Updated Breast Pathology Lecture to medical students.

1. Knowledge is a burden,
If it robs you of innocence,
If it makes you feel you are special,
If it gives you an idea you are wise,
If it is not integrated into life,
If it does not bring you joy,
If it does not set you free.
Sri Sri Ravi Shankar,
Humanitarian and founder of the Art of Living Foundation, India.

2. CPC 4.5 – 42y Woman, sore R. breast.
Mrs JM is a 45y old woman, primary school teacher, living in Weipa.










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
“odd change in my left breast when I was showering last week”
Duration.
Noticed it 8 days ago
What? “My left breast feels a bit thicker – points to upper outer quad*
Pain No, Nipple discharge: No, Trauma to breast: No
Menstrual cycle: regular, Mastalgia: not usually
LMP: about 4/52 ago; K due now.
Age of menarche: 13 years*, Parity: none* (failed IVF / infertility*)
Appetite, Weight : stable*
was on COCP* ages 17yrs – 30 yrs.
Cervical smear: Never*
Menarche aged 13yrs*
Has never had mammogram/breast USS* ‘I check regularly’ *

3. CPC 4.5- Examination
Key .. ?
Fibrocystic
o R breast NAD, L breast firm thickening ? upper
Tumor
outer axillary tail ?; no discrete mass ? no skin
Cancer
tethering ? / changes; no nipple inversion ?; no
areola changes ?, no axillary or supracla. LN. No Cancer
Paget’s
nipple discharge(blood/pus) ?
Cancer
 What Differentials:
Papilloma
 Benign proliferations, Breast malignancy
Duct ectasia
 What further investigations?
 Mammogram, FNAB, CT Scan, PET Scan,
Biopsy + immunochemistry (HER2) ?
Labs:
ER
PR
HER2
BRC

4. CPC 4.5- Examination




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Mammogram – solid* non mobile* irregular* mass lying at
the 10 o’clock position of the L breast. Mass has prominent
radiating spicules*; 2 x small calcifications* within the mass.
Overall mass 1x 1.5x 1cm.
US guided FNAB: High grade infiltrating ductal carcinoma ?
CT scan: no sign metastatic disease in liver or lung
Bone scan: no sign of metastases.
Immunochemistry : ER: ++ PR: neg HER2: +++.. ? ? ?
(? Sub types, Luminal B)

5. CPC 4.5 – 42y Woman, sore R. breast.
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

6. CPC 4.5- Core Learning Issues
Pathology Major CLI:
•
•
•
•
•
•
Pathology of Breast – overview, classification & common dis..
Breast Lumps - Differential diagnosis.
Trauma, infections & Inflam. – Mastitis, fat necrosis, abscess.
Hyperplasia – Fibrocystic disease
Tumours – Benign – Fibroadenoma, giant fibroadenoma.
Breast cancer – etiology, pathogenesis, morphology &
complications, Laboratory diagnosis, including markers.
Pathology Minor CLI:
•
•
•
•
Duct ectasia,
Breast Cysts.
Paget’s disease.
Gynecomastia & male breast disorders.

7. Case studies:

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
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.

8. 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.


9. “Strength does not come from winning,
Struggles & Hardship develop strength.
- - Arnold Schwarzenegger
Bodybuilder, Actor & Leader.

10. Pathology of Breast
Dr. Venkatesh M. Shashidhar
Associate Prof. & Head of Pathology

11. CPC- 44 – Core learning Issues

Major CLI:

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
Pathology of breast diseases – over view
Congenital, Inflammatory & Neoplastic disorders.
Breast Lumps – Hyperplasia – Fibrocystic disease.
Benign neoplasms: Fibroadenoma, Duct papilloma &
Breast cancer – Ductal Carcinoma & DCIS.
Minor CLI:





Cong:
Hypertrophy, atrophy, accessory, supernumerary..
Mastitis (acute/chronic), Breast trauma, fat necrosis.
Phyllodes tumor, other carcinoma (Lobular etc)
Duct ectasia.
Paget’s disease.

12. Introduction: Anatomy
Modified
sweat glands.
Lobes and lobules of gland
in fat tissue stroma.
Ducts emerge from acini of glands
Smaller ducts join to form
lactiferous ducts
Lactiferous ducts merge just
beneath the nipple to form a
lactiferous sinus.
Then individually open on nipple

13. Anatomy
T4 level

14. Breast Physiology:
Male
Female

15. Normal Breast – glands & stroma
Dense stroma
Loose stroma
Acinus

16. Normal Breast – glands & stroma
Loose stroma
Acinus
Dense stroma

17. Breast – Acini (SEM)

18. Age changes in breast:
Puberty
Fibrous

Adult (Lactating)
Fibro-Fatty

Menopause
Fat

19. Disorders of Breast:

Congenital

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
Inflammatory

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Acute: lactational* / Chronic Mastitis
Trauma – Traumatic Fat necrosis
Duct ectasia – chronic, discharge, sinus,
Galactocele
Proliferative Conditions



Aplasia : turners / Juvenile hypertrophy
Accessory/ectopic breasts – along milk line
Fibrocystic disease – common cause of lumps
Cysts, Adenosis, Metaplasia & mixed.
Neoplastic


Benign – Fibroadenoma, duct papilloma
Malignant – Ductal Carcinoma & DCIS – several types.

20. Disorders of Breast:

21. Gynecomastia:



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

Breast enlargement in men.
Estrogen excess –
Klinefelter’s, Hyperthyroidism, pitu
itary & adrenal tumors, testicular
failure, hormonal.
Liver failure, cirrhosis
Lung, Testicular Cancer
diethylstilbestrol therapy for
prostatic carcinoma.
Drugs (Spironolactone, H2
antagonists, Neuroactive agents).
Microscopy – only duct & stromal
hyperplasia. (no acini)

22. Acute Mastitis:

Acute Mastitis:


Non Lactational
(central, periductal, rare)
Lactational (periphery, common)





First few weeks after delivery.
Crack in the nipple – entry point.
Staph. aureus, Strep. pyogenes.
Localized inflammation, Swelling erythema
& pus.
Chronic Mastitis:



Granulomatous (TB, Fungal, Silicone
etc.)
Traumatic fat necrosis: Chronic
granuloma, foam macrophages, radial
scar – dd Ca.
Diabetic mastopathy: DM1, rubbery
lymphocytic.

23. Duct Ectasia:
Mimics Ca.
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>50y, multiparous. Periareolar mass
with white, cheesy nipple discharge.
Duct obstruction/destruction,
inflammation, dilation, fibrosis with fat
globules & foamy macrophages in
lumen.
Recurrent abscess / fistula.
Scarring with nipple inversion may
mimic Ca.

24. Lump in Breast: Diagnosis & Features
Clinical presentation
<25 years
25-35 years
35-55 years
>55 years
Mobile lump (single)
Fibroadenoma
Fibroadenoma
Fibroadenoma
Phyllodes
tumour
Phyllodes
tumour
ill-defined lump/s or lumpy
areas – cyclic pain.
Uncommon
Fibrocystic
change
Uncommon
Firm lump tethering
(fixed)
Uncommon
Fibrocystic
change
Sclerosing
adenosis
Carcinoma*
Carcinoma
Carcinoma
Fat necrosis
Nipple discharge
Clear/pus
Uncommon
Uncommon
Duct ectasia
Duct ectasia
Bloody
Uncommon
Uncommon
Duct papilloma
Duct papilloma
In situ
carcinoma
Paget's
disease
In situ
carcinoma
Paget's
disease
Nipple adenoma
Nipple
adenoma
Nipple ulceration, eczema
Nipple
adenoma
Nipple adenoma

25. Fibrocystic Disease/change:
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Pathology: Harmone induced acinar
hyperplasia. Oestrogens*
Clinical: Commonest (40%) cause of
lumps in 20-40y. Irregular induration/
lumps. Cyclic pain/discomfort.
Gross: Grey white scar tissue with
cysts.
Micro: Fibrosis, cysts, hyperplastic
glands.
Pathogenesis: Hyperplasia of glands
and stroma  DCIS  Carcinoma.

26. Fibrocystic Disease

27. 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.

28. FCD: Cysts, Fibrosis & Proliferation

29. FCD + Ductal Hyperplasia*
Hyperplasia may progress to DCIS
(Duct Carcinoma In-Situ).
Progress to duct carcinoma.

30. FCD: Ep. Hyperpl. - Sclerosing Adenosis*
Small duct proliferation.
Clinical & biopsy
mimics carcinoma.

31. Fibrocystic Disease-Blue dome cyst
When single large cyst - blue

32. Education must instill the fundamental
human values; it must broaden the vision to
include the entire world and all mankind.
Education must equip man to live happily.
-- Satya Sai Baba

33. 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)

34. Fibroadenoma
Types
Solitary
Few (< 5 / breast )
Multiple (> 5 / breast )
Giant (> 4 / 5 cms) & Juvenile
Low grade
Benign
Natural history
Majority remain small & static
50% involute spontaneously
No future risk of malignancy
High grade

35. 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.

36. Mammogram - Benign

37. Fibroadenoma
Note: well demarcated, capsulated, nodular tumour

38. Fibroadenoma

39. Fibroadenoma
In
P
P
In
P
C = capsule; In = intracanicular pattern; P = pericanicular pattern

40. Fibroadenoma
Summary:
 Small discrete mobile.
 Stromal neoplasm with
reactive glands.
 No malignant potential.
 Regress / calcify in
menopause.
 Increase in pregnancy.

41. Giant Fibroadenoma
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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..

42. Fibroadenoma
Flat slit glands, fibrous stroma, Benign.
– Giant Fibroadenoma
Branching leaf like glands, Cellular stroma
Benign 85%  malignant 15%.

43. Intraductal papilloma
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Clinical: Middle age, Bloody
discharge, sub areolar lump.
Duct wall
Gross: Solitary, Intra-ductal
papillary Proliferation.
Micro/Path: Benign papillary
proliferation of lactiferous duct
epithelium.
Stalk & papillae
Prognosis: recurrent, but no risk of
malignancy. (rare)

44. Education has two important
characteristics. One is learning of a
subject & skill. The other is the
personality to apply this knowledge to
the benefit of community.
--Baba
One without the other is either useless or dangerous…. !
Knowledge, Skill & Attitude
* JCU graduate attributes..

45. Breast Carcinoma – Aus. stat.

The most common cancer among Australian women (also
in aboriginals). (20%)
 UK 1 in 10 women, 1 in 8 in US, 1 in 9 Aus.
 One in nine women before the age of 85.
 28% of all cancer diagnoses in 2006.
 Increased from 5,289 in 1982 to 12,614 in 2006
 Commonest cause of death in young < 55y
 Rare before age 30. (30-50 genetic, >50 sporadic)
 Much less incidence in Asia, Japan.
 Majority of cancers arise in the ducts.
 Survival is improving with therapy. (96% 5y – 2006)

46. Etiology of Breast Carcinoma:
• HER2/NEU
• RAS & MYC
• BRC A1, A2.
Environment
Hormone
• Family history – First degree relative.
• Premenopausal & bilateral.
• Early menarche/Late menopause.
•
•
•
•
Genetics
• Estrogen therapy.
• Alcohol, Smoking.
• High fat diet, Obesity.
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

47. Pathogenesis of Breast Cancer.
Duct Ca. in-Situ
DCIS
Hyperplasia  Dysplasia  DCIS  Carcinoma
Fibrocystic change  Cancer

48. Pathogenesis:

49. Ductal Carcinoma in Situ (DCIS)

Dysplastic cells filling ducts with
Ca+, no invasion. Pre-cancer state.
 Increasing incidence of DCIS due to
mammographic screening. (diffuse
irregular firm/lumpy areas)
 Spreads throughout ductal system to
produce extensive lesions.
 Many types: solid
cribriform, papillary, and
micropapilary, comedo type or mixed
pattern. (dysplasia: low – high grade)
 Progress to invasive carcinoma.

50. Ductal Carcinoma in Situ, DCIS

51. DCIS – Comedo type (high grade)
DCIS
Central necrosis (comedo)

52. Myoepithelial Cells in DCIS
(imunoperoxidase stain note intact BM & ME cells)
DCIS
All ducts, ductules and acini are separated from the interlobular and intralobular
connective tissue (stroma) by a basement membrane & Myoepithelial cells.

53. DCIS- High grade

54. Ca Breast: Histological Types
Histologic Type
Freq. (UK)
InfiltratingDuct Ca
63.6 (75)
Lobular Carcinoma
5.9 (10)
InfiltratingDuctal & Lobular Ca
1.6
Medullary Carcinoma
2.8 (3)
Mucinous (colloid) Carcinoma
2.1 (3)
Comedocarcinoma
1.4
Carcinoma-In-Situ
5%

55. Prognostic / Genetic Classification: (new)
1. Luminal A – 50% of NST. ER+, HER2 –ve. Low grade, slow
L
growing, post menopausal, respond to harmone therapy. –
Better prognosis.
2. Luminal B – 20% of NST. ER+, HER2/neu +ve. (triple
positive ca.) high grade, respond to chemo.
3. Basal like – (Triple neg) 15% of NST. ER-, HER2/neu –
H
ve, BRCA1+, young. Poor prog.
4. HER2 positive – 10% ER- HER2 +, high grade, poor
prognosis, early brain mets. (Trastuzumab)
HER - Human Epidermal Growth factor Receptor  Growth.
ER - Estrogen receptor  function.
ER is good & HER is bad…!

56. Breast Ca-Clinical
Lymphnode mets.
Skin Puckering
Nipple retraction

57. Breast Carcinoma





Irregular, hard, grit
ty Painless
nodule.
Tethering/puckerin
gfixation
Nipple retraction
Oedema
Lymphnodes

58. 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)

59. Mammogram - Ca

60. Breast Carcinoma Inflammatory / medullary



Inflamed, bulging without
nipple/skin retraction.
Uncommon.
High grade / medullary type
(HER2 & BCRA1)

61. Breast Carcinoma - Schirrous

62. Infiltrating Duct Carcinoma: small hard

63. Typical Invasive Ductal Carcinoma / Duct Ca (NOS)
Ca-tubules
collagen stroma

64. DCIS component within Duct Ca (NOS)
DCIS

65. Infiltrating Duct Carcinoma

66. Breast Ca. Lymphedema
Pathogenesis of Peu-de Orange in High grade Ca.
Tumor in lymph Vessel
Tumour emboli within lymphatic vessels  obstruction  Lymphedema
(also radiation induced lymphangitis can cause peu-de orange)

67. Medullary type (high grade): * note lymphocytes, no collagen/scar
Expansile tum
Ca. cells
Lymphocytes

68. Lobular Carcinoma:



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

Multifocal, Bilateral.
Small cells, uniform, no tubules.
Target like growth around
normal tubules.
‘Indian file (single cell lines)
between collagen bundles. No
tubule formation.
Lobular Ca-in-situ(LCIS)
E-cadherin –ve (unlike IDC)
ER/PR neg, HER2/neu pos.

69. Spread of Breast
Carcinoma:

70. Pagets Disease

Spread of Breast cancer
cells to skin (areola) &
resulting in Eczematous
reaction.
Ca. Cell
Ca. Cells

72. Diagnosis: History First….!






Mammorgraphy
Fine Needle Aspiration Biopsy
Core/Needle Biopsy
Excision Biopsy
Ultrasound
Special molecular tests on Biopsy:


Immunoperoxidase – HER2, ER & PR.
Molecular techniques – Gene detection (BRCA).
Triple Assessment  Clinical,
Imaging & Biopsy

73. Breast clinic: incidence

74. Breast clinic: incidence

75. Mammorgram
• Low
radiation (0.1rad)
• Light compression by plates to stabilize
and spread its interior structures.
• Detect Fibrosis & Calcifications <100 µm
• Reveals a lump 1-2y before BSE.
• Women >40y should have yearly* mammogram.
• More for those at risk or symptoms.

76. Mammogram
:
Normal – 18y
Normal 40y
Carcinoma
Dusty Ca+
Malignant
Cancer

77. Breast Ca. screening: new research

Cochrane Summaries:
 Research involving 600,000 women, results showed “for
every 2000 women screened



one will avoid dying of breast cancer
10 healthy women will be treated unnecessarily.
>200 experience distress due to false positive findings.

78. Breast Cytology - FNAB
Benign
Malignant

79. Tumor Markers
in Breast Ca.
ER: Estrogen Receptors.
PR: Progesterone Receptors.
HER2/neu: Human Epidermal growth factor
Receptor 2
E-Cadherin: Cell adhesion protein.
BRCA: Breast Carcinoma Antigen.

80. Immunoperoxidase stain: (ER, PR, HER, BCL, p53, E-Cad),
Neg
1+
2+
3+

81. Nuclear ER positivity - 3+

82. Gene expressions
portraits of breast
carcinomas.
(micro array)
Identify new breast
cancer subtypes
(“luminal A,”
“HER2/neu
positive,” & “basallike”).

83. HER2 (Human Epidermal growth factor Receptor 2)

The HER2 proto-oncogene encodes a cell surface
receptor that is over expressed in approximately 25%30% of breast cancers. (normally 2 copies).
 HER2 positive breast cancers grow quickly and spread
more than others. (poor prognosis)
 HER2 testing (Immunohistochemistry/FISH) results are
critical to ensuring that patients who may benefit from the
anti-HER2 antibody therapy.
 Trastuzumab (Herceptin®) is the first monoclonal antibody
that targets the extra cellular domain of the HER2
protein, and inhibits growth of breast cancer cells that over
express this protein.

84. BRCA1







(FISH Technique)
52% of genetic type (2%
overall)
Young age.
Risk of Ca – 40-90%
High
grade, necrosis, inflam (..
Medullary)
Triple –ve (ER,PR, HER2)
F/H of
ovarian, prostate, pancre
as ca.
Chromosome 17q







BRCA2
32% of genetic type (1%
overall)
Not specific.
Risk of Ca 30-90%
Low grade, NOS type.
Scaring (..Schirrous)
ER positive.
F/H of male breast ca
(ovary, prostate also)
Chromosome 13q.

85. Progression of Breast Ca: (new)

86. Common Ca. Breast: NST / NOS / Schirrhous Ca / Infiltrating duct Ca.
Mammogram: Stellate Lesion on Mammogram
Gross: Hard irregular - Schirrhous
Micro: Pleomorphic cells forming tubules in dense fibrous stroma.

87. 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.

89. Sign or symptom
Pathological basis
LUMP
DIFFUSE
Fibrosis, epithelial hyperplasia and cysts in fibrocystic change
DISCRETE
Neoplasm or solitary cyst
MOBILE
Benign neoplasm (usually fibroadenoma)
TETHERED
Invasive neoplasm (carcinoma)
SKIN FEATURES
OEDEMA (PEAU
D'ORANGE)
Impaired lymphatic drainage due to carcinoma
PUCKERING AND
TETHERING
Invasion of skin by carcinoma
ERYTHEMA
Increased blood flow due to inflammation or tumour
NIPPLE
DISCHARGE
Milky-pregnancy or prolactinoma
White/green-duct ectasia
Bloody-duct papilloma or carcinoma (rare)
RETRACTION
Tethering by invasive carcinoma
ERYTHEMA AND SCALING
Paget's disease of nipple (cancer) or eczema
BREAST PAIN
CYCLICAL
Benign breast changes – fibrocystic change
ON PALPATION
Inflammatory lesion (e.g. mastitis)
MICROCALCIFICATION
invasive carcinoma (also in cysts, benign changes, DCIS)
BONE PAIN OR FRACTURE
Possibly due to metastatic breast carcinoma or associated with hypercalcemia

90. Confusion
Distinction and explanation
Fibroadenoma &
Fibroadenosis
Fibroadenoma is a localized circumscribed benign neoplasm comprising
epithelial cells and specialised fibrous tissue. Fibroadenosis is an obsolete
name for fibrocystic change, a diffuse hyperplastic lesion.
Fibroadenoma &
phyllodes tumour
both comprise neoplastic epithelial and fibrous tissue components. However,
in phyllodes tumours the fibrous tissue component is more cellular and
abundant, and the lesion has less well defined margins; borderline and
malignant variants occur.
Ductal epithelial
hyperplasia &
ductalcarcinoma
in situ
Ductal epithelial hyperplasia is a benign proliferation of duct epithelium,
whereas ductal carcinoma in situ has undergone neoplastic transformation,
although it is not yet invasive. These lesions can have morphological
similarities. A proportion share genetic alterations.
Radial scar &
complex
sclerosing lesion
Radial scars and complex sclerosing lesions differ only in size: the latter are
>10 mm diameter. Both mimic carcinomas radiologically and histologically,
but they are benign non-neoplastic lesions.
Medullary
carcinoma of the
breast & of the
thyroid
The term medullary refers only to the soft consistency (resembling the
medulla of the brain). There is no other relationship between these lesions.
Paget's disease of
the nipple & of
bone
Both lesions were described by Sir James Paget (1814-1899). There is no
other relationship between these lesions.

91. Benign









Young <35y
Multiple
Painful
No bleeding
Soft, cystic,
rubbery
Regular, nodular
Mobile
No lymphnodes
No weight loss.
vs
Malignant



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Old >35y
Single
Painless
Bleeding
Hard gritty
Irregular
Fixed
Lymphnodes
Weight loss

92. What is this? 
•
•
•
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What is PET Scan?
What contrast is used?
What does it show?
What are its Indications ?
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Positron Emission Tomography.
Radiolabelled glucose by IV.
High metabolic rate cells (cancer cells)
3D view of cancer spread over body.

93. Infections
2. NonLactational infections : Central

Usually due to Periductal mastitis

Affects younger women. Often smokers
in the West

May present as : inflammation +/mass, abscess, mammary duct fistula

Aerobic + anaerobic organisms may
be involved
Treatment :

Antibiotics (E.G. Co amoxyclav etc)
before pus formation

Abscess : Repeated aspiration / mini
incision with topical anaesthetic cream
( I& D under GA occasionally)

MDF : Excision fistula + Total duct
excision