"Powered by intellect,Driven by Values..!”
Life motto of Infosys founder and Chairman, Narayana Murthy. INDIA
1
Tip for Success in life….!
T4W1: Week overview:2013 Term 4 CPC 1
Title: MSK
System: RheumatologyAim: To train students in:
History taking + clinical examination of patient with joint pain ; pathology of physiologyof rheumatological diseases; process of care + population health especially in rural and remote areas
Learning Outcomes:
Students will be able
to
1. Demonstrate competency in history taking & clinical examination of patients
presenting with joint pain2. Describe the Pathophysiology of
• 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: Ms F.M. 19 year old student – Scenario 2: Mr J.W. 45 year old foot, 1st metatarsal – Scenario 3: Mrs N.M 69y retired Sports teacher.
• 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
Rheumatoid A Gouty Arthritis Osteoarthritis
4
COMMON CLINICAL ARTHRITIS
Differentiating Features:
5
Rheumatoid Arthritis:• Young, small joints• Autoimmune.• Synovial Inflammation• synovium Cartilage
Osteoarthritis:• Old age, Large joints• Degenerative.• Cartilage degeneration.• Cartilage Synovium
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
8
Normal Osteoarthritis
Osteoarthritis: Ankylosis
9
• varus deformity of the knee and collapse of the joint space with destruction of the medial cartilage and the subchondral cortex (open arrowheads).
OA Hip:
10
RA - Pathophysiology
11
Autoimmune TH1, TH17 & B cellsMMPs, TNF, PGE2
Synovial Inflam & Proliferation withPapillary projections
Chronic Inflam.Lymphocytes &Lymphoid follicles
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.
• Large deposits – Tophi
13
Tophus
Acute Chronic
Degenerative Disc Disease (DDD)
• Ageing / trauma• Low back pain/deformity.• Complication:
– Nerve damage
Common Disc degenerations
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 CPC 2
Title: Renal Disease (Glomerulonephritis)
System: Nephrology – Renal DiseaseAim: • Clinical, Pathology & population study of patients with kidney
function disorders.• Pathology & clinical diagnosis of patient with chronic illness—
chronic kidney diseasesLearning
outcomes: The student
will be able to
1. Demonstrate competency in history taking & clinical examination of patients with renal disease.
2. Describe the Investigation and first line management of UTIs, 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.
2. 2 year old boy presents with sudden onset polyuria, proteinuria following mild fever.
3. 8 year old girl presents with fever, oliguria, smoke coloured urine & hypertension following upper respiratory tract infection.
4. 49y, nephrotic syndrome non-responsive.
5. 18y male recurrent painless hematuria, 3-6 days, usually following fever, URTI.
MGN
MCD
PGN
IgA
FSGS
Anatomy of Renal System
Cortex
Medulla - pyramid
Renal Papilla
Renal calyx
LR
Anatomy of Kidney
Note the positions of Glom, PCT, Loop, DCT, CT
Glom, PCT, DCT
Aldosterone
ADH
Renin
Renal Physiology: Urine, Hormones & Homeostasis
Hypertonic media
Normal Kidney: Histology
DCT
PCT
Gl.Cap
Mesang.
Aff.Art JGA
* 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
• Oliguria• Hematuria• Non selective Proteinuria.• GFR, Cr, BUN• Edema (salt and water
retention)• Hypertension• RBC & Protein casts.
Nephrotic
• Proteinuria (“nephrotic range” >3.5g/24h)
• Edema (retention+Hypoalbuminemia)
• Hyperlipidemia• Lipiduria• Protein casts.
urineurine
Synonyms:
Incidence:
Etiology:
ClinicalFeatures:
LabFeatures:
Pathology:
ClinicalCourse:
Nil disease, lipoid nephrosis, foot process disease
Idiopathic. Loss of net negative charge destruction of podocyte foot processes.
Nephrotic syndrome. History of recent URI in 30%. Association with Hodgkin’s lymphoma. Overlap with FSGS patients.
Nephrotic urine (polyuria, Selective proteinuria. (albuminuria).
Spontaneous remission in 25-40%. Complete remission in 65-70% of patients. Steroid resistant patients may progress to FSGS.
Normal Microscopy. IF - Negative.EM loss of foot processes.
80% of nephrotic syndrome in children (1-8 yrs.), mostly male. Adults in 2nd-3rd decade.
Minimal Change GN:
Normal Microscopy
Loss of foot process - EM
Focal Segmental GN: Adults
Synonyms:
Incidence:
Etiology:
ClinicalFeatures:
LabFeatures:
Pathology:
ClinicalCourse:
Focal segmental Sclerosis
Idiopathic - ? Auto Immune. No deposits. (Similar to minimal change).
Nephrotic syndrome. History of recent URI in 30%. Association with Hodgkin’s lymphoma. Overlap with MCD patients.
Nephrotic urine (more, clear) Selective proteinuria. No specific laboratory findings.
Spontaneous remission 30% , 50% progression to chronic renal failure, 20% rapid progression.
Podocyte damage, Segmental collapse of glom. increase in matrix (pink).
10 - 35% of nephrotic syndrome in adults.
Synonyms:
Incidence:
Etiology:
Clinical:
Lab:
Path:
ClinicalCourse:
membranous GN
Immune complex deposition. Idiopathic in most patients, associated with infections, drugs, carcinomas, and heavy metals.
Nephrotic syndrome in 80%, asymptomatic proteinuria in 20%. Microscopic hematuria.
Non-selective proteinuria ± hematuria.
Excellent prognosis in children. Some adults develop ESRD. Exclusion of other diseases is required.
Diffuse, uniform BM thickening with subepithelial projections (“spikes”). Diffuse, coarsely granular IgG and C3 deposits along basement membranes. Electron-dense subepithelial deposits.
40-60 Years, 50% of adult nephrotic syndrome.
Membranous GN:
Wireloop
Synonyms:
Incidence:
Etiology:
Clinical:
Lab:
Path:
ClinicalCourse:
Acute proliferative glomerulonephritis, acute post-infectious GN.
Glomerular trapping of circulating immune complexes. (Group A, Beta-hemolytic streptococci, type 12).
Acute nephritic following strep. pharyngitis or pyoderma. (Other infections rare)
Nephritic urine (little, dark, smoky) RBC casts, non selective proteinuria. Decreased serum complement. Evidence of strep inf.
Children - Excellent prognosis. Adults - Worse prognosis, some develop progressive disease.
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.
children (3-14). Sporatic, mostly winter and spring.
Acute Post Strept, Diff, Prol GN:
• 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 Nephropathy (Berger’s)
IgA dep.
Normal
IgA dep.
Progression of GN:
Renal Failure
Renal Insufficiency
Endstage
Decreased Renal reserve
GFR
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
Glom. Norm
Necrotic PCT(no nuclei)
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 + RenalAim: Understanding pathology ,presentation and clinical
diagnosis of patients with urinary obstruction & urinary tract infections.
Learning outcomes:
The student will be able to
1. Demonstrate competency in history taking & clinical examination of patients with urinary symptoms.
2. Demonstrate competency in the clinical examination of 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 BPH6. Describe the anatomy and histology of bladder,
urethra + prostate;
Week Learning outcomes:2013 Term 4 CPC 3 Title: Male Genitourinary
System:GU + RenalAim: Understanding pathology ,presentation and clinical
diagnosis of patients with urinary obstruction & urinary tract infections.
Learning outcomes:
The student will be able to
7. Describe the pathology of BPH, prostate cancer, renal and bladder tumours ,and renal and bladder calculi
8. Outline the Professional, ethical & legal issues in 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
Calcium Oxalate
Nephrolithiasis: Organic matrix(3%) + salts (97%) ~
• Calcium stones (80%): oxalate/phosphate/urate salts. – 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. • Cystine stones (2%)
– Genetic disorder - Failure of reabsorption
Staghorn Calculus:
Male Urogenital System - anatomy
Ca
BPH
Zonal Histology:
BPH
Ca.
Normal Histology: Fibro-Musclular-Gland
Two Layer Ep.
Fibromuscular stroma
Secretions
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
Cystic Gl
Nodule of BPH
Secret
ions
BPH-Complications:
1. Obstructive Uropathy2. Bladder hypertrophy3. Trabeculation4. Diverticula formation5. Hydroureter – bilateral6. Hydronephrosis7. Lithiasis / stone.8. 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
Benign: Double layer. Secretion (clear cytopl) Uniform cells Papillary folds
Malignant Single/crowded. Less/no secretion. Uniform/Pleomorphic No papillary folds. But
crowding & clustering.
Normal
Ca.
Normal
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-OrchitisSystem: Male Genital System
Aim: Clinical, Pathology & Population study of patients with male genitalsystem disorders & sexually transmitted disease (STD) using a case of epididymo-orchitis with a differential diagnosis of testicular torsion and testicular tumour.
Learning Outcomes The student will be
able to
1. Demonstrate competency in history taking & the clinical examination of male patients with genital disorders
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. 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.
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 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 recurrent attacks of sharp pain in right groin with small painful bulge, disappears on laying down.
68y male, erythematous, irregular, raised papule on penis/glans since 6 months.
Torsion
Seminoma
Ep.Orchitis
Hernia
Bowen/EQ
Structure, origin, Lymphatics:
Normal Testes:Leydig Cells
Sperms
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.
- 9m
- 3mAbdominal
Inguinal
Suprascrotal
Normal
~ 1 yearNormal Atrophy
Testes Atrophy:
Bilateral in Hypopituitarism, Chronic Alcoholism, chemotherapy or radiation.
Hormonal, infection, Cryptorchidism. Mumps – Patchy. Sertoli only, Leydig cell hyperplasia.
high chance of neoplasms.
Normal
Atrophic
Normal SpermatognesisFew Leydig cell cluster outside
AtrophySertoli 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 SchwarzeneggerBodybuilder, Actor & Leader.
T4W5: Week overview:
2013 Term 4 CPC 5 Title: Breast Cancer System: Breast
Aim: Clinical, Pathology & population study of patients breast disease
Learning outcomesThe student will be
able to
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.
3. Describe the Pathophysiology of breast disease (benign and malignant)
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 Adult (Lactating) MenopauseFibrous Fibro-Fatty Fat
Disorders of Breast:
Fibrocystic Disease
FibroCystic Disease: types
A. Simple Fibrocystic change.B. Lobular hyperplaisa without atypica (adenosis)C,D - Ductal hyperplasia without atypia (E. with atypia - cribriform)F. Lobular hyperplasia.
Non prol. / low grade
Prol. / High grade
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
Slit like glands
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.
StromaTumour
N. Breast
Capsule
Breast fat
N. Fat
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..
Leafy folds
Etiology of Breast Carcinoma:
• 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
GeneticsHormone
Environment
• Family history – First degree relative.
• Premenopausal & bilateral.• Early menarche/Late menopause.
• Estrogen therapy.• Alcohol, Smoking.• High fat diet,
Obesity.
• HER2/NEU• RAS & MYC• BRC A1, A2.
Pathogenesis of Breast Cancer.
Hyperplasia Dysplasia DCIS CarcinomaFibrocystic change Cancer
Duct Ca. in-SituDCIS
Pathogenesis:
Infiltrating Duct Carcinoma: Breast Ca.
Note: Fibrotic tumor, radiating fibrous scar around resulting in nipple retraction & skin pulling (puckering)
(NOS or Classic or typical “Schirrhous carcinoma”)
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. Cells
Ca. Cell
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
98
T4W6: Week overview:
2013 Term 4 CPC 6 Title: Female Gynaecological 2System: Female genital tract
Aim: Understanding pathology & clinical diagnosis of female patients with 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 tract5. Describe the difference in presentation in STIs in women and men6. Discuss the screening program for cervical cancer in Australia7. Construct a management plan for patients with normal and
abnormal PAP smears8. 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.
Case studies:• 8year girl, vaginal bleeding and discharge.• 21year female, itchy vaginal discharge foul
smelling.• 26 year old thick white cheesy discharge.• 25 year old, whitish yellow pus discharge.• 31year female, irregular heavy bleeding. • 34year female, irregular & post coital bleeding.• 28y G2 P1, second trimester vaginal bleed.• 69year female, vaginal bleeding
Trauma
Chlamy..
Candida
Gonoco..
DUB
CaCx
Molar preg.
Endo.. Ca
100
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.
101
Vaginal disorders:Sarcoma Botryoides
Sarcoma, 1-5 year children
102
Pelvic Inflammatory Disease (PID):
Infertility
Pain & Fever
Mass
103
HPV: Condyloma acuminatum
Ano-genital wart, soft, HPV 6 & 11, STI, Benign,
A. Small, warty, Cauliflower-like growth.
B. Koilocytes: peri nuclear halo + viral particles
C. Mild Dysplasia. (Cx. CIN-1)
A B C
104
Transformation Zone:
105
Colposclopy & Acetic acid test
mosaic pattern resembling inlaid woodwork. (LSIL)
Erythematous patch in the transformation zone.
Before acetic acid After acetic acid
http://www.operationalmedicine.org/ed2/images/Cervix/Cervix.htm
106
Normal Ectocervix :Strt. Sq. Ep
SUPERFICIAL
INTERMEDIATE
BASAL
107
PAP: CIN I-III Comparison (note nuclei)
Normal CIN I (LSIL)
CIN II (HSIL) CIN III
PAP Smear
CINPathogenesis & Features
25y 30y 35y 45y
109
Low Risk
– 6,
11.
High Risk 16, 18
HPV - Pathogenesis:
Vulva, Vagina, Cx
Benign Wart(CIN1/LSIL)
???
Cx-Transition Zone - HPV
Smoking, Estrogens, Genetics..E6, E7 protein Rb & p53
Carcinoma
CIN1/LSIL
CINII-III/HSIL
LSIL: Lowgrade Squamous Intraepithelial Lesion (CIN1)HSIL: Highgrade Squamous Intraepithelial Lesion (CIN II, III)
110
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.
111
Cervical Dysplasia: HSIL margin
HSIL/DysplasiaNormal
112
Cervical Dysplasia: HSIL
?
113
HSIL early invasion: Ca
Invasion
“We choose our joys and sorrows long before we experience them!”
--Khalil Gibran
115
• Myometrium: – Benign – Leiomyoma– Malignant – Leiomyosarcoma
• Endometrium:– Endometritis.– Endometrial Hyperplasia – polyp, diffuse, atypical.– Endometriosis, Adenomyosis.Endometrial tumor:– Malignant – Endometrial Carcinoma.
Disorders of Uterus & Endo..
116
Endometrial Hyperplasia & Polyp:• Hyper-estrogenemia.• Hyperplasia of endometrium, may form
polyp.• Common cause of uterine bleeding - DUB• Risk of malignancy – more with
atypical/dysplasia.
117
Uterus Adenomyosis:
Endometrial Cavity
Cervix
Adenomyosis
118
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,
119
Endometrial Ca:• Adenocarcinoma (not HPV)• Estrogen – risk factor.• Post-menopausal bleeding.• Irregular, polypoid, bleeding.• Dysplastic back to back glands• Little/no stroma. Adenocarcinoma
Hyperplasia
We are responsible for what we are…
You are the stone, You are the chisel, and You are the sculpture….!
www.akshardham.com
LAST LECTURE !CPC47-Ovary
T4W7: Week overview:Term4 CPC 7 Title: Female Gynaecological 2
System Female genital tract
Aim: Understanding pathology & clinical diagnosis of female patients with abnormal vaginal bleeding
Learning Outcomes:
The student will be able to
1. Demonstrate competency in History taking & the clinical examination of patients with abnormal vaginal bleeding.
2. Demonstrate competency in history taking and clinical examination ofpatients with menopausal symptoms3. 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
123
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,
124
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.
125
Endometriosis: chocolate cysts
Frozen Pelvis - adhesions
126
Classification of Ovarian Tumours
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.
128
Tooth..!
FatHair
Dermoid Cyst
Dermoid Cyst
Dermoid Cyst
Immature Teratoma
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..
129
130
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.
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).
131
132
Mole/Molar pregnancy1. 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.
133
Complete Mole Partial• All villi cystic, no BV• No fetal parts• Diffuse trophoblastic
hyperplasia• Diploid (2 sperms)• Choriocarcinoma 2%• High βHCG levels.
• Partially cystic, few BV.• Fetal parts +• Focal hyperplasia of
trophoblasts• Triploid (ovum+2 sperms)• Rare carcinoma• Relatively less βHCG.
134
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,
Remember the Challenge….!Dec 2011:
4th Year Students at JCU School of Medicine set new record.…!!!100% Pass & Class Average over 70%
Yes We Can…!
136
Asking quality questions is the key!
“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
What am I doing? - Where am I going?(Where I want to be in 5 years?)
"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..
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