Pathology Review-Term4

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

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

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)

“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….!

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.

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.

Male Urogenital System anatomy

BPH

Normal Histology: Fibro-Musclular-Gland

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

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:

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.

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.

Age changes in breast:

Puberty
Fibrous



Adult (Lactating)
Fibro-Fatty



Menopause
Fat

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

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



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

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

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..

Pathology Review-Term4

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