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MED 411 - Term 1 > Week 4 - Breast Mass > Flashcards

Week 4 - Breast Mass Flashcards

1
Q

State the basic breast imaging principles and procedures to evaluate symptomatic women

A

Available modalities (imaging):

  • Mammography
  • Ultrasound
  • MRI

Biopsy (ultrasound guided)

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2
Q

Describe the cutaneous innervation of the skin overlying the breast

A

Nerve Supply for skin that covers breast:
- 2nd to 6th intercostal nerves

Nipple: by the 4th intercostal N.

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3
Q

Describe the vascular supply and lymphatic drainage of the breast

A 
Vascular supply
Blood supply 
- Axillary (artery)
- Internal thoracic (artery)
(also Ant. intercostal)

Lymphatic drainage
Axilla lymph nodes - vessels - parasternal lymph nodes communicate with the other side of the sternum (cancer can spread from one breast to the other this way)

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4
Q

List key components of a patient-centred medical interview

A

?

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5
Q

List the mechanisms of protein synthesis, modification and targeting within a cell

A

The life cycle of proteins - summary
(Didn’t include synthesis)

  • Protein targeting signals are zip codes that determine the targeting of proteins to various organelles
  • Proteins are translated directly into the ER lumen following SRP dependent targeting of ribosomes to the ER membrane
  • Chaperones help protein folding and prevent the accumulation of protein aggregates

For transmembrane protein - stop transfer sequence in the middle

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6
Q

Explain the various ways that proteins may be degraded within a cell

A

Ubiquitin proteasome pathway
- proteins tagged with ubiquitin will be degraded by proteosomes

ER associated degradation (ERAD)
- misfolded/mislocalized substrates recognized and extracted through the ER membrane, also ubiquitinated

Lysosomal pathways
- Endocytic vesicle and autophagosomes can target proteins to lysosomal degradation

*need to know details?

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7
Q

Describe the fate of (some) mutant/variant proteins and some examples of links between mutation and disease

A

Leigh syndrome - neurometabolic disorder - can be caused by mutations of the mitochondrial genome

Cystic fibrosis - mutation in CFTR gene, plasma membrane channel, protein misfolding and degradation

Gaucher’s disease - mutation in b-glucosidase, lysosomal enzyme responsible for degradation of lipids

Multiple Myeloma - cancer, relies on ubiquitin pathway (how?)

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8
Q

Describe checkpoints in the cell cycle and their regulators

A

Cell cycle)
G0: Mitogens induce G1 (macaroni linker molecules)
G1: Mitogens induce Cyclin formation, Cyclin/CDK complexes form to progress the cell through the cell cycle
S: more cyclin/cdks
G2: more cyclin/cdks
M: Prophase, Metaphase, Anaphase, Telophase/Cytokinesis (Mitosis is your dog: Please don’t Pee on the MAT)

3 DNA checkpoints. One before S, one after S, one before M

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9
Q

Identify the 3 major components of the cytoskeleton, and their distinct functions

A

Microfilaments: dynamic, important in cell adhesion, contractile force, cell shape, surface projections (e.g. microvilli)

Intermediate filaments: more stable, tensile strength within cells and across tissues (cell-cell/cell-ECM), maintain cell and nuclear structure, **helpful markers of specific tissues in histopathology, determining origin of tissue

Microtubules: cylinders of tubulin, polar, grow from + end, held in position by microtubule organizing centre, motors move along bringing cargo

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10
Q

Recognize the structure and function of 4 major cell-cell junctions

A

“Cell-cell:
(Zonula = belt)

  1. Zonula adherens** (Need to know names of junctional molecules) - belt around cell, lateral adhesion
  2. Tight Junctions (Zonula Occludens) - apical, forms barrier and regulates the movement of macromolecules between cells
  3. Desmosomes (Macula Densa) - not a belt, spots (appear on electron micrographs), link to intermediate filaments increase tensile strength; physically link cells together (prominent in skin)
  4. Gap junctions - channels that link cells and allow for the passage of small molecules and ions between cells
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11
Q

Recognize the structure and function of 2 major cell-extracellular matrix (ECM) junctions

A

Cell-ECM
Hemidesmosomes - heterophilic (bind to ECM proteins), intermediate filaments
Focal Adhesions - heterophilic, actin filaments, contractile force, highly dynamic, critical for cell migration

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12
Q

What are the components of Zonula adherens?

A

Components:
Cadherins - receptor, calcium dependent adherence molecules, will bind similar cadherins on other cells

Catenins - link cadherins to cytoskeletal elements

Actin - make the junction dynamic, can form/release/reform along lateral cell wall

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13
Q

Dysplasia vs metaplasia

A

Dysplasia

  • A pre-malignant change in cells (usually epithelium) characterized by disordered growth and morphologic changes in the cell nucleus
  • In mammary gland, same epithelium, but cells look different (dysmorphic) and epithelium is disorderly - can transform into carcinoma

Metaplasia

  • a mature, differentiated cell type is replaced by another mature, differentiated cell type (doesn’t necessarily indicate cancer)
  • In mammary gland, replacement of epithelium with another type of cell, but it appears normal - can transform into carcinoma
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14
Q

Carcinoma

A

Malignant epithelial neoplasm

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15
Q

Define cell signal transduction pathways

A

Involves the binding of extracellular signaling molecules and ligands to receptors located on the cell surface or inside the cell that trigger events inside the cell, to invoke a response.

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16
Q

Oncogene + MOA

A

Oncogene: Oncogenes code for proteins and factors involved in cell growth; Mutations in these genes lead to an increase cell
division (mutation turns ON - cancer)

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17
Q

Tumor suppressor gene + MOA

A

Tumor suppressor gene: prevent abnormal proliferation of cells, promote cell death (e.g. p53 gene); mutation turns OFF - cancer

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18
Q

Describe the Gompertzian pattern of tumor growth

A

Number of cancer cells by time

-Diagnostic threshold (1cm)

  • Limit of clinical detection (earliest)
  • Cell death (when cancer cells outgrow food source and die)

**Look at picture

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19
Q

What are the characteristic features of cancer development?

A
  • Genomic instability
  • Inappropriate cell proliferation, evasion of cell death
  • Angiogenesis
  • Invasion and metastasis
20
Q

Describe inappropriate cell proliferation in cancer development

A

Neoplastic state, there is an imbalance (cell division>cell death)

  • normal cells will reproduce until they come into contact with other cells (in malignant cells - there is a loss of contact inhibition)
  • evasion of the immune system by inhibition through targeting PD1 on T cells (stops them from killing)
21
Q

Describe angiogenesis in cancer development

A
  • generally, the creation of blood vessels to provide nutrients/O2 - occurs during life and growth;
  • Neoplastic tissues recruit new blood vessels from pre-existing ones, controlled by regulators secreted by the tumor and stroma (+ regulators - by oncogene, - regulators -by tumor suppressor)
22
Q

Describe invasion in cancer development

A
  • Invasion occurs when neoplastic cells show a disordered structure with piling up of cells; can be as a result of:
    Imbalance between proteinases and proteinase inhibitors in ECM (the underlying basement membrane and ECM are degraded)
    Alterations in Cell Adhesion Molecules (allow detachment of cancer cells, enhance cell mobility)
23
Q

Describe metastasis in cancer development

A
  • intravation of primary tumour into vessel through the basement membrane, circulates, extravation of tumor cells into new tissue at different location
24
Q

Hyperplasia

A
  • An increase in the number of cells within an organ. Occurs in response to a stimulus.
    When the stimulus is removed, the cells return to normal size.
25
Q

Malignant neoplasia

A

• Grow rapidly • Poorly circumscribed • Infiltrate and destroy adjacent tissues • Metastasize • Histologically may poorly resemble tissue of origin • Often fatal • Surgically cured only in the early stages

26
Q

Neoplasm

A

Abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the adjacent normal tissues. The mass persists in the same excessive manner even after the stimulus or cause is removed.

27
Q

Hypertrophy

A

An increase in the size of cells within an organ. Occurs in response to a stimulus.
When the stimulus is removed, the cells return to normal size.

28
Q

Atrophy

A

A reduction in either the size of cells or the number of cells within an organ.
This process is reversible when it represents part of a response to an external stimulus or it can be part of the normal aging process.

29
Q

High grade dysplasia aka. Carcinoma in-situ

A
  • High-grade dysplasia has most of the cellular morphologic changes of cancer cells but is not invasive and cannot therefore metastasize.
    By molecular analysis high-grade dysplasia has fewer mutations than invasive cancer.
30
Q

Benign neoplasia

A

• Slow growing • Usually circumscribed • A mass that pushes aside adjacent tissues • Does not infiltrate adjacent tissues • Do not metastasize • Histologically resemble the tissue of origin • Good prognosis • Can be cured by surgical removal • Can be a precursor for malignant neoplasms

31
Q

Malignant neoplasia

A

• Grow rapidly • Poorly circumscribed • Infiltrate and destroy adjacent tissues • Metastasize • Histologically may poorly resemble tissue of origin • Often fatal • Surgically cured only in the early stages

32
Q

Identify the important steps required to diagnose carcinoma-in-situ and invasive cancer

A

History and Exam

Tissue sample - Distinguishes malignant from benign • Establishes the cancer type – e.g. lymphoma from carcinoma • Can confirm the site of origin of the cancer
Tools for tumour diagnosis and classification:
- Morphology – what the tumour looks like
- Immunophenotype – proteins expressed by the tumour
- Molecular tests - FISH for copy number changes and translocations; Sequencing for gene mutations

Predictive biomarkers

Staging investigations - where is the cancer?

33
Q

Describe the development of the mammary gland

A

Glands made up of:

  • epithelial tissue (functional unit of glands - parenchyma)
  • connective tissue (supportive unit - stroma)

Dynamic organ that only develops into a mature functional state in pregnancy/lactation (look at how changes throughout life)

34
Q

Describe normal breast tissue and how it changes in response to hormonal changes throughout life

A

Fetal:
15 - 20 or 25 ducts present at birth
Milk line that regresses to pectoral region

Puberty:
Increase in estrogen and progesterone that induces proliferation of the ducts resulting in elongation and branching
Terminal end buds (possibly 2 cell layer)
Slight increase in adipose tissue

Adult/Resting:
Continued duct elongation with each ovarian cycle
Branching also continues
Growth/branching continues until 35 years old

Pregnancy/Lactation:
Prolactin is introduced due to drop in progesterone (48 - 72 hours after delivery)
Oxytocin introduced, induces contraction of myoepithelia and lactation
Stroma reduces, parenchyma increases
Terminal ends become alveolar through morphogenesis

Involution (post-weaning):
Reverts back to adult/resting stage through apoptosis
Caused by decrease in prolactin, oxytocin, and estrogen and progesterone revert back to normal cycles

Post-menopausal Involution:
Decrease in estrogen and progesterone
Increased adipose tissue

35
Q

List the different types of pre-malignant conditions and different key types of breast cancer that can occur

A

changes occurring gradually from normal breast tissue, to development of atypical ductal hyperplasia, then ductal carcinoma in-situ (DCIS), then invasive ductal carcinoma

invasive lobular (carcinoma?): 10-15%
-atypical: 5-10%
36
Q

Describe what a mammogram is and the difference between screening and diagnostic mammography

A

Type of low dose x-ray designed to image breast tissue.

Screening
• Asymptomatic women
• Limited views

Diagnostic
• Symptomatic women or
women with history of
cancer or with implants 
• Additional views
37
Q

State the basic breast screening policy in BC

A

Letters sent out to Women age 50-69 years (Service also available to women age 40-49 & 70+)

Every 2 years (controversial)

Two-view screening mammogram

Higher risk (one 1st degree relative with breast cancer) - every year 
Can be under 40 if strong family history or mutation
38
Q

Define specificity vs. sensitivity

A

Specificity: reducing false positives

Sensitivity: reducing false negatives

39
Q

How are cancers staged?

A

TNM (tumour, nodes, metastasis) system is universally used in solid cancers
• T - Primary tumour characteristics (Size and depth of invasion)
• N - Nodal status (Involved or not, number involved, size)
• M - Metastasis (Present or absent and extent)

TNM is specific to the individual cancer type

40
Q

Describe the models for genetic counseling and genetic testing (of cancers)

A

Traditional Approach - referral - HCP appointment - assessment - call back
Oncologist-Led Genetic Testing - oncologist initiates testing, reduces
Group Genetic Counseling
DNA-Direct Genetic Counseling - (Call and mail in sample?)

41
Q

Describe and compare different molecular methods for hereditary cancer diagnosis and tumour testing

A

** Skip this, need to go over lecture**

  • Site specific
  • Single gene
  • Gene panel
  • Whole exome
  • Whole genome

Tumour testing - performed for diagnosis and treatment decisions
Tumour phenotype can reflect germline

First tumour approach

42
Q

Explain the difference between exocrine and endocrine glands

A

Endocrine gland secrets chemical substances directly to the blood stream, while exocrine gland secrets its product into a duct

43
Q

Indicate which cranial nerves and spinal nerves carry sympathetic and parasympathetic fibers out of the central nervous system

A

Sympathetic:

Parasympathetic:

44
Q

Describe in general how pain from the viscera is referred to regions innervated by somatic nerves

A

-

45
Q

Describe in general terms how parasympathetic nerves are distributed in the head

A

–

46
Q

Describe in general terms how sympathetic nerves get into the head

A

-

MED 411 - Term 1 (2 decks)

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