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General Surgery > Breast And Endocrine > Flashcards

Breast And Endocrine Flashcards

1
Q

DCIS vs LCIS

A

Both are non-invasive, and are characterised by absence of stromal invasion

Ductal carcinoma in situ
25% of all newly dx breast ca
Usually unifocal
Frequently has a pattern of grouped microcalcifications
High risk of subsequent invasive carcinoma (ipsilateral)

VS

Lobular Carcinoma in Situ
0.5-1.5% of benign breast biopsies
Usually multi focal
Microcalcifications are rare
Not a true premalignant condition, if left untreated won’t progress to invasive
It is a marker of risk
High risk of subsequent invasive ca both breasts equally predisposed (but not limited to area of LCIS

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2
Q

IDC vs ILC

A

Invasive ductal carcinoma
70-80% of all invasive breast carcinoma
Unilateral localisation
Unifocal
More aggressive

Invasive lobular carcinoma
10-15% of all invasive br ca
Bilateral or unilateral
Multi focal
Less aggressive than ductal
Slower metastasis than ductal

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3
Q

Treatment of noninvasive breast carcinoma

A

DCIS:
-Breast conserving therapy or Mastecomy
-If BCT not feasible, do Mastectomy and Sentinel lymph node biopsy

LCIS
-Life long surveillance and chemoprevention with hormone therapy TAMOXIFEN
-surgery only if unsure of dx
-noninvasive doesn’t require systemic tx but radiotherapy might be indicated

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4
Q

Management of Invasive breast carcinoma

A

Stage 1&2
1. Surgery: breast conserving therapy followed by radiation therapy
2. Mastecomy for pt unable to undergo BCT or requests aggressive mx
3. Intra-Op lymph node evaluation (SLNB) to assess potential lymph node spread of ca cells to a axillary lymph node (indicated for all pt with neg preOp axillary LN.
-Axillary LN clearance for pt clinically positive preOp Axillary LN

Adjuvant systemic therapy
-Hormone and targeted biological therapy in all ER/PR+ (estrogen or progesterone receptor) or HER2+ patients
-Chemo in high risk pt

Stage 3 ca management
1. Neoadjuvant (before surgery) systemic therapy+ surgical resection (BCT or mastectomy) + Axillary LN resection
2. Followed by adjuvant therapy +/- radiation

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5
Q

Indications for chemotherapy

A

Metastatic LN
Aggressive tumour
Histology: HER2 positive or triple negative breast cancer
Locally advanced br ca (stage 3 I think)

Agents : Anthracycline and Taxane regimens

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6
Q

Side effects and contraindications of Chemo

A

Alopecia
Myelosuppresion
Hypersensitivity
Cardiotoxicity
Contraindicated in 1st trimester of pregnancy

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7
Q

Indications for hormone therapy (which agents to use)

A

Oestrogen receptor positive tumours

Premenopause:
1st line: Tamoxifen (serum estrogen receptor modulator), estrogen receptor antagonist, acts as agonist on uterus and bone. Often used in conjunction with ovarian suppression or ablation

Post menopausal
Aromatise inhibitors eg Arimidex (Anastrozole)

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8
Q

Side effects of hormone therapy in breast cancer tx

A

Page 211 lol

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9
Q

Side effects of hormone therapy in breast cancer tx

A

Page 211 lol

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10
Q

Complications of breast cancer

A
  1. Metastatic disease : bone metastasis
  2. Recurrence
  3. Paraneoplastic syndrome (hypercalcemia of malignancy)

Tx ass/complications
1. Endometrial ca promoted by Tamoxifen
2. Cardiotoxicity by certain chemo drugs
3. Anaphylactic reaction by certain drygs
4. Lymphadema or the arm
5. Angiosarcoma of the breast (or lymphangiosarcoma or hemangiosarcoma)
6. Skin changes and sensitivity from radiotherapy (post rad mastitis, joint stiffness, damage to underlying joint tissue)

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11
Q

What are the prognostic factors on breast cancer

A

Axillary lymph node status (most important)
Tumour size
Patient age
Receptor status (ER/PR neg, HER 2 pos and triple negative ass w worse prognosis)
Histological grade and subtype

HER2 positive ass/w aggressive tumour growth and high recurrence therefore poor prognosis
Since tx with trastuzumab prognosis has improved

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12
Q

What is the survival rate for pt with breast cancer

A

Early disease without LN involvement : 10y survival rate is 70%
Node positive disease: Hugh risk of recurrence without radiotherapy
Metastatic disease: 3 year survival rate of 48-71%

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13
Q

Differentials for a breast discharge

A

Introduction papilloma
Ductal actasia
Breast ca
Lactation or pregnancy
Medication

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14
Q

Causes of bilateral gynaecomastia

A

Drugs: spironolactone, steroids, HAART (efavirenz), diazepam, TCAs, cimetidine, digoxin, ca channel blockers
Liver/ renal failure
Recreational: Alcohol, marijuana, heroin, amphetamine
Testicular carcinoma

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15
Q

Causes of unilateral gynaecomastia

A

Breast cancer
Benign breast lump

+ all causes of bilateral as below

Drugs: spironolactone, steroids, HAART (efavirenz), diazepam, TCAs, cimetidine, digoxin, ca channel blockers
Liver/ renal failure
Recreational: Alcohol, marijuana, heroin, amphetamine
Testicular carcinoma

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16
Q

Differentials for a breast lump

A
  1. Benign: fibroadenoma, fat necrosis, cyst, galactocoele, lipoma, abscess, granulomatous inflammation
  2. Malignant: invasive carcinoma, ductal carcinoma in-situ, phyllodes tumour, metastases, lymphoma, sarcoma

• Fibroadenomas:
o Benign lumps that arise from the lobular component
o Typically affects women aged 15-25
o Firm, well-circumscribed, <3cm, hypoechoic on U/S
o Patients over 20 may need a U/S to confirm. Patients over 25 may need U/S and core biopsy to confirm
o Any mass that feels like a fibroadenoma but is associated with skin/nipple changes, discharge, rapid growth etc. warrants further investigation
o Surgical excision only warranted if: large (>5cm), patient request, patient over 30, diagnostic uncertainty

• Fat necrosis: occurs at any age following trauma. May require triple assessment with U/S +/- mammogram, and biopsy

• Breast cysts: common in 40’s-50’s. Caused by blockage on terminal ducts. Anechoic on U/S. Treated with aspiration of straw-coloured fluid and biopsy of remaining mass. Blood-stained aspirate may indicate papillary cystic carcinoma

• Galactocoele: occurs in a woman who is lactating or lactated recently. Caused by obstruction of the lactiferous duct. Aspiration of milky contents confirms diagnosis. May need oral antibiotics if secondarily infected

• Abscess: (lactational) treat with flucloxacillin and drainage. (non-lactational) treat with augmentin and drainage with biopsy to rule out inflammatory carcinoma

• Granulomatous inflammation: typically presents with a unilateral, firm, discrete breast mass with inflammation of overlying skin +/- nipple retraction. Treat with corticosteroids +/- wide local excision if required

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17
Q

Risk factors for breast cancer

A

Personal hx of breast cancer
Increase oestrogen exposure
-nulliparous
-wide window- early mernache late menopause
-high number of menstrual cycles
-first pregnancy after 35
-exogenous oestrogen (eg HRT)
BRCA1/2 gene mutations
Positive family hx
Prev radiation
Lifestyle: smoking, obesity, alcohol,low fibre high fat diet

18
Q

Genetic disorders associated with breast cancer

A
  1. Li-fraumeni syndrome
    -Autosomal dominant inherited mutation of the p53 tumour suppressor gene
    Multiple malignancies at early age
    -breast cancer, osteosarcoma, leukaemia, lymphoma, brain tumour, adrenocortical carcinoma
  2. Peutz-Jeghers syndrome
19
Q

Signs of breast cancer

A

Palpable lump on breast
Skin dimpling
Skin redness
Nipple discharge (blood)
Nipple changes/inversion

20
Q

Signs of benign vs malignant breast mass on mammogram

A

Benign:
-well defined circumscribed mass
-halo sign (radiolucent ring surroundings)
-diffuse microcalcifications or course calcifications

Malignant
-focal mass with poorly designed margins
-speculated margins
-clustered microcalcifications
-skin thickening or dimpling
-abnormal LN

21
Q

Signs of breast cancer on U/S (benign vs malignant)

A

Benign
Well defined, circumscribed mass
Wider than tall

Malignant:
Hypoechoic lesion
Irregular margins
Taller than wide
Posterior shadowing

22
Q

What are Desmond tumours

A

Desmond tumours are aggressive or deep fibromatosis, they are not sarcomas but represent neoplasms of fibroblastic tissue that lacks ability to metastasise.

23
Q

Complications of Desmond tumours

A

Local recurrence even after complete excision
Capacity to cause local morbidity
Death

24
Q

Risk factors for Desmoids (who is it common in)

A

Pregnancy (mostly Postpartum)
Familial Adenomatous Polyposis (FAP) in the mesenteric route

25
Q

Which conditions are associated with sarcomas

A

Multiple neurofibromatosis
Li Fraumeni syndrome
Gardeners syndrome
Lymphodema
Irradiation
HIV infection (Kaposi Sarcomas)

26
Q

Common sites from sarcomas

A

Soft tissues (80%)
Bone

Basically in bulks of soft somatic tissue e.g buttock, thigh, upper extremity, torso, retroperitoneum, head and neck

27
Q

Sarcomas subtypes

A

Undifferentiated soft tissue sarcoma (Sarcoma NOS)
Liposarcoma
Leiomyosarcoma
Synovial sarcomas
Malignant peripheral nerve sheath tumour

28
Q

Conditions Pheochromocytoma are ass/w

A

Men 2
Neurofibromatosis
Von Hippel Lindau Syndrome

29
Q

Contraindications to breast conserving therapy

A

Large tumour to breast ratio
Multifocal tumours within breast
Diffuse microcalcifications
Tumour fixed to chest wall
If excision with negative tumour margins is not guaranteed
Involvement of skin and nipple
Prev Radiation
BRACA mutation

30
Q

What are the risk factors for thyroid cancer

A

Female
Exposure to Ionizing Radiation
Fx hx of thyroid cancer
Men 2A and 2B
Papillary thyroid cancer: Gardner Syndrome, Cowden syndrome, familial are adematous polyposis

31
Q

Clinical presentation of hypercalcemia

A

 Renal calculi – Commonest
presentation of PHPT.
 MSK – musculoskeletal pain/
fibromyalgia / “arthritis” symptoms;
osteopenia; osteoporosis;
pathological fractures (severe cases).
 GIT – dyspepsia; gastric ulcers;
cramping; pain.
 Neuropsychiatric – depression; short
term memory loss; fatigue;
personality changes; confusion &
delirium (w’ very high levels).
 Asymptomatic – Many pts.

32
Q

Investigations for hyperparathyroidism

A

Primary hyperparathyroidism
High calcium
High PTH

Familia Hypocalceuric hypercalcemia
High calcium
High PTH
Low urine calcium
Low phosphate

Secondary hyperParathyroid
(Renal failure = failure to hydroxylate vit D and resorb calcium in kidneys= low calcium. PTH stimulated=bone resorption(bone sx) =normal Ca)
High PTH
High Phosphate
Low ca or normal (from bone resorption)

Tertiary Parathyroidism
High calcium
PTH high
(After renal transplantation, PTH remain elevated and calcium rises)

Imaging
US
SestaMIBI scan
CT scan and MRI not often not done

33
Q

Treatment of primary hyperthyroidism

A

Focus parathyroidectomy

34
Q

Management of secondary parathyroidism

A

Surgery of 3 1/2 of the parathyroid, forth gland can be left there o transplanted into the arm for easy access.

35
Q

Causes of hypercalcemia

A
  1. Primary hyperparathyroidism (PHPT)
    is the commonest cause of
    hypercalcaemia in the community.
     In a hospital population, however,
    malignant disease w’ bony
    metastases make up at least half of
    the cases.
    Other Less Common Causes…
     High bone turnover – thyrotoxicosis;
    long term bed rest; thiazide
    diuretics; vit A toxicity; multiple
    myeloma.
     Renal disease – tertiary
    hyperparathyroidism.
     Vit D disorders – hypervitaminosis D;
    sarcoidosis.
36
Q

Calcium metabolism

A

Hormones: Parathyroid hormone and vitamin D
Organs: Kidney, GIT, Bone

PTH:
 Released in response to low serum
calcium.
 Acts to increase serum calcium by…
- Acting on kidneys to increase
calcium reabsorption.
- Acting on bone to activate
osteoclasts to release calcium &
phosphate.
- Promote hydroxylation of vit D in
the kidneys to increase calcium
absorption in the GIT.
 Also regulates phosphate metabolism
by encouraging renal excretion of
phosphate.
Vit D:
 Promotes absorption of dietary
calcium.
 Activated in the liver and kidneys.

 99% of total body calcium is found in
bone as calcium-phosphate
complexes.
 Non-bone (serum) calcium occurs in
both the ionised and non-ionised
forms.
 Non-ionised calcium is bound mainly
to albumin, and ionised calcium is
found in complexes with calcium
phosphate, calcium carbonate, and
calcium oxalate.
 As 50% of serum calcium is bound to
albumin, abnormal measurements of
total calcium may result from
Hypoalbuminaemia.
 Serum calcium plays a critical role in
extra- and intracellular signalling,
nerve impulse transmission, and
muscle contraction.
 Calcium homeostasis is regulated
through PTH & vit D.

37
Q

Functions of calcium

A

Bone
Skeletal strength
Dynamic store for intra and extracellular calcium stires

Serum/blood
Muscle contraction
Nerve impulse transmission
Intra and extracellular signalling

38
Q

Complications of parathyroid surgery

A

Hematoma
Haemorrhage
Injure recurrent laryngeal nerve
Hypocalcemia

39
Q

Symptoms of secondary hyperparathyroidism

A

Chronic renal failure + osteopenia
Pruritis
Pathological bone fractures
Bone pain
Ectopic soft tissue calcification
Vascular calcifications
Skin ulcers (calciphylaxis)

40
Q

Pathophysiology if familial hypocalceuric hypercalcemia

A

Pg 225

General Surgery (6 decks)

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