better prognosis -solid or cystic -mass projecting from wall of an endometriotic cyst filled with chocolate-coloured fluid -usually malignant -b/l, 30% have concomitant endometrial carcinoma -teratomas of germ-cell origin -neoplasms of germ-cell origin -younger px = greater is likelihood of malignancy -90% - benign cystic mature teratomas -dermoid cysts – cyst lined by recognizable epidermis replete with adnexal appendages -ectodermal differentiation of totipotential germ cells -u/l, m/c right -sebaceous secretion with hair, teeth, bone, cartilage, etc -prone to torsion -found early -bulky, solid on transaction, random necrosis -differentiation toward cartilage, bone, muscle, nerve, etc -struma ovarii – mature thyroid tissues  hyperthyroidism -small, solid, u/l, brown ovarian masses -ovarian carcinoid -either ascending through birth canal (hematogenous) -ascending m/c, bacterial, premature birth or transplacental

2) Immature malignant teratomas 3) Specialized teratomas

Disease of Pregnancy Placental inflmn and infxn

Ectopic pregnancy Gestational Trophoblastic Disease 1) hydatidiform mole

2) Invasive mole 3) choriocarcinoma


-Candida or mycoplasmas -hematogenous – syphilis, TB, listeriosis, some viruses -TORCH complex -usually oviducts -hydatidiform mole, invasive mole, chroriocarcinoma -high hcG -like grapes, cystically dilated, chorionic villi -complete – do NOT have fetal parts, partial does -abN fertilization -complete – empty egg with 2 sperm -partial – normal egg with 2 sperm  triploid -high hcG with no heart sounds -usually can’t completely remove because invasive -remain high hcG -very aggressive -from gestational chorionic epithelium or gonads -bloody, brownish d/c with high hcG w/o uterine enlargement -usually widespread dissemination -if from gestational chorionic epithelium 100% cure -HTN with proteinuria and edema in 3rd trimester -eclampsia – seizures  DIC -inadequate blood to placenta -usually 24-25 wks

Male Genital System Penis Malformations Inflammatory lesions 1) balanitis and balanoposthitis 2) phimosis and paraphimosis 3) genital candidiasis Penile neoplasms

Scrotum, Testes, Epididymis Hydrocele Hematoceles and

-hypospadias: urethra open on ventral aspect -epispadias: urethra open on dorsal aspect -see UTI infections -often uncircumcised males -local inflammation of glans penis or glans and prepuce -smegma: desquamated epithelium, sweat, debris -prepuce can’t be retracted over glans -para: stenotic prepuce forcibly retracted -circulation compromised with resultant congestion -DM risk -usually squamous cell carcinoma -usually uncircumcised -poor hygiene, HPV 16 and 18 -gray, crusted, popular lesion, on glans or prepuce -uncommon metastases -scrotal skin – fungal infections -neoplasms unusual – scc m/c -m/c cause of scrotal enlargement -accumulation of serous fluid w/ tunica vaginalis -infection, tumours, or idiopathic -blood or lymph in tunica vaginalis

chyloceles Cryptorchidism

Inflammatory lesions

Testicular neoplasms

-severe lymphatic obstruction  elephantiasis -failure of testicular descent into scrotum -malpositioning, hormonal, testicular AbN, mechanical -b/l  sterility, 4x testicular malignancy -orchiopexy -m/c in epididymis -venereal ds -nonspecific epididymitis and orchitis: begin as UTI -orchitis complication of mumps -TB: epididymitis, 2 to testes, inflammation, necrosis -m/c cz of firm, painless enlargement of testis -usu from germ cells (malignant) -non germ cell may make steroid hormones -testicular dysgenesis – increase testicular CA -germ cell tumours 2 categories: -1) seminomas – single histologic pattern -2) nonseminomatous germ cell – multiple pattern -embyonal carcinomas, yolk sac choriocarcinomas, teratomas -tumour markers – hcG and a-fetoprotein


Prostate Prostatitis Nodular hyperplasia


-acute bacterial – E.coli, concomitant in urethra and UB -chronic – bacterial or not (prostatodynia) -normal prostate has glandular and stromal elements surrounding urethra -aka BPH -causes: androgens and estrogens -if castrated before puberty – no incidence -DHT – stimulate glandular and stromal proliferation -older males -androgens play a part -if castrated, no development -bone mets are common -PSA – early dx -T pallidum -human only natural hosts -active cutaneous or mucosal lesion -can be congenital -common in HIV px -hard chancre -painless, well-defined indurated margins, moist base -see spirochetes -serologic tests often negative in early stages -self limiting -w/in 2 months of primary -palms, soles, feet -condylomata lata – broad, elevated, moist areas -last several weeks, then 1 year latent phase -strongly positive Ab tests

STD Syphilis

Primary syphilis

Secondary syphilis

Tertiary syphilis Congenital syphilis

Serological tests for Syphilis Gonorrhea

Nongonococcal Urethritis and Cervicitis

Lymphogranuloma Venereum Chancroid (soft chancre)

Granuloma Inguinale


Genital Herpes Simplex HPV

-1/3 px after 5 years -nontreponemal Ab may be –ve, antitreponemal Ab +ve -can lead to stillbirth -infantile – chronic rhinitis, desquamating rash -late or tardive – Hutchinson triad: notched central incisors, interstitial keratitis with blindness, deafness from CN VIII -saddle nose, mulberry molars -non-treponemal Ab and antitreponemal Ab tests -non-treponemal Ab – often –ve in early stages of disease -antitreponemal Ab tests – T. pallidum Antibodies -humans only natural host -need direct contact with mucosa -in females – lead to salpingitis, infertility -disseminated infection: less common -sxs: tenosynovitis, arthritis, skin lesions -rare endocarditis and meningitis -gonococcal infection – can go to infants – opthalmia neonatorum -m/c STD today -C trachomatis, t. vaginalis, u. urealyticm, m. hominis -C trachomatis: gram –ve, indistinguishable from N. gonorrhoeae -HLA-B27 +ve -Reiter’s syndrome -chronic, ulcerative ds -C. trachomatis -sexual promiscuity -acute, ulcerative -H ducreyi -lower SES, tropical areas -m/c cause of genital ulcers in Africa and SE Asia -co-factor for HIV-1 -chronic inflmn -c. donovani -rural and tropical areas -sexual promiscuity -scarring, elephantiasis -t vaginalis -sticks to mucosa -itchy, profuse, frothy, yellow vaginal d/c -dysuria -often asxs in males – but can look like nongonococcal urethritis -HSV 2 -direct contact with mucosal surface -neonatal herpes infection -codylomata acuminate – venereal warts – HPV 6 and 11 -cervical CA – HPV 16 (also 18, 31, 45)

KI and Collecting System Manifestations of Renal Diseases

-azotemia – elevation of blood urea nitrogen and creatinine -related to decrease GFR

Glomerular Disease

Immune Complex Nephritis in Situ

Cell Mediated Immune GN Mediators of Immune injury

-uremia – when azotemia has clinical ss/sxs and biochem abN -glomerular capillary wall has fenestrated endothelial cells, GBM, visceral epithelial cells (podocytes) and foot processes (pedicels) -supported by mesangial cells (contractile and secretes -GFR: high permeable to water and small solutes) -secondary glomerular diseases: affect glomerulus -primary GN or glomerulopathy – affect KI -2 forms of Ab-associated injury: -1) deposits of circulating Ag-Ab complexes in glomerulus -glomerulus does not incite rxn -Ag endogenous or exogenous -if Ag exposure cts, repeated immune cycles chronic -2) Ab reacting in situ in glomerulus -anti-glomerular basement membrane disease -Ab vs fixed Ag in GBM -spontaneous anti-GBM nephritis – autoAb vs GBM -Goodpasture syndrome – anti-GBM cross-react in LU and KI -severe glomerular damage -sensitized T cells from cell-mediated immune rxn -glomeular damage, loss of barrier function -proteinuria and mb reduced GFR -complement-leukocyte-mediated mechanism – mainly C5a and recruit neutrophiles and monocytes -neutorphils release proteases  destroy GMB -free radicals  Cell damage -arachidonic acid  reduce GFR -Abs to epithelial cell Ag or toxin -see morphologic change in visceral epithelial cells -proteinuria -detachment of visceral epithelial cells caused by alterations in nephrin and cytoskeletal proteins -protein leakage -reduce GFR to 30-50%  end stage renal ds -proteinuria and glomerulosclerosis -rest of glomeruli hypertrophy  handle additional load  injury  capillary collapse and sclerosis -1) massive proteinuria -2) hypoalbuminemia -3) edema -4) hyperlipidemia and lipiduria -increase permeability to plasma proteins -depleted serum albumin -edema d/t decrease osmotic P b/c hypoalbuminemia and primary retention of salt and water by KI  decrease plasma volume  decrease GFR  aldosterone secretion promotes retention of salt and water -adults usu systemic ds; children usu KI prob -systemic: DM, amyloidosis, SLE

Epithelial Cell Injury

Renal Ablation glomerulopathy

Nephrotic Syndrome

1) minimal change disease

2) Membranous GN

3) focal glomerulosclerosis

4)membranoproliferative GN

Nephritic Syndrome

Acute Prolif GN

Berger Disease

-primary glomerular lesions: membranous GN, lipid nephrosis (minimal change disease), focal glomerulosclerosis, membranoprolif GN -benign ds, m/c caouse of nephrotic syndrome in children -glomeruli that look normal in light microscope but diffuse loss of epithelial foot processes in electron microsope -ds of T cells  loss foot processes and proteinuria -subepithelial Ig deposits in GBM -diffuse thickening of capillary wall -cz: infections, tumours, SLE, AI conditions, inorganic salts, NSAIDs, idiopathic -Abs react to endogenous glomerular Ag -Heymann nephritis – idiopathic MGN -C5b-C9 on cell  leaky and liberates proteases and oxidants -sclerosis affecting some but not all glomeruli and only segments of each glomerulus -IgM -injury  disrupts epithelial cells -mb ass with nephrotic syndrome -can occur with HIV, heroin, secondary, congenitally, primary, or part of glomerular ablation nephropathy -hematuria and HTN -proteinura  renal ds -no response to corticosteroids -altered BM and mesangium, prolif of glomerular cells -2 types -1) immune complexes with hep B and C, SLE, infxn -2) C3 nephritic factor  alt complement pathway -hypocomplementemia (more type II) -acute onset -1) hematuria -2) oliguria and azotemia -3) HTN -some proteinuria and edema -maybe SLE or primary glomerular ds -post strep, postinfectious -1-4 weeks in child after group A strep -usu initial infxn in pharynx or skin -immune complex with IgG and complement on GBM -hypocomplementemia -IgA nephropathy -children and young adults -1-2 days after URTI -gross hematuria, every couple months, loin pain -IgA in mesangium -over IgA production -celiac ds -LV ds – defective hepatobiliary clearance of IgA (secondary IgA nephropathy) -m/c of glomerular disease

Hereditary Nephritis Chronic GN Ds affecting Tubules and Interstitium Tubulointerstitial Nephritis

-Alport syndrome – nephritis with deafness, eye ds -BM defect -chromo 2 -cause end stage renal ds -develops insidiously -tubular injury -bacterial -renal pelvis -pyelonephritis -interstitial nephritis – noninfxs -acute or chronic -UTI -E. coli, proteus, klebsiella, enterobacter, pseudomonas -recurrent infections -either by bloodstream of LUTI, more in females -interstitial inflammation and scarring in renal parenchyma -deformity of pelvicalyceal system -cause of chronic renal failure: -1) chronic obstructive PN -2) reflux PN – superimposed UTI on veicoureteral reflux and intrarenal reflux  chronic renal insufficiency -1) acute – m/c synthetic penicillin, 15 days post exposure -sxs: fever, eosinophilia, rash, renal abN -drugs act as haptens, bind to tubular  immunogenic -IgE -2) analgesic – large consumption  chronic inflmn often with renal papillary necrosis -mix drus -covalent damage and oxidative damage -inhibit PG synthesis  ischemia (loss of v-dilation) -destruction of tubular epithelial cells and acute suppression of renal function -m/c cause of acute renatl failure -24 hr urine < 400mL -d/t inadequate blood flow, or nephrotoxic -benign HTN with hyaline arteriolosclerosis -usu with primary KI dx -mild proteinuria -usu die of HTN HT ds or CV prob -less common -renal vascular damage (d/t benign one or arteritis or sclerotic injury)  renal ischemia  stim angiotensin sys  v-constriction  more ischemia -malignant arteriolosclerosis – HT throughout body -microangiopathic hemolytic anemia, thrombocytopenia, renal failure -childhood HUS – follow E.coli

1) acute pyelonephritis

2) chronic pyelonephritis

Drug induced interstitial nephritis

Acute Tubular Necrosis

Ds involving BV Benign Nephrosclerosis

Malignant HTN and nephrosclerosis

Thrombotic microangiopathies

-major cause of acute renal failure in children -bacterial verocytotoxin on endo  thrombosis, v-constrict Cystic Dx of KI Simple Cysts -innocuous -fill with clear fluid -usu in cortex -dialysis-associated acquired cysts – end stage renal ds with prolong dialysis, in cortex and medulla, hematuria -adult -autosomal dominant -chromo 4 or 16 -multiple expanding cysts in both KI, destroy parenchyma -child -autosomal recessive -chromo 6 -small cysts in cortex and medulla -urolithiasis -predispose to bacterial infxn -increased urine concentration, supersaturation -most likely calcium, hypercalciuri/emia -Mg ammonium P (struvite) – UTI -uric acid stones – gout and leukemias -cystine stones – defect in renal transport -dilation of renal pelvis and calyces -atrophy of parenchyma b/c obs of urine flow -congenital or acquired -below ureters – b/l; above or at – u/l -still have glomerular filtration  affected calyces and pelvis become dilated -LUT are 2x as common as renal cell carcinomas -cortical -LT dialysis, smoking, cadmium -1) clear cell carcinoma -2) papillary renal cell carcinoma: MET protooncogene -3) chromophobe renal carcinoma – good prog -more common in young children -all mesodermal -transitional epithelium  epithelial tumours -UB common  50x more if exposed to b-naphthylamine -can recur and infiltrative obs of ureters rather than malignant

Polycystic KI ds

Urinary Outflow Obs Renal stones


Tumours Renal Cell Carcinoma

Wilms Tumour Tumours in UB and collecting system

MSK System Hereditary Diseases of Bone


Osteogenesis imperfecta


-inherited -impaired maturation of cartilage -cause dwarfism – osteochondrodysplasia -constant activate fibroblast growth factor receptor 3 on chromo 4 (supposed to inhibit normal cartilage prolif) -shortening of proximal extremities, bowing legs, lordotic -“brittle bone ds” -abN development of type I collagen (sin, joints, eyes) -varying severity of bone fragility -multiple bone fractures -can result in abN dentition, hearing loss, blue sclera -“marble bone ds” -deficient osteoclastic activity -abnormally thickened, mineralized brittle bone -anemia, thrombocytopenia, infections, fractures -dramatic decrease amt of marrow space for hematopoiesis -can compress nerve roots  CN palsies

Osteoporosis and acquired metabolic ds Osteoporosis

Rickets and Osteomalacia

Bone Ds Associated with Hyperparathyroidism


-low bone mass, deterioration with increase in bone fragility and susceptibility to fractures -senile osteop -postmenopausal osteo – women after menopause -bone resorption > formation -RANK ligand has to be expressed on stromal cells or osteoblasts so macrophages can differentiate into osteoclasts -RANK R is stimulus to bone resorption -peak bone mass important determinant of risk -most vulnerable white females -spine and femoral necks – common fracture site -decrease in osteoblastic and increase in osteoclastic activity -hormonal factors, need estrogen -genetic factors: need Vit D -mechanical – weight bearing -diet – Ca and vit D -vit D xu - defective mineralization of bone -increase nonmineralized osteoid -osteo – total bone decrease but mineral content of remaining bone is normal -rickets – children -osteomalacia – defective mineralization of bone that has completed its normal development -PTH – calcium homeostasis (osteoclast activation, increased bone resorption, calcium mobilization, increase resoprtion of Ca by renal tubules, increase vit D by KI which increases Ca absorption from gut and moves Ca from bone) -net effect: raise serum Ca level, should inhibit further PTH -xs PTH, renal insufficiency (no vit D)  abN osteoclasts -Inflammation of bone and marrow cavity -infections only

Pyogenic Osteomyelitis

Tuberculous Osteomyelitis

Paget Disease

Bone Tumours Bone forming tumours 1) osteoma

2) osteoid osteoma and osteoblastoma

3) osteosarcoma (Terry Fox)

-3 routes: hematogenous, direct extension nearby, surgical -Staph aureus – m/c  has R for bone matrix that help stick -chronic is sequelae -sequestrum (necrotic bone), if big, surrounded by rim of reactive bone called involucrum -Brodie abscess – rim with residual abscess -organisms can live in sequestered area -hematogenous spread -long bones and vertebrae -synovium common site of initial infection  epiphysis  inflammatory rxn with necrosis and bone destruction -Pott disease  TB of vertebral bodies -cold abscess in psoas -aka Osteitis Deformans -osteoclastic  mixed clast and blast  osteosclerotic phase (dense, mineralized bone with little cellular activity) -end result: xs abN, unstable bone -infection? Paramyxovirus-like -more metastatic lesions – prostate, breat, LU, KI, GIT, thy -usu osteolytic (prostate  blast) -production of osteoid by neoplastic cells -osteoblastic metastases – osteoid by osteoblasts -reactive growth -head and neck -localized, solitary hard growth on surface of bone -Gardner syndrome – multiple lesions -not malignant -benign neoplasms -osteoid osteoma: femur, tibia, males, <2cm,local pain relieved by aspirin -osteoblastomas: vertebral column, males, pain, hard to localize, not responsive to ASA -malignant -neoplastic cells make osteoid -primary and secondary forms -knee, distal femur, proximal tibia -males, TP53 tumour suppressor gene -aka exostoses – benign prolif with bone and cartilaginous cap -mostly asxs -from metaphysis  bony firmly anchored with cap of hyaline cartilage -stop once skeletal growth completed -mature hyaline cargilate -hands and feet -Ollier ds – multiple, one side of body -Maffucci syndrome – multiple chondroma with angiomas -well-circumscribed lesion in medullary cavity of bone -multiple ones  chondrosarcomas

Cartilaginous Tumours 1) osteochondroma

2) Chondroma

3) Chondrosarcoma Other Tumour Stuff Giant Cell Tumour Ewing Sarcoma Family Fibrous Dysplasia

-malignant neoplasms with mesenchymal cartilaginous matrix -neoplatic cells do NOT form osteoid




-aka osteoclastoma -epiphyses -giant cells with mononuclear cells -EWS and PNET -neural origin and presence of chromosomal translocations -normal trabecular bone replaced by fibrous tissues and malformed bone -m/c monostotic fibrous dysplasia – from teens -polyostotic fibrous -polyostotic fibrous with endocrime – café au lait, precocious puberty (McCune-Albright syndrome) -aka degenerative joint disease -degeneration of articular cartilage -not really inflammation -aging and mechanical effects -Herberden nodes -tissue accumulation of xs uric acid (purine met) -tophi – large crystalline aggregates -primary overproduction of uric acid -Lyesch-Nyhan syndrome – last HGPRT, only males (x-linked), xs uric acid, severe neurological ds, self mutilation -salmonella if px has sickle cell -with local pain, fever, neutrophilic inflmn -Lyme Ds – Borrelia burgdorferi, deer ticks -3 stages: erythema chronicum migrans, early disseminated stage, late disseminated stage -chornic arthritis, smtms with severe damage to large joint and encephalitis -ex: floppy infant syndrome -progressive atrophy -bedridden with glucocorticoid usage -endogenous hypercortisolism -type II – fast twitch -acquired AI -Ab vs Ach-R -usually with small cell carcinoma of LU -increase in amp of AP with repetitive stimulation -Ab vs presynp of NMJ -polymyositis and dermatomyositis -idiopathic, m/b parasites or viral -spontaneous, progressive degeneration of MSK fibers -DMD – X-lined, absence of dystrophin -impaired conractile activity -BMD – x linked, mutation of dystrophin gene

Diseases of Joints 1) OA

2) Gout

3) infectious arthritis

Ds of Skeletal Muscle Neurogenic Atrophy Type II Myofiber atrophy Myasthenia Gravis Lambert-Eaton Myasthenic Syndrome Inflammatory Myopathies Muscular Dystrophies Duchenne and Becker Muscular Dystrophy

Other Myopathies Soft Tissue Tumours Tumours of Adipose Tumour-Like lesions of fibrous tissue Nodular fasciitis Fibromatoses

-Less severe that DMD -intrinsic metabolic errors and exogenous toxic insult -usu benign -local mass -lipoma – subQ tissue, sporadic lesions, slowly enlarging -liposarcoma – malignant neoplasms of adipocytes, visceral sites, lower extremity, and abdomen, often to LU

Fibrosarcoma Fibrohystiocytic tumours a) fibrous histiocytoma b) dermatofibrosarcoma protuberans c) malignant fibrous histiocytoma Neoplasms of MSK Rhabdomyosacoma

-self-limited, reactive fibroblastic -rapidly enlarging, may be painful -usually upper extremity and trunk, hx of local trauma -grow in infiltrative fashion -superficial – dupuytren contracture, penile fibromatosis (Peyronie ds) – structural deformity -deep – abdomen, trunk, extremeties -can be part of Gardner syndrome – polyps in colon, osteomas of bone, fibromatsoses -malignant neoplasms of fibroblasts -keep tissues in thigh, knee, and retroperitoneal area -slow growth, recur often to LU -well-defined mobile nodule in dermis or subQ -interlacing spindle cells -intermediate tumour b/w benign and malignant -dermis and subQ, slow growing -often recur, infiltrative -aggressive soft tissue sarcoma, aggressive -deep muscular tissues in extremities, retroperitoneal area -neoplasm of infancy, childhood, and teens -malignant mesenchymal neoplasm -embryonal rhabdomyosarcoma -in head, neck, GUT, retroperitoneum -alveolar rhabdomyosarcoma – extremity -pleomorphic rhabdomyosarcoma – rare in soft tissue -leiomyomas - benign -leiomyosarcoma – malignant smooth muscle tumours -synovial sarcoma – mesenchymal cells around joints (not always), chromosomal translocation

Smooth Muscle Tumour Misc Neoplasms

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