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Pathology Review-Term4
 

Pathology Review-Term4

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Medical school pathology lectures, year review of term 4 - Kidney, Urogenital system and tropical infections.

Medical school pathology lectures, year review of term 4 - Kidney, Urogenital system and tropical infections.

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    Pathology Review-Term4 Pathology Review-Term4 Presentation Transcript

    • Tip for Success in life….! "Powered by intellect, Driven by Values..!” Life motto of Infosys founder and Chairman, Narayana Murthy. INDIA 1
    • T4W1: Week overview: 2013 Term 4 CPC 1 Title: MSK System: Rheumatology Aim: To train students in: History taking + clinical examination of patient with joint pain ; pathology of physiology of rheumatological diseases; process of care + population health especially in rural and remote areas Learning 1. Demonstrate competency in history taking & clinical examination Outcomes: of patients Students will be presenting with joint pain able 2. Describe the Pathophysiology of to • Rheumatoid arthritis (RA) • Sero-negative arthritis • Osteoarthritis (OA), • Gout 3 Describe differential diagnoses for patients presenting with joint pains. 4 Formulate a first line management plan for patients presenting with joint pains, demonstrating a knowledge of indications and side effects of commonly used medications prescribed for treatment of joint pain.
    • CPC 4.1 – MSK-Rheumatology – Scenario 1: Rheumatoid A  Ms F.M. 19 year old student Gouty Arthritis  Mr J.W. 45 year old foot, 1st metatarsal – Scenario 2: Osteoarthritis  Mrs N.M 69y retired Sports teacher. – Scenario 3: • Notes to Tutors: – Discuss DD - variety of clinical scenarios. – Remember/revise serious causes of acute joint pain esp. septic arthritis, rheumatic fever (Jones criteria). – DD to include fibromyalgia, polymyalgia rheumatica, SLE etc. • Investigations: – FBC, RFT, ESR/CRP, ALP, Auto Ab.P, RF & Anti-CCP, HLA B27, 3
    • COMMON CLINICAL ARTHRITIS 4
    • Differentiating Features: Rheumatoid Arthritis: • Young, small joints • Autoimmune. • Synovial Inflammation • synovium  Cartilage Osteoarthritis: • Old age, Large joints • Degenerative. • Cartilage degeneration. • Cartilage  Synovium 5
    • Degenerative - Inflammatory • • • • • • • Both sexes equal. Pain through the day No morning stiffness. Stiffness, less pain. Bony swelling. No soft tissue swelling Uni/Bilateral, Asymmetrical. • • • • • Females more. Morning stiffness >1h. Less with movement. Pain & redness Inflammation & swelling of soft tissue. • Late bone swelling. • Bilateral, Symmetrical. 6
    • Early Destruction of cartilage in RA: 7
    • Normal -- Femur Head -- OA Normal Osteoarthritis 8
    • Osteoarthritis: Ankylosis • varus deformity of the knee and collapse of the joint space with destruction of the medial cartilage and the subchondral cortex (open arrowheads). 9
    • OA Hip: 10
    • RA - Pathophysiology Autoimmune TH1, TH17 & B cells MMPs, TNF, PGE2 Synovial Inflam & Proliferation with Papillary projections Chronic Inflam. Lymphocytes & Lymphoid follicles 11
    • RA Joint destruction, ankylosis: 12
    • Gout: • 1%, Males common, • High serum uric acid + monosodium urate crystals in & around joints. – Primary 90% - congenital – Secondary 10% (malignancies, renal disesase, high protein diet) – Acute / Chronic. Tophus • Large deposits – Tophi Acute Chronic 13
    • Degenerative Disc Disease (DDD) • Ageing / trauma • Low back pain/deformity. • Complication: Common Disc degenerations – Nerve damage Online Animation (Spine Universe.com)
    • Arthritis Comparison: 15
    • “To be a great champion you must believe you are the best. If you’re not, pretend you are….!” – Muhammad Ali Fake it until you make it….!
    • T4W2: Week overview: 2013 Term 4 Title: Renal Disease (Glomerulonephritis) CPC 2 System: Nephrology – Renal Disease Aim: • Clinical, Pathology & population study of patients with kidney function disorders. • Pathology & clinical diagnosis of patient with chronic illness—chronic kidney diseases Learning 1. Demonstrate competency in history taking & clinical examination of outcomes: patients with renal disease. The student 2. Describe the Investigation and first line management of UTIs, will be able to recurrent UTIs, acute and chronic renal failure including chronic kidney disease. 3. Outline the basic sciences relating to fluid balance, kidney function, urine production & urination (including bladder & urethra). 4. Outline the autonomic nervous system + signs of autonomic neuropathy 5. Describe the Pathophysiology & Pathology of renal disease (nephrotic, nephritic & renal failure acute & chronic). 6. Outline the different types of glomerulonephritis. 7. Describe the epidemiology, community & rural health issues in renal disease, renal dialysis & transplantation.
    • Renal Case Scenarios 1. 35y female, Tired for years, Worsened since two months. She has noted swelling of her legs and puffiness around eyelids. MGN 2. 2 year old boy presents with sudden onset polyuria, proteinuria following mild fever. MCD 3. 8 year old girl presents with fever, oliguria, smoke coloured urine & hypertension following upper respiratory tract infection. PGN 4. 49y, nephrotic syndrome non-responsive. FSGS 5. 18y male recurrent painless hematuria, 3-6 days, usually following fever, URTI. IgA
    • Anatomy of Renal System Cortex R L Renal Papilla Renal calyx
    • Anatomy of Kidney Glom, PCT, DCT Note the positions of Glom, PCT, Loop, DCT, CT
    • Renal Physiology: Urine, Hormones & Homeostasis Renin Aldosterone ADH Hypertonic media
    • Normal Kidney: Histology PCT DCT Aff.Art JGA Mesang. Gl.Cap * Revise: JGA, Renin, Angiotensin, Aldosterone, BP & Electrolyte control.
    • Filtration Membrane: Endothelium Basement Mem Epithelium
    • Clinical Presentations of Renal Function Dis. 1. Nephrotic Syndrome: – Massive albuminuria, hypoalbuminemia, edema, hyperlipidemia, lipiduria. 2. Nephritic Syndrome: – Oliguria, Hematuria, mild Proteinuria, azotemia, Hptn. 3. Painless hematuria / Proteinuria: – Mild forms of glomerulonephritis. 4. Acute Renal Failure (ARF): – Pre-Renal, Renal & Post-Renal. 5. Chronic Renal Failure (CRF): – Chronic progressive kidney damage (Diabetes, Hptn.) UTI, Nephrolithiasis, Cysts & Neoplasms.
    • Nephritic Nephrotic • • • • • • Proteinuria (“nephrotic range” >3.5g/24h) • Edema (retention+Hypoalbumi nemia) • Hyperlipidemia • Lipiduria • Protein casts. Oliguria Hematuria Non selective Proteinuria. GFR , Cr , BUN Edema (salt and water retention) • Hypertension • RBC & Protein casts. urine urine
    • Minimal Change GN: Synonyms: Nil disease, lipoid nephrosis, foot process disease Incidence: 80% of nephrotic syndrome in children (1-8 yrs.), mostly male. Adults in 2nd-3rd decade. Etiology: Idiopathic. Loss of net negative charge destruction of podocyte foot processes. Clinical Features: Nephrotic syndrome. History of recent URI in 30%. Association with Hodgkin’s lymphoma. Overlap with FSGS patients. Lab Features: Nephrotic urine (polyuria, Selective proteinuria. (albuminuria). Pathology: Normal Microscopy. IF - Negative. EM  loss of foot processes. Clinical Course: Spontaneous remission in 25-40%. Complete remission in 65-70% of patients. Steroid resistant patients may progress to FSGS. Normal Microscopy Loss of foot process - EM
    • Focal Segmental GN: Adults Synonyms: Focal segmental Sclerosis Incidence: 10 - 35% of nephrotic syndrome in adults. Etiology: Idiopathic - ? Auto Immune. No deposits. (Similar to minimal change). Clinical Features: Nephrotic syndrome. History of recent URI in 30%. Association with Hodgkin’s lymphoma. Overlap with MCD patients. Lab Features: Nephrotic urine (more, clear) Selective proteinuria. No specific laboratory findings. Podocyte damage, Segmental collapse of glom. increase in matrix (pink). Pathology: Clinical Course: Spontaneous remission 30% , 50% progression to chronic renal failure, 20% rapid progression.
    • Membranous GN: Synonyms: membranous GN Incidence: 40-60 Years, 50% of adult nephrotic syndrome. Wireloop Etiology: Immune complex deposition. Idiopathic in most patients, associated with infections, drugs, carcinomas, and heavy metals. Clinical: Nephrotic syndrome in 80%, asymptomatic proteinuria in 20%. Microscopic hematuria. Lab: Non-selective proteinuria ± hematuria. Path: Diffuse, uniform BM thickening with subepithelial projections (“spikes”). Diffuse, coarsely granular IgG and C3 deposits along basement membranes. Electron-dense subepithelial deposits. Clinical Course: Excellent prognosis in children. Some adults develop ESRD. Exclusion of other diseases is required.
    • Acute Post Strept, Diff, Prol GN: Synonyms: Acute proliferative glomerulonephritis, acute post-infectious GN. Incidence: Etiology: children (3-14). Sporatic, mostly winter and spring. Glomerular trapping of circulating immune complexes. (Group A, Beta-hemolytic streptococci, type 12). Clinical: Acute nephritic following strep. pharyngitis or pyoderma. (Other infections rare) Lab: Nephritic urine (little, dark, smoky) RBC casts, non selective proteinuria. Decreased serum complement. Evidence of strep inf. Path: Enlarged, hypercellular glomeruli with endothelial and mesangial cell proliferation, neutrophils, IgG and C3 in very coarsely granular pattern along GBMs. Discrete, subepithelial “hump-like” deposits. Clinical Course: Children - Excellent prognosis. Adults Worse prognosis, some develop progressive disease.
    • IgA Nephropathy (Berger’s) • Commonest form of GN – Nephritic. • Young 15-30y, males, Asia-Pacific. • IgA deposits in mesangium, High serum IgA, varied severity • Episodic asymptomatic hematuria • microscopic hematuria (40%) • Bouts of macro hematuria (40%) • Nephritic or Nephrotic (rare). • Renal failure (10%) • Slowly progressive CRF in 1/3 patients. IgA dep. Normal IgA dep.
    • Progression of GN: Decreased Renal reserve Renal Insufficiency Renal Failure Endstage G F R
    • Acute Tubular Necrosis: • Necrosis of tubular cells – fall of as casts. • Most common cause of ARF. • Ischemic (patchy PCT & DCT) – Hypovolemia – Shock • Toxic (PCT only) – Drugs… – Toxins – Mercury, CCL4, Radiocontrast.
    • Acute Tubular Necrosis(ATN): toxic Necrotic PCT (no nuclei) Glom. Norm Normal DCT (Pro. cast inside) PCT early necrosis
    • “Look at the sky. We are not alone. The whole universe is friendly to us and conspires only to give the best to those who dream and work.” - Wings of Fire: An Autobiography of Dr. APJ Abdul Kalam.
    • T4W3: Week overview: 2013 Term 4 CPC 3 Title: Male Genitourinary System:GU + Renal Aim: Understanding pathology ,presentation and clinical diagnosis of patients with urinary obstruction & urinary tract infections. Learning 1. Demonstrate competency in history taking & clinical outcomes: examination of patients with urinary symptoms. The student will be 2. Demonstrate competency in the clinical examination of able to the abdomen and pelvis 3. Describe the Laboratory investigations for patients with bladder outflow obstruction and haematuria 4. Demonstrate competency in debating the use of the PSA in individual patients and as a screening test. 5. Describe the first line management of prostate cancer and BPH 6. Describe the anatomy and histology of bladder, urethra + prostate;
    • Week Learning outcomes: 2013 Term 4 CPC 3 Title: Male Genitourinary System:GU + Renal Aim: Understanding pathology ,presentation and clinical diagnosis of patients with urinary obstruction & urinary tract infections. Learning 7. Describe the pathology of BPH, prostate cancer, renal outcomes: and bladder tumours ,and renal and bladder calculi The student will be 8. Outline the Professional, ethical & legal issues in able to diagnosis & management of patients with benign prostatic hyperplasia (BPH) and prostate cancer 9. Outline the Epidemiology & Public Health issues of BPH and prostate cancer
    • SAQ: UT Obstruction • What are differential diagnosis? • What complication he has? Or he may develop? • Should PSA be tested for all? Diagnostic levels? • When is biopsy indicated? • Does BPH lead to Carcinoma? • What is the best screening test for Ca? • What investigations are available? • BPH & Carcinoma – microscopy? • Gleason grading of prostate carcinoma?
    • Self Assessment: • • • • • • Common obstructions of LUT – age Etiology, pathogenesis, morphology: BPH PSA levels in diagnosis – debate. Cystic diseases of Kidney – ADPKD Urinary Tract Infections – Microbiology. Nephrolithiasis – common stones morphology. • Transitional cell carcinoma – brief • U:C ration – significance, diagnosis.
    • Core Learning Issues: (CLI) Major: • Disorders of Prostate – Prostatitis, BPH & Ca. • Nephrolithiasis: Features, Types, Pathogenesis. • Tumors of Kidney. – RCC, TCC, Wilms. • Urinary Tract Infection – Common Microbiology. Minor: • hematuria, strictures, obstructions, polyps. • Tumors of Urinary tract and bladder. • Kidney Cysts, Hydronephrosis, Recurrent UTIs, Pyelonephritis, renal abscess, Congenital disorders of kidney.
    • When you lose, don’t lose the lesson! Lao Tzu Everyone makes Mistakes, only intelligent learns from it.
    • Causes of Obstructive Uropathy  INTRINSIC:  Calculi - Lithiasis  Strictures – congenital, inflammatory (UTI)  Tumors – Transitional cell papilloma & Carcinoma.  Blood clots, necrotic tissue (Papillary necrosis)  EXTRINSIC:  Pregnancy  Inflammation- STI / PID, peritonitis, diverticulitis, salphingitis.  Tumors: Prostate, rectum, bladder, ovaries etc.
    • Nephrolithiasis: • Usually unilateral, small 1-3 mm, • Flank pain & tenderness – renal capsule. • Passage marked by Paroxysmal, intense colicky pain in the back (loin) with radiation to anterior (renal or ureteral "colic“) • “writhing in pain, pacing about, and unable to lie still” • Hematuria macro/micro • Larger stones that cannot pass produce hydronephrosis or hydroureter.
    • Levels - Clinical symptoms • Ureteropelvic junction - deep flank pain No radiation. Distension of the renal capsule. (Symp. T11-L2) • Ureter – Acute, severe, colicky pain in the flank and ipsilateral lower abdomen with radiation to the testes/vulva (ilioinguinal n.). nausea / vomiting. – Upper ureter – cholecystitis. – Middle – appendicitis – Distal ureter – Pelvic Infl. Dis. • Ureterovesical junction - Cause irritative voiding, urinary frequency and dysuria. Calcium Oxalate
    • Nephrolithiasis: Organic matrix(3%) + salts (97%) ~ • Calcium stones (80%): oxalate/phosphate/urate salts. Calcium Oxalate – Increased gut absorption or defective tubular reabsorphtion of calcium – Common, high pH. – Hyperparathyroidism (10%) – Hyperuricosuria – high pH • Struvite Stones (15%) magnesium ammonium phosphate (triple phos). Staghorn stone. – Chronic UTI with gram-negative rods (split urea) pH >7 – Proteus, Pseudomonas, and Klebsiella (not E. coli). • Uric acid stones (6%): – pH <5.5, high protein (meats), malignancy, 25% have gout.
    • Staghorn Calculus:
    • Male Urogenital System anatomy BPH
    • Zonal Histology: BPH Ca.
    • Normal Histology: Fibro-Musclular-Gland
    • Benign Prostatic Hyperplasia:
    • BPH-Bladder Gross – Identify Cues?       Trabeculations Hypertrophy of wall Stone - urolithiasis Inflammation Median lobe- ball valve. Enlarged prostate.
    • BPH: Nodular, Gland+stromal hyperplasia Nodule of BPH
    • BPH-Complications: 1. 2. 3. 4. 5. 6. 7. 8. Obstructive Uropathy Bladder hypertrophy Trabeculation Diverticula formation Hydroureter – bilateral Hydronephrosis Lithiasis / stone. Secondary infection. • Not a risk factor for Carcinoma prostate.
    • Pathogenesis: PIN & carcinoma 1. Prostatic Intraepithelial Neoplasia (PIN) Multilayered, pleomorphic. 2. Malignancy is single layered, & well differentiated at start…!
    • Adeno-Ca Prostate • Posterior Lateral lobes: Carcinoma • Rectal examination. • Solid, hard, adenocarcinoma
    • Gleason Grading & Scoring of Prostatic Ca.
    • Summary: BPH/Ca Normal  Benign:      Double layer. Secretion (clear cytopl) Uniform cells Papillary folds Ca. Malignant     Normal Single/crowded. Less/no secretion. Uniform/Pleomorphic No papillary folds. But crowding & clustering. Ca.
    • Transitional cell Neoplasms:     90% of bladder ca. Males 3:1 Fem, 50-70y Painless hematuria, Malignant cells in urine Papillary(low gr), Flat / Infiltrative (high gr) Risk F: β-naphthylamine. Cigarette smok, chronic cystitis, schistosomiasis
    • “No one who does good work will ever come to a bad end, either here or in the world to come” – Bhagavad Gita 6:6
    • T4W4: Week overview: 2013 Term 4 CPC 4 Title: Epididymo-Orchitis System: Male Genital System Aim: Clinical, Pathology & Population study of patients with male genital system disorders & sexually transmitted disease (STD) using a case of epididymo-orchitis with a differential diagnosis of testicular torsion and testicular tumour. Learning Outcomes 1. Demonstrate competency in history taking & the clinical The student will be examination of male patients with genital disorders able to 2. Outline the Laboratory investigations and first line management of common infections including STIs. 3. Outline the Investigations and first line management of testicular torsion and testicular carcinoma 4. Outline the anatomy and histology of male genital system. 5. Describe the Microbiology of common STIs; Pathology of Penis & testicular disorders including torsion and tumours. 6. Relate the Professional, Ethical & Legal issues in diagnosis & management of patients with STIs. 7. Describe the Epidemiology & Public Health issues of STIs, testicular torsion, testicular cancer.
    • CPC4.4:Testes: Common presentations. Torsion 12y boy, woke up in the night with sudden severe scrotal pain. O/E tender, swollen testes high up in the scrotal sac does not allow to touch.  Seminoma 35y man, dragging sensation in scrotum since 6 weeks. O/E enlarged, smooth, non tender, firm testes on one side.  28y man, severe aching pain in the left groin Ep.Orchitis radiating to the scrotum since 3 days with associated fever and rigors. O/E a 4 cm, hot, swollen, tender, (left epididymis & testis).  35y man, smoker, chronic cough, presents with Hernia recurrent attacks of sharp pain in right groin with small painful bulge, disappears on laying down. Bowen/EQ 68y male, erythematous, irregular, raised papule on penis/glans since 6 months.
    • Structure, origin, Lymphatics:
    • Normal Testes:
    • Condyloma Accuminatum • HPV serotypes 6 & 11 • Fleshy / warty Papillary epithelial overgrowth. • Glans & periurethra • Acanthosis & Koilocytes
    • Bowen’s & Erythroplasia of Queyrat: • • • • • Epithelial hyperplasia & dysplasia. HPV type 16, 18 On Glans: Erythroplasia of Queyrat On Shaft : Bowens Disease. Premalignant  Sq. Cell Ca.
    • Carcinoma Penis: (Sq cell)            Hygiene, smegma irritation Smegma carcinogen? Smoking is a risk factor* HPV 16, 18 * Circumcision known to prevent. Phimosis increases risk. Starts as erythroplakia/leukoplakia. Well diff. sq.ca – Epithelial pearls. Slow growth, Good prognosis Inguinal & iliac LN spread. 70% 5 year survival.
    • Cryptorchidism: “undescended testes”       Normal descent: 3m to pelvis, 9m to scrotum. Non descent 5% at birth, 1% at 1y (10% bilateral) Cause: Hormonal, intrinsic & mechanical. Common in Patau, Prader willi sy. etc. Atrophy, - sertoli & Leydig cell hyperplasia. 3-5 fold increase in Germ cell Malignancy – even in the other testes. (not in other types of atrophy)  Orchiopexy – reduces risk of sterility & cancer. Normal Abdominal - 3m Inguinal Suprascrotal - 9m Normal Atrophy ~ 1 year
    • Testes Atrophy: Normal  Bilateral in Hypopituitarism, Chronic Alcoholism, chemotherapy or radiation.  Hormonal, infection, Cryptorchidism.  Mumps – Patchy.  Sertoli only, Leydig cell hyperplasia. high chance of neoplasms. Atrophic Normal  Spermatogne sis Few Leydig cell cluster outside  Atrophy Sertoli only inside, Leydig cell Hyperplasia outside
    •  Hydrocele: Common, Clear Fluid in Tunica vaginalis. Cong./Acquired (inflam).  Varicocele: Engorged spermatic cord veins (pampiniform plexus). Common cause of infertility oligospermia. Primary / Secondary  Spermatocele: Epididymis dilatation trauma/infection, multilocular, sperms.  Hematocele: Blood in tunica vaginalis. Trauma, tumours.
    • To measure the man, measure his heart. -- Malcolm Stevenson Forbes
    • Epididymo-Orchitis:  Symptoms: • Testicular pain - unilateral • Erythema / oedema of the scrotum • Urethritis, dysuria / urethral discharge.  Etiology: • Gonococcal – Neisseria gonorrhoeae. Non Gonococcal - (chlamydia, Mycoplasma..)  Gross: swollen, hot, Acute inflammation, edema  Micro: Edema, neutrophils, necrosis.  Investigations: • Exclude torsion/trauma in <30 years, • Microbiology: C/S, Elisa, etc.
    • Genital herpes:  STD - HSV (Herpes Simplex Virus) type 2.  Itching  closely grouped vesicles surrounded by erythema.  Vesicles burst to form painful ulcers.  Multinucleate giant cells with viral inclusion.
    • Syphilis:  Treponema pallidum  Primary chancre on penis: ulcerated nodule inguinal lymphadenitis  Secondary stage: condylomata lata, (2-8w)  Painless, broad, moist Grey white to red plaques. Highly infectious.  Tertiary stage: gumma, often in the testis
    • Lymphogranuloma venereum  Chlamydia trachomatis, serotypes L1-L3  Genital Painless papule - 2-5 days.  1-4 wk. suppurative necrotic Inguinal lymphadenitis.  Suppurative granuloma (neutrophil abscess) & Chlamydial inclusions in microscopy.
    • Reiter’s Syndrome:  Common Inflammatory polyarthritis in young men.  Chlamydia trachomatis (rarely salmonella & shigella)  HLA-B27 – risk factor in 70%  Fever, malaise, myalgia, asymmetric arthritis & Conjunctivitis.  Knee, ankle & feet common.  Chronic, recurrent.  Disability in ~ 20% cases. Sausage toe Inflammed ankle
    • Testes Tumors: Features:  Commonest tumour of young males.  Etiology: • Idiopathic, Undescended testes, estrogens.  Clinical features: • • • • • Adults 40-50y – Seminoma. Children <10y – NSGT- Yolksac tum. Painless, enlargement, unilateral, Hydrocele, Gynaecomastia. Metastases – Para aortic LN*.  Origin: • 95% Germ cell, • Seminoma 40-50% • Non seminoma (NSGT) (Embryonal ca 25%, Terato ca 25%, Teratoma 5%, Chriocarcinoma 1%, 15% mixed.) • 5% Sertoli/Leydig cell tumours.
    • Seminoma:  Commonest Germ cell tumour, 30-50y, hCG  Firm, grey, smooth, painless, (many subtypes: classical, spermatocytic, anaplastic, etc.)  Microscopy: uniform cells, Pale, vacuolated cytoplasm contains glycogen, plenty lymphocytes.  Mixed seminoma  Seminoma + Teratoma, embryonal carcinoma or choriocarcinoma etc.
    • Embryonal Ca.  Children (Yolksac/Endodermal sinus) • Pink AFP globules in cells. • Schiller-Duvall bodies (embryo like)  Adults: Embryonal Ca. • Primitive, pleomorphic cells in clusters, embryoid structures.  Pathology: Germ cell tum.  Clinical: painless swelling of testes. malignant, poor prognosis, metastases.  Gross: Hemorrhagic, necrotic tum.  Micro: Pleomorphic cells, embryoid structures.
    • “Strength does not come from winning, Struggles & Hardship develop strength. - - Arnold Schwarzenegger Bodybuilder, Actor & Leader.
    • T4W5: Week overview: 2013 Term 4 CPC 5 Title: Breast Cancer System: Breast Aim: Clinical, Pathology & population study of patients breast disease 1. Demonstrate competency in history taking & the clinical examination of patients with breast disease. 2. Describe the first line investigation and management of patients with breast disease or symptoms. Learning outcomes The student will be 3. Describe the Pathophysiology of breast disease (benign and malignant) able to 4. Outline the basic sciences relating to function of the breasts. 5. Describe the Epidemiology and aetiology of breast disease in Australia and world wide. 6. Illustrate the advantages and disadvantages of the breast screening program in Australia
    • Case studies: • 22year female, noticed small mobile round lump in her right breast, lower inner quadrant. • 39year female, multiple small lumps, irregular, firm, tender more during mid cycle. • 41year female, two left axillary LN, no pain, no breast mass. mild loss of weight. • 34year female, diffuse firm left breast. FNAC reports abnormal cells. No LN. • 39year female, painful lump, chronic pus discharge from nipple. • 71year old female. Rough, red scaling pruritic patch on left nipple and areola. • 26y nurse, right breast lump 5m, firm irregular, 6cm firm, fixed lump. • Fibroadenoma • Fibrocystic dis • Ca breast. • DCIS • Duct ectasia • Paget’s dis • BRCA Ca.
    • Self assessment: • • • • • • • • • Clinical features of benign, malignant & reactive… Breast cancer screening guidelines. Hyperplasia / tumour features. Familial vs Non familial breast Ca features. Screening Mammogram – policy, procedure & interpretation. Fibrocystic disease, fibroadenoma & cancer. Breast cancer common types & features (gross, microscopy, complications etc.) Duct carcinoma, lobular carcinoma, other types. BRCA testing in familial breast ca.
    • Anatomy T4 level
    • Age changes in breast: Puberty Fibrous  Adult (Lactating) Fibro-Fatty  Menopause Fat
    • Disorders of Breast:
    • Fibrocystic Disease
    • FibroCystic Disease: types Non prol. / low grade Prol. / High grade A. Simple Fibrocystic change. B. Lobular hyperplaisa without atypica (adenosis) C,D - Ductal hyperplasia without atypia (E. with atypia - cribriform) F. Lobular hyperplasia.
    • Breast Neoplasms:  Benign: (round, smooth, soft, mobile)  Fibroadenoma  Duct Papilloma  Others – rare.  Malignant: (irregular, rough, hard, fixed)  Ductal carcinoma – classic.  Lobular carcinoma  Others - rare Fibrocystic Disease (Not a neoplasm)
    • Fibroadenoma Pathology: Benign tumor of acini tissue (gland & stroma) Clinical: Well demarcated, mobile, round/nod (mouse) Gross: Capsulated, firm grey, nodular tumour, cysts+/-. Micro: Compressed slit like ducts/glands in cellular stroma.
    • Giant Fibroadenoma • Pathology: Benign(young) to malignant(adult) tumor of acinii. • Clinical: young (Low grade) /adult (high grade)*, unilateral macromastia, recurrent, metastasis 15%. • Gross: Large 10-15cm . Giant. With linear “leaf-like” clefts and slits – Giant/Juvenile in young - Phyllodes tumor in adult. • Micro: Both stroma & glands are hypercellular & pleomorphic. glands show branching..
    • Etiology of Breast Carcinoma: • HER2/NEU • RAS & MYC • BRC A1, A2. Environment Hormone Genetics • Estrogen therapy. • Family history – First degree • Alcohol, Smoking. relative. • High fat diet, • Premenopausal & bilateral. Obesity. • Early menarche/Late menopause. • Overexposure to oestrogens and underexposure to progesterone • No definite relationship to oral contraceptives • Some tumours contain hormone receptors and respond to hormone manipulation • No good evidence for viral involvement
    • Pathogenesis of Breast Cancer. Duct Ca. in-Situ DCIS Hyperplasia  Dysplasia  DCIS  Carcinoma Fibrocystic change  Cancer
    • Pathogenesis:
    • Infiltrating Duct Carcinoma: Breast Ca. (NOS or Classic or typical “Schirrhous carcinoma”) Note: Fibrotic tumor, radiating fibrous scar around resulting in nipple retraction & skin pulling (puckering)
    • Typical Invasive Ductal Carcinoma / Duct Ca (NOS) Ca-tubules collagen stroma
    • Pagets Disease • Spread of Breast cancer cells to skin (areola) & resulting in Eczematous reaction. Ca. Cell Ca. Cells
    • Summary: • • • • Anatomy & Physiology. Congenital, Inflammatory & Neoplastic dis. Fat Necrosis, Abscess, Duct ectasia. Proliferative Disorders: – Fibrocystic Disease – hormonal, benign. • Neoplastic Disorders – Benign – Fibroadenoma, papilloma – Malignant – Invasive Duct Carcinoma, Lobular Carcinoma, – DCIS – Ductal carcinoma in-situ.
    • If through a broken heart you become a better person then, thank him for breaking your heart! ~ Oswald Chambers 
    • T4W6: Week overview: 2013 Term 4 CPC 6 Title: Female Gynaecological 2 System: Female genital tract Understanding pathology & clinical diagnosis of female patients with Aim: abnormal vaginal discharge Learning Outcomes (The student will be able to..) 1. Demonstrate competency in History taking & clinical examination of patients with an abnormal vaginal discharge. 2. Demonstrate competency in the Physical examination of abdomen and pelvis. 3. Outline the Investigation and first line treatment of common causes an abnormal vaginal discharge including pelvic inflammatory disease. 4. Outline the anatomy and histology of female genital tract 5. Describe the difference in presentation in STIs in women and men 6. Discuss the screening program for cervical cancer in Australia 7. Construct a management plan for patients with normal and abnormal PAP smears 8. Relate the Professional, ethical & legal issues in diagnosis & management of victims of violent crime. 9. Describe the Epidemiology & Public Health issues of cervical cancer and STIs. 98
    • Case studies: Trauma • 8year girl, vaginal bleeding and discharge. Chlamy.. • 21year female, itchy vaginal discharge foul smelling. Candida • 26 year old thick white cheesy discharge. Gonoco.. • 25 year old, whitish yellow pus discharge. DUB • 31year female, irregular heavy bleeding. CaCx • 34year female, irregular & post coital bleeding. Molar preg. • 28y G2 P1, second trimester vaginal bleed. Endo.. Ca • 69year female, vaginal bleeding
    • CPC4.5- Female Genital System-1 - CLI • Pathology Major Core Learning Issues: – – – – Sexually Transmitted Infections – Microbiology* Pathology of Cervical disorders, cervical cancer. Pap smear, biopsy & CIN, Ca Cx grading & staging. Endometrial - hyperplasia, polyps, cancer. • Pathology Minor Core Learning Issues: – – – – Pelvic Inflammatory Disease (PID)* Disorders of Vulva & Vagina. Infections & inflammations – vulvovaginitis, cervicitis, Endometriosis & Adenomyosis. 10
    • Sarcoma Vaginal disorders: Botryoides Sarcoma, 1-5 year children 10
    • Pelvic Inflammatory Disease (PID): Infertility Mass Pain & Fever 10
    • HPV: Condyloma acuminatum A B C Ano-genital wart, soft, HPV 6 & 11, STI, Benign, A. Small, warty, Cauliflowerlike growth. B. Koilocytes: peri nuclear halo + viral particles C. Mild Dysplasia. (Cx. CIN-1) 10
    • Transformation Zone: 10
    • Colposclopy & Acetic acid test mosaic pattern resembling inlaid woodwork. (LSIL) Before acetic acid Erythematous patch in the transformation zone. After acetic acid http://www.operationalmedicine.org/ed2/images/Cervix/Cervix.htm 10
    • Normal Ectocervix :Strt. Sq. Ep SUPERFICIAL INTERMEDIATE BASAL 10
    • PAP: CIN I-III Comparison (note nuclei) Normal CIN II CIN I (LSIL) (HSIL) CIN III 10
    • PAP Smear 25y  30y  35y  45y CIN Pathogenesis & Features
    • HPV - Vulva, Vagina, Cx Pathogenesis: Cx-Transition Zone - HPV CIN1/LSIL Smoking, Estrogens, Genetics.. E6, E7 protein  Rb & p53 Benign Wart CINII-III/HSIL (CIN1/LSIL) ??? Carcinoma LSIL: Lowgrade Squamous Intraepithelial Lesion (CIN1) HSIL: Highgrade Squamous Intraepithelial Lesion (CIN II, III) 10
    • CIN Progression: • CIN (Stage 0) – CIN I – LSIL, HPV 6,11. – CIN II & III – HSIL, HPV 16, 18. • Stage 1: Limited to Cervix. – Ia. Preclinical by microscopy • Ia1. Microinvasive <3 mm x <7 mm. • Ia2. <5mm x <7mm wide. • • • • – Ib Larger - Confined to cervix. Stage 2: Beyond Cx. Stage 3: To pelvic wall/lower vagina. Stage 4a: Bladder, Rectum Stage 4b: Beyond pelvis. LSIL / CIN-1 is virtually a transient HPV infection and not a cancer precursor. 11
    • Cervical Dysplasia: HSIL margin Normal HSIL/Dysplasia 111
    • Cervical Dysplasia: HSIL ? 11
    • HSIL  early invasion: Ca 11
    • “We choose our joys and sorrows long before we experience them!” --Khalil Gibran
    • Disorders of Uterus & Endo.. • Myometrium: – Benign – Leiomyoma – Malignant – Leiomyosarcoma • Endometrium: – Endometritis. – Endometrial Hyperplasia – polyp, diffuse, atypical. – Endometriosis, Adenomyosis. Endometrial tumor: – Malignant – Endometrial Carcinoma. 11
    • Endometrial Hyperplasia & Polyp: • Hyper-estrogenemia. • Hyperplasia of endometrium, may form polyp. • Common cause of uterine bleeding - DUB • Risk of malignancy – more with atypical/dysplasia. 11
    • Uterus Adenomyosis: Adenomyosis 11
    • Endometriosis: • Definition: Endometrial spread beyond uterus. – Spread through Fallopian tube – Pelvic veins or Lymphatic spread. – Metaplasia of coelomic epithelium. • Cause: Hyper Oestrogenemia. • Sites: – Endometriosis Interna – Adenomyosis. – Endometriosis Externa • Clinical: Periodic Pain, pelvic inflammation, fibrosis, • Complications: infertility, 11
    • Endometrial Ca: • • • • • • Adenocarcinoma (not HPV) Estrogen – risk factor. Post-menopausal bleeding. Irregular, polypoid, bleeding. Dysplastic back to back glands Little/no stroma.  Adenocarcinoma  Hyperplasia 11
    • You are the stone, You are the chisel, and You are the sculpture….! We are responsible for what we are… www.akshardham.com
    • LAST LECTURE ! CPC47-Ovary
    • T4W7: Week overview: Term4 CPC 7 Title: Female Gynaecological 2 System Aim: Learning Outcomes: The student will be able to Female genital tract Understanding pathology & clinical diagnosis of female patients with abnormal vaginal bleeding 1. Demonstrate competency in History taking & the clinical examination of patients with abnormal vaginal bleeding. 2. Demonstrate competency in history taking and clinical examination of patients with menopausal symptoms 3. Outline the Investigation and first line management of patients with abnormal vaginal bleeding: menopausal symptoms. 4. Illustrate the advantages and disadvantages of HRT 5. Outline the anatomy and histology of the female genital tract; the physiology of menstrual cycle and menopause including anovulatory menstrual cycles and polycystic ovarian syndrome 6. Describe the pathology of common disorders of the uterus and ovaries including polyps, tumours -both benign and malignant. 7. Relate the Professional, ethical & legal issues in diagnosis & management of patients with abnormal vaginal bleeding. 8. Describe the Epidemiology & Public Health issues of menopause, ovarian
    • Core Learning Issues: Pathology Major CLI: • Ovary – disorders overview. • PolyCystic Ovary Syndrome (PCOS) • Tumors of Ovary – overview (common: Cystadenoma, dermoid cyst) • Gestational Pathology – Overview Pathology Minor CLI: • Ectopic pregnancy. • Eclampsia & Pre-Eclampsia, Gestational tumours. • Disorders of placenta, Hydatidiform mole,choriocarcinoma. • Other tumours of ovary – teratocarcinoma, 12
    • Polycystic Ovary Sy: PCOS • Arrested follicle development, anovulation. • Teens/young adults, acne, oligemenorrhoea, hirsutism, obesity, HPTN, DM2. • Multiple subcortical follicular cysts. • Excess androgens & estrogens. • Stromal hyperplasia & anovulation. • Complications: – Important cause of infertility, – Endometrial hyperplasia. 12
    • Endometriosis: chocolate cysts Frozen Pelvis - adhesions 12
    • Classification of Ovarian Tumours 12
    • Cystadenoma: • • • • • • Serous more common, 75% benign. Serous frequently bilateral Multi-loculated / single cyst. Benign cystic  Malignant solid. Single layer ep  papillary. CA125 Tum marker (epithelial) followup.
    • Germ Cell Tumours: Teratoma • Many types of tissues inside. • Benign/mature Teratoma  mature tissues. (common Dermoid cyst) • Malignant/solid Teratoma  multiple cancers on microscopy. Dermoid Cyst Dermoid Cyst Tooth..! Immature Teratoma Dermoid Cyst Hair 128 Fat
    • Chorioamnionitis: • Infection & inflammation of chorionic membrane & villi. – 1-4% of normal births, – 40-70% of premature births. • Risk factors: Early rupture of membranes, nulliparity, prolonged labour, race/ethnicity. • Local: Vaginal flora, genital mycoplasma, Candida. • Systemic: TB, Syphilis, Toxo, Rubella, CME (TORCH). • Inflammation, WBC, infarctions. • Neonatal sepsis, asphyxia, death.. 12
    • Eclampsia & pre-eclampsia • Diagnosis: HPTN, proteinuria, edema in 3rd trimester (pre-Ecl.) + Seizures, DIC (Eclamp.) • 5-10% pregnancies. • Etiology: Unknown/genetic/immune. • Risk Factors: Primi / molar preg, later age. • Pathogenesis: Placental Ischemia. – Abnormal spiral arteries  Decreased placental vasodilators and Renin Angiotensin inhibition  Hypertension & Glomerulonephritis. • Placental infarction or hemorrhage. • Chorionic villi underperfusion, cytotrophoblast hyperplasia. • Complications: DIC, CCF, fatal. 13
    • Ectopic Pregnancy: • • • • • Implantation outside uterus. 1% pregnancy, 90% in fallopian tubes. Ovary, abdomen, etc. rare. Risk factors: Obstruction, PID, stricture, IUD, tumours, endometriosis etc. in 50%, rest idiopathic (50%). • Embryo / placental tissue within dilated tube filled with hemorrhage. • Complications: Abortion, bleeding, chorioamnitis, Choriocarcinoma (rare). 13
    • Mole/Molar pregnancy 1. Gestational Trophoblastic Disease: 2. Spectrum of trophoblast neoplasms. 3. Benign to malignant: – Partial mole – Benign, fetal parts+ Ovum+2 sperms. (triploid) – βHCG – Complete mole – no fetal parts, 2% ChorioCa. 2 sperms (diploid) – Invasive mole. aggressive. – Choriocarcinoma. Malignant.  βHCG  High grade  Poor prognosis. 13
    • Complete • All villi cystic, no BV • No fetal parts • Diffuse trophoblastic hyperplasia • Diploid (2 sperms) • Choriocarcinoma 2% • High βHCG levels. Mole Partial • Partially cystic, few BV. • Fetal parts + • Focal hyperplasia of trophoblasts • Triploid (ovum+2 sperms) • Rare carcinoma • Relatively less βHCG. 13
    • Core Learning Issues: Pathology Major CLI: • PolyCystic Ovary Syndrome (PCOS) • Tumors of Ovary – overview (Common: Cystadenoma, dermoid cyst, carcinoma) • Gestational Pathology – chorioamnionitis, mole/Ch.Ca. Pathology Minor CLI: • Ectopic pregnancy. • Eclampsia & Pre-Eclampsia, Gestational tumours. • Hydatidiform mole, invasive mole, choriocarcinoma. • Other tumours of ovary – Teratoma / Teratocarcinoma, 13
    • Dec 2011: Remember the Challenge….! 4th Year Students at JCU School of Medicine set new record.…!!! 100% Pass & Class Average over 70%
    • Asking quality questions is the key! 13
    • What am I doing? - Where am I going? (Where I want to be in 5 years?) “Identifying your Goal is like identifying the North Star, you fix your compass on it and then use it as the means of getting back on track when you tend to stray” -- Marshall Dimock
    • "I learned that good judgment comes from experience and that experience grows out of mistakes!" – Omar Bradley
    • Education is what remains after we have forgotten all the facts taught in the class! --
    • “A man must be big enough to admit his mistakes, smart enough to profit from them, and strong enough to correct them!” --John C. Maxwell
    • Wish you all Success, Health, & Happiness in life. Need help for exams? You can still contact me..