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pipi&pi3 > Cancer > Flashcards

Cancer Flashcards

1
Q

What is a tumor?

A
  • An abnormal mass of tissue
    ~ Either benign or malignant
  • Uncontrollable/autonomous growth
    ~ Persists even after cessation of the stimuli that initiated it
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2
Q

What are the general characteristics of benign tumors?

A
  • Typical of tissue of origin
  • Well-differentiated
  • Few mitosis and normal
  • Strictly local, often encapsulated with no metastasis
    ~ Capsule and basement membrane not breached
  • Slow growth rate
  • Rare tumor necrosis
  • Rare recurrence after treatment
  • Good prognosis
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3
Q

What are the general characteristics of malignant tumors?

A
  • Anaplastic
    ~ With abnormal cell size and shape
    ~ Not well-differentiated
  • Many mitoses
  • Rapid growth rate and may be abnormal
  • Infiltrative/frequent metastases
    ~ Capsule and basement membrane breached
  • Tumor necrosis common
  • Recurrence common after treatment
  • Poor prognosis
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4
Q

What are the main phases of tumor development and growth?

A

1) Transformation
- Benign cells
~ Mostly well-differentiated
~ Resemble the cell from which they originated

  • Malignant
    ~ Transforms into anaplasia (final stage)
    ~ Nuclear and cellular pleomorphism (size and shape)
    ~ Abnormal nuclear morphology
    ~ Loss of polarity
    ~ Abundant mitoses

2) Rate of growth of transformed cells
- How differentiated the cells are
~ Well-differentiated: Resembles mature cells of tissue of origin
~ Poorly-differentiated: Primitive cells
~ Undifferentiated: Anaplastic
- Less differentiated = faster growth

3) Invasion of tumor cells to surrounding tissues
- Benign cells
~ Cohesive with a rim of condensed connective tissue/capsule

  • Malignant
    ~ Local invasion (Detachment, attachment, degradation & migration)

4) Metastasis of tumor cells to distant sites
- Lymphatic, hematogenous and seeds into body cavities
- Intravasation, embolisation, adhesion, extravasation, metastatic growth

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5
Q

What are the different ways that cells can transform in cancer?

A

HHN DMA (HHN Done More Amazing)

1) Hypoplasia
- Fewer cells than normal
~ Usually benign
- eg postpubertal female breast underdevelopment /micromastia

2) Hyperplasia
- More cells than normal
- Controlled by normal proliferation mechanisms
- Due to external stimuli
~ eg callus exposed to pressure

3) Neoplasia
- ^ cell number
- Abnormal multiplication
~ Loss of normal proliferation regulation
~ Absence of stimuli

4) Dysplasia
- Change in normal shape, size and organisation
- Usually in response to chronic irritation
- Reversible changes if stimulus is removed
~ If not, cells become metaplastic

5) Metaplasia
- Change in cell type
- After prolonged irritation
- Reversible changes if stimulus is removed
~ If not, cells become anaplastic

6) Anaplasia
- Reversal in differentiation OR
- Loss of structural and functional differentiation of normal cells
- Not reversible in nature
- Characteristic of cancerous tumors

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6
Q

What are some abnormal nuclear morphology?

A
  • Hyperchromasia
  • High nuclear cytoplasmic ratio
  • Chromatin clumping
  • Prominent nucleoli
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7
Q

What are the steps in local invasion of cancer cells?

A

1) Detachment of tumor cells from each other

2) Attachment of tumor cell to matrix components

3) Degradation of matrix components
- To allow slow invasion through
- eg using collagenase

4) Migration of tumor cells

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8
Q

What are the steps in metastasis?

A

Clonal expansion, growth, diversification, angiogenesis into metastatic subclone -> Adhesion to and invasion of basement membrane -> Passage through extracellular matrix -> (1)

1) Intravasation
- Passage of cancer cells into blood vessels

2) Embolization
- Interaction with host lymphoid cells forms a tumor cell embolus/clump which travels along the BV

3) Adhesion
- Embolus adhesion to the basement membrane

4) Extravasation
- Passage of cancer cells out of blood vessels into distant tissues
- Metastatic deposit
- Angiogenesis and growth

5) Metastatic growth

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9
Q

What is the significance of nodal metastasis?

A

T1N0M0:
- Small
- No spread to regional lymph nodes
- No metastasis
- Considered stage 1

T4N1M1:
- Large
- Spread to regional lymph nodes and other organs
- Considered stage 4

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10
Q

What is the nomenclature for cancers?

A

Benign:
- Suffix of -oma
- eg osteoma, lipoma, papilloma

Malignant:
- -carcinoma
~ If originated from epithelial cells
~ eg squamous cell carcinoma, adenocarcinoma

  • -sarcoma
    ~ If originated from mesenchymal cells
    ~ eg fibrosarcoma, osteosarcoma, angiosarcoma
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11
Q

What are the predisposing factors for cancer?

A
  • Age
  • Childhood cancers
  • Obesity
  • Chronic inflammation
  • Precancerous conditions
    ~ Chronic ulcerative colitis
    ~ Atrophic gastritis of pernicious anemia
    ~ Leukoplakia of mucous membranes
  • Genetic factors
    ~ Point mutation
    ~ Translocation
    ~ Amplification
    ~ Familial cancer symptoms
  • Environmental factors
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12
Q

What are the environmental factors that increases the risk of cancer?

A
  • Chemicals
    ~ Hormones, grilled meats, asbestos
  • UV light/ionizing radiation
    ~ Usually causes basal cell carcinoma, squamous cell carcinoma, melanoma
  • Viral infx
    ~ HPV (squamous cell carc)
    ~ EBV (Burkitt lymphoma, NPGL carc)
    ~ HBV (hepatocellular carc)
  • Vices
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13
Q

What is the molecular basis of malignancy?

A

Failure of DNA repair or cell mutations ->
- Activation of growth-promoting hormones + Inactivation of tumor suppressor genes
~ Unregulated cell proliferation

  • Alterations in genes that regulate apoptosis
    ~ Decreases apoptosis
  • Clone expansion + Angiogenesis + Additional mutations + immunity escape
    ~ Tumor progression and malignant neoplasm
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14
Q

What are the regulatory genes targeted in carcinogenesis?

A
  • Proto-oncogenes
    ~ Normal genes that promote cell proliferation
    ~ Only switched “on” for short periods by growth-promotion factors
    ~ Mutates into oncogenes when damaged by carcinogens
    ~ Oncogenes are dominant and function autonomously
    ~ RAS genes, MYC genes, ABL genes
  • Tumor suppressor genes
    ~ Inhibits cellular proliferation
    ~ Stimulates apoptosis
    ~ BRCA1/2 genes, p53 genes, RB genes
  • Genes regulating apoptosis
  • Genes revolved in DNA repair
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15
Q

What is the ABL gene?

A
  • ^ tyrosine kinase activity to ^ RBC division
  • Forms Philadelphia chromosome when ABL gene on chromosome 9 translocates to chromosome 22
    ~ Allows unregulated tyrosine kinase activity for ^ cell division/unregulated growth
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16
Q

What are the RB genes, BRCA1/2 genes and p53 genes?

A

RB
- Associated with retinoblastoma
- On chromosome 13
- Inactivated in HPV infx
- Implicated in almost all cancers

BRCA
- 1 on chromosome 17, 2 on chromosome 13
- Usually repairs damaged DNA and destroys unrepairable cells
- Most common in breast cancer, but also in colon and prostate cancer

p53
- on chromosome 17
- linked to apoptosis
- Activated when the cell is stressed or injured
~ Prevents cell division, repairs DNA and triggers apoptosis
- When gene is damaged, tumor suppression decreases

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17
Q

How to stage neoplasms?

A

Tis: in situ, non-invasive
T1: Small, minimally invasive
T2: Larger but still within primary organ site
T3: Larger and invasive beyond margins of the primary organ site
T4: Very large and invasive, with spread to adjacent organs

N0: No lymph node involvement
N1: Nearby LN
N2: Regional LN
N3: More distant LN involvement

M0: No distant metastasis
M1: Distant metastases

18
Q

How to grade neoplasms?

A

I: Well differentiated
- Easiest to control

II: Moderately differentiated

III: Poorly differentiated

IV: Nearly anaplastic
- Poorest prognosis

19
Q

What are the diagnostic methods for neoplasia?

A
  • Hx and PExam
  • Radiography (presence and location of mass lesions)
  • Lab analyses and tumor markers
    ~ Prostate specific antigen (PSA)
    ~ CEA, AFP, HCG
  • Genetic testing
  • Cytology
    ~ Pap smear
    ~ Fine needle aspiration
  • Tissue biopsy
  • Autopsy
20
Q

What are the effects of tumors on the host?

A

1) Anatomic encroachment
- eg SVC syndrome

2) Hormone production
- eg prolactinoma

3) Bleeding, inf

4) Cachexia (fat + muscle loss)
- Reduced diet
~ Fat loss > muscle loss
- TNF alpha, IL-1, Proteolysis Inducing Factor (PIF)

5) Para-neoplastic syndromes
- Not directly related to the tumor spread
- Mediated by humoral factors (eg hormones or cytokines) excreted by tumor cells
- eg Acanthosis nigricans in gastric/lung cancers, clubbing in lung cancer, Trousseau / migratory thrombophlebitis in pancreatic cancer

6) Acute symptoms
- eg rupture, infarction

21
Q

What are the common complications of cancer treatment or at stage 4 cancer?

A
  • Superior vena cava syndrome (SVCS)
  • Hypercalcemia
  • Spinal cord compression
  • Tumor lysis syndrome
22
Q

What are some s/s of SVCS?

A
  • Non-productive cough
  • Fatigue
  • Worsening dyspnea
    ~ on exertion and when lying down
  • Hoarseness
  • Progressively enlarging veins on the chest to neck
  • Increasing neck and face swelling
  • Sensation of blacking out
23
Q

What are the mechanism of SVCS?

A

1) Extrinsic compression
- eg by tumor
- Pressure exerted externally reduces venous return
~ Blood backs up into the veins of the upper body
~ Venous congestion and elevated pressure lead to swelling/edema of the face, neck, and upper extremities

2) Intravascular thrombosis
- Clot impedes venous blood flow
~ Stagnation and congestion in the upstream venous system
- Inflammatory processes around the thrombus can further exacerbate the obstruction

24
Q

What are the investigations for SVCS?

A
  • CXR, CT contrasted
  • Tumor markers (AFP< HCG)
  • FBC
  • PT/PTT/aPTT
  • Biopsy, histology
25
Q

What are the complications of SVCS?

A

If px collapses during procedure:
- CTVS team, CTICU and HD team

If SVC collapses:
- Urgent stenting
- Removal of external compression

If tumor breaks down spontaneously:
- Management of tumor lysis syndrome

26
Q

IMPT:
What is the management of SVCS?

A
  • Treat the cause and complications of mediastinal mass
  • Look out for complications of treatment
    ~ eg chemotherapy toxicity (neutropenic fever, N/V, central line sepsis, renal impairment)
    ~ fluid overload
  • Do not increases SVC return
    ~ No IV plugs and BP taking on upper limbs
    ~ Head of bed at 30 degrees
    ~ Advocate for central line insertion give treatment lately
  • Fall precaution or neurological changes
  • Strict I/O
  • Daily weight if needed
27
Q

What are the s/s of hypercalcemia?

A
  • Bone pain
  • Fractures
  • Renal stones/calculi
  • Anorexia
  • N/V
  • Constipation
  • Abdominal pain
  • Pancreatitis
  • Fatigue
  • Confusion/acute delirium
  • Depression
28
Q

What are the causes of hypercalcemia?

A
  • Hyperparathyroidism
  • Hyperthyroidism
  • Cancer
  • Vitamin D intoxication
  • Excessive Vitamin A
  • ^ Calcitriol
  • Thiazide diuretics
  • Acromegaly
29
Q

What is the grading of hypercalcemia?

A

Mild: <3mmol/L

Moderate: 3-3.5mmol/L

Severe: >3.5mmol/L

30
Q

What is the management of hypercalcemia?

A
  • NS 3L/day x3/7, 1.5L/day x2/7
  • IV Pamidronate 60mg in 500 ml over 6hrs
  • Treat cancer w chemo/radiotherapy
  • Treat symptoms of s/s of hypercalcemia
  • Look out for complications of treatments
    ~ Hyperhydration - fluid overload
    ~ Biphosphonate & denosumab - hypocalcemia and osteonecrosis of jaw
  • Strict I/O
  • Daily wights
  • Give furosemide PRN based on dr’s orders
  • Pain charts
31
Q

What is the treatment for hypercalcemia?

A

Mild/moderate/asymptomatic:
- Does not require immediate treatment
- Remove factors that aggravate hypercalcemia
- Ensure adequate hydration

Severe/symptomatic:
- Immediate, aggressive treatment
- Aggressive hydrations (200-300l/hr)
~ In case of CCF or CKD, use CALCITONIN instead (rapid response within 12-24 hrs) but can cause rebound hypercalcemia or tachyphylaxis)
- Furosemide
- Biphosphonates
~ ZOLENDRONIC ACID/PAMINDRONATE
- RANKL inhibitor
~ DENOSUMAB

32
Q

What are the s/s of spinal cord compression?

A
  • Back pain
  • Motor findings
    ~ eg mechanical instability of the spina
    ~ difficulty in moving
  • Sensory findings
  • Bladder and bowel dysfunction
  • Ataxia
  • Cauda equina syndrome
    ~ Medical emergency from when nerves at the end of the spinal cord get compressed
33
Q

What are the investigations for spinal cord compression?

A
  • Spine MRI
  • CT (but not ideal)
  • PET-CT
    ~ If primary site of disease is not known / newly diagnosed
  • Biopsy, histology
  • Labs PT, aPTT, FBC
  • Tumor markers
34
Q

What is the epidural spinal cord compression grading scale?

A

Grade 0: Tumor confined to bone

Grade 1a/b: No contact with spinal cord

Grade 2: Tumor that displaces or compresses spinal cord

Grade 3: Tumor with circumferential epidural extension that causes severe spinal cord compression with obliteration of the CSF space

35
Q

What is the medical management of SCC?

A

If spine unstable:
- Surgical fixation
~ eg pedicle screws, percutaneous cement injection

If pain:
- Glucocorticoids
~ High dose dexamethasone
- RT
- Chemo-sensitivity
- Opioids

Prophylaxis:
- Venous thromboembolism prophylaxis
~ Especially for advanced cancers
~ Prophylactic low molecular weight heparin, CLEXANE

36
Q

What is the management for SCC?

A
  • Log rolling
    ~ for unstable spine
  • Assessment of neurological involvement and spinal stability
    ~ Using SINS scoring tool
  • Management of urinary retention and constipation
    ~ IDC
    ~ Laxatives
    ~ I/O chart
  • VTE prophylaxis
    ~ Calf compressors
    ~ Bed exercises
  • Fall precaution
37
Q

What is tumor lysis syndrome?

A
  • Oncologic emergency caused by massive tumor cell lysis
  • Releases large amounts of potassium, phosphate and nucleic acids into blood
    ~ Results in hyperkalemia, hyperphosphatemia, secondary hypocalcemia, hyperuricemia and AKI
  • Potassium and Breakdown of nucleic acids
    ~ Highly insoluble products
    ~ Forms crystals in the renal distal tubules (crystal deposition leads to AKI)
  • Phosphate (conc. is x4 higher in cancer cells)
    ~ Calcium binds to phosphate -> precipitation -> hypocalcemia -> AKI and cardiac arrhythmias
38
Q

What are the types of tumor lysis syndrome?

A
  • Spontaneous
    ~ Often without hyperphosphatemia
  • Treatment-induced
39
Q

What are the risk factors for tumor lysis syndrome?

A

Px factors:
- Pre-existing hyperuricemia or renal disease
- Oliguria or acidic urea
- Dehydration especially during treatment

Tumor specific:
- Large tumor burden (large, ^ WBC count, bone marrow involvement, LDH >x2 normal)
~ Easily lysed by treatment
- Blood cancer
- Chemo/radiosensitivity

40
Q

What is the management for tumor lysis syndrome?

A

1) Treat electrolyte abnormalities
- Hyperkalemia
~ Serum potassium levels
~ Continuous cardiac monitoring
~ Oral potassium-lowering agents (SODIUM POLYSTYRENE SULFONATE)

  • Hyperphosphatemia
    ~ Aggressive hydration with concurrent use of diuretics
    ~ Phosphate binder therapy (CALCIUM CARBONATE)
  • Hypocalcemia
    ~ If calcium phosphate product is >60mg/dL, no calcium should be given until hyperphosphatemia is treated
    ~ Calcium replacement given at lowest dose to relieve symptoms

2) Target hyperhydration
- Strict I/O
- Daily weight
- Renal dialysis management for px with severe AKI
- Furosemide

41
Q

What is the preventive management for TLS?

A
  • IV hydration
  • Hypouricemic agents
    ~ ALLOPURINOL
    ~ RASBURICASE (for high risk px but need to do G6PD check before giving)

pipi&pi3 (24 decks)

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