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Oncology - Seminars Flashcards

1
Q

Types of lung cancer? (3)

A
  1. Adenocarcinoma
  2. Squamous cell carcinoma
  3. Small cell carcinoma
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2
Q

Types of esophageal cancer? (2)

A
  1. Adenocarcinoma
  2. Squamous cell carcinoma
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3
Q

What does the Grade of cancer tell us?

A

The degree of interruption in cell differentiation and morhphology of the tissue affected. In other word, the severeity of dysplasia of the cells within the tissue affected.

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4
Q

What does the TNM in TNM staging stand for? And what are the parameters?

A
  • T: Tumor stage
  • N: Nodal status
  • M: Metastasis
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5
Q

Explain the Tumor staging (the T) in TNM:

A
  • T0: no tumor
  • TIS: Carcinoma in situ
  • T1: < 2cm (invades mucosae or submucosae)
  • T2: 2 - 4cm (invades muscularis propria)
  • T3: > 4cm (invades subserosa)
  • T4: > 4cm (invades peritoneum or other organs)
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6
Q

Explain the Nodal status part (the N) of TNM staging:

A
  • N0: no nodal malignancy
  • N1: single node, < 2cm
  • N2: single node,
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7
Q

Explain the Metastasis part (the M) of TNM staging:

A
  • M0: no metastasis
  • M1,2: metastasis, differs in type and location of metastasis
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8
Q

Some TNM stagings also include an “S” at the end, what does the “S” represent?

A

S - tumor markers

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9
Q

What is EGFR a molecular marker for?

A

Lung cancer

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10
Q

Tumor markers for Colon cancer?

A
  1. KRAS
  2. NRAS
  3. Ca19-9
    4.
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11
Q

What is BRAF a molecular marker for?

A

Melanoma

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12
Q

What is HER2 a molecular marker for?

A

Breast cancer

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13
Q

What do we mean by the term “Palliative” in oncology when compared to what it usally means?

A

In Oncology, “Palliative” means to treat the cancer well enough to prolong life, but not enough to remove it. Patient with end stage cancer may not be able to be cured, but palliative treatment can prolong their limited time of life.

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14
Q

Which factors can make cancer treatment more curative?

A
  1. Localized solid tumor
  2. Oligometastases
  3. High chemotherapy sensitivity (like in testicular cancer and certain leukemias and lymphomas)
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15
Q

Which factors can make cancer treatment more palliative than curative?

A
  1. Stage IV solid tumors
  2. Locally advanced tumors
  3. Patient in poor physical condition, unable to get curative treatment
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16
Q

What is RECIST?

A

Response Evaluation Criteria in Solid Tumors

  • CR - complete response
  • PR - partial response (> 30%)
  • SD - stable disease
  • PD - progressive disease
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17
Q

Tumor marker for prostate cancer?

A

PSA

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18
Q

Tumor marker for germinal tumors?

A
  1. B-HCG
  2. AFP
  3. LDH
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19
Q

Tumor marker for gastric cancer?

A
  1. CEA
  2. Ca19-9
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20
Q

Tumor marker for pancreatic cancer?

A

Ca19-9

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21
Q

Tumor marker for ovarian cancer?

A
  1. Ca 125
  2. HE4
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22
Q

Tumor marker for Hepatocellular cancer?

A

AFP

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23
Q

Tumor marker for Medullary thyroid cancer?

A

calcitonin

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24
Q

What is CTC AE?

A

Common Terminology Criteria for Adverse Events

Lets us know how toxic our treatment is.

G1 - G2: mild

G3 - G4: Severe

G5: Fatal

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25
Q

What is Zubrod scale and how is it organised?

A

A scale for checking how well the patients’ physical health is. Just like ECOG. Higher score = less suitable for chemo

Daytime spent in bed:

  • PS0: asymptomatic
  • PS1: symptomatic, but in good condition
  • PS2: <50% daytime in bed
  • PS3: >50% daytime in bed
  • PS4: bedbound
  • PS5: fatal
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26
Q

What is the most common type of head & neck cancer?

A

SCC (Squamous Cell Carcinoma)

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27
Q

Most common cause of head and neck cancers?

A

Smoking and alcohol

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28
Q

Viruses that may cause H&N cancers?

A
  1. HPV (oropharynx)
  2. HSV-1, HSV-2 (oral cavity)
  3. EBV (nasopharynx and salivary gland)
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29
Q

What is the field cancerization theory?

A

H&N have an increased risk of cancer throughout life due to those areas being more exposed to possible carcinogens (e.g breathing in smoke, eating carcinogenic products etc…) and thereby also increased risk of recurrence

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30
Q

Initial signs of H&N cancer? (4)

A

Irregularities in:

  1. Deglutition
  2. Phonation
  3. Respiration
  4. Hearing
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31
Q

Signs of cancer in oral cavity? (3)

A
  1. Swelling
  2. Ulcer
  3. Plaque
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32
Q

Sign of cancer in oropharynx?

A

Silent area, maybe dysphagia

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33
Q

Signs of cancer in larynx? (2)

A

Hoarseness or dyspnea

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34
Q

Signs of cancer in nasopharynx? (2)

A
  1. Epistaxis
  2. Stuffy nose
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35
Q

Gold standard imaging type for H&N cancers?

A

CT, rules out node involvement and liver metastasis

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36
Q

Which area of H&N cancers i surgery preferred?

A

Oral cavity

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37
Q

Which areas of H&N cancers is radiotherapy preferred?

A
  1. oropharynx
  2. larynx
  3. nasopharynx
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38
Q

Criteria for Surgery + postsurgical Radiotherapy: (5)

A
  1. T3-T4 primary tumor
  2. N2 or more
  3. Neural or vascular invasion
  4. Poorly differentiated tumor
  5. Short margins
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39
Q

Criteria for Surgery + postsurgical chemoradiotherapy: (2)

A
  1. Positive surgical margins
  2. Extracapsular extension (to other lymph nodes)
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40
Q

Advantages of starting cancer treatment with surgery rather than radiotherapy:

A

Helps us assess the grade and stage of the tumor and thereby the severity + possibility for biopsy.

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41
Q

What is the difference between adjuvant and neoadjuvant chemotherapy?

A
  • Neoadjuvant: chemotherapeutic medications given BEFORE the primary treatment
  • Adjuvant: chemotherapeutic medications given AFTER the primary treatment
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42
Q

2 examples of medication-combo given as neoadjuvant chemotherapy:

A
  1. Cisplatin + 5FU
  2. Cisplatin + 5FU + Paclitaxel
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43
Q

Anti-EGFR-antibody, similar effect to Cisplatin with less morbidity. Name the drug.

A

Cetuximab

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44
Q

Most frequent chemotherapy regimen for H&N cancers?

A

Cisplatin + 5FU combo (+ Cetuximab sometimes)

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45
Q

What do you give patients in too poor condition to handle normal cis/5fu comno therapy?

A

Metothrexate

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46
Q

Response rate and survival after chemo in H&N cancer patients?

A
  • Response rate 30%
  • 6-12month survival
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47
Q

Explain the 4 phases within a cell-cycle:

A
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48
Q

What can mutation of protooncogenes or tumor supressor genes cause in general? (3)

A

Uncontrolled proliferration due to:

  1. Increased growth factor production
  2. Change in receptor sensitivity and connecte pathways
  3. Change in cycle transducers (Cyclins, Cdk’s, Cdk inhibitors)
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49
Q

Which cell phase are most anticancer drugs effective on?

A

S phase (often cause DNA damage –> apoptosis)

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50
Q

What kind of normal healthy cells exhibit most of the side effects seen in chemotherapy? (5)

A

Rapidly-dividing cells like:

  1. Bone marrow cells
  2. Skin cells
  3. Hair follicle cells
  4. GI cells
  5. Gametes
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51
Q

Difficulties to consider when treating a tumor with chemo: (4)

A
  1. The cells in the tumor do not all proliferate continously
  2. The tumor may outgrow abaility to maintain blood supply (harder drug delivery)
  3. The tumor has empty compartments and only 5% of it is made of cells
  4. Resting cells in G0 may not be activated, then get activated to G1 after end of treatment –> recurrence
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52
Q

Types of cytotoxic agents used in chemotherapy: (4)

A
  1. Alkylating agents
  2. Antimetabolites
  3. Cytotoxic antibiotics
  4. Plant derivatives
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53
Q

What are antimetabolites? What to they consist of? (3)

A

Analogs of molecules necessary for enzymes and structures in S phase (in other words, bad ingredients for making DNA–> bad DNA structures made by the cancer cells).

Consist of analogs to purines, pyrimidines and folate.

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54
Q

2 Chemotherapeutic agent types that work on tumor cells throughout the whole cell cycle?

A

Damage the DNA directly and indirectly.

  1. Alkylating agents
  2. Antitumor antibiotics
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55
Q

What is HIPEC? Why it is used

A

Hyperthermic Intra-Peritoneal Chemotherapy

  • Chemo is directly infused into the peritoneal cavity to treat cancer with peritoneal dessimination
  • Used because peritoenal cancers get their nutrients from peritoneal fluids and can grow without blood supply
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56
Q

What is Transarterial Chemoembolization?

A

Catheter is placed in femoral artery and then is guided to the liver where it secretes chemo directly on the tumor.

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57
Q

What is endocrine therapy useful for?

A

Useful for tumors of cells that usally respond to certain hormones during proliferation (e.g mammary, endometrial etc…)

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58
Q

3 receptors commonly targeted in Endocrine therapy:

A
  1. Estrogen receptor
  2. Androgen receptor
  3. Progesterone receptor
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59
Q

Which cancers may have tumors with Estrogen receptors (3), and how are they destimulated during endocrine therapy (3)?

A
  • Breast cancers, Ovarian cancers, Endometrial cancers
  • Endocrine therapy:
  1. Estrogen receptor blockers - Tamoxifen & Fulvestrant
  2. Estrogen synthesis blockers (aromatase inhibitors)
  3. Estrogen deprivation - aGNRH antagonist
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60
Q

Which cancers may have tumors with Androgen receptors (2), and how are they destimulated during endocrine therapy (3)?

A
  • Prostate cancer, Breast cancer
  • Endocrine therapy:
  1. Androgen receptor blockers
  2. Androgen deprivation - aLNRH antagonist
  3. Androgen synthesis blocker - Abiraterone
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61
Q

Which drugs are Androgen receptor blockers? (3)

A
  • AMIDE suffix:
  1. FlutAMIDE
  2. BikalutAMIDE
  3. EnzalutAMIDE
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62
Q

Which susbtance do we use in endocrine therapy of tumors with progesterone receptors?

A

Progestrogens

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63
Q

Which substance do we use for endocrine therapy in leukemias and lymphomas?

A

Glucocorticoids

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64
Q

Ways for certain tumor cells to resist endocrine therapy: (3)

A
  1. By autocrine signaling pathways (they produce their won stimulating hormone that goes on to bind to the receptor)
  2. By increasing the number of receptors (thereby needing higher doses of chemo to treat)
  3. By making activation trough co-regulators like prolactin and GH instead of the main regulator like Androgen for example (thereby the cell has many activating pathways)
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65
Q

Types of drugs used against Growth Factor Receptors?

A
  1. Monoclonal antibodies (often against EGFR) like Cetuximab and Panitumumab
  2. Erbitux - anti-EGFR antibody (though not monoclonal)
  3. Trastuzumab
  • also a monoclonal antibody
  • Binds HER-2 and is against EGFR
  • also induce p21 and p27 cell-cycle inhibitors
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66
Q

Why do we have angioneic therapies?

A

Tumors often release growth factors that cause angiogenesis in close blood vessels –> increased vascularization of tumor –> increased growth

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67
Q

Which drug types are used in angiogenic therapy?

A
  1. Tyrosine Kinase inhibitors (VEGF/PDGFR inhibitor)
  • SorafeNIB
  • SunityNIB
  1. Serine-Threonine (mTOR) inhibitors
  • TemsiROLIMUS
  • EveROLIMUS
  1. VEGF Neutralization
    * Bevacizumab
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68
Q

What is HER2 and what does ocerexpression of it mean?

A

HER2 is a prognostic marker in breast cancer and overxpression of it can be masured to assess the cancer severity and prognosis during treatment.

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69
Q

Drugs used in treating breast cancer? (2)

A
  1. Trastuzumab (main drug)
  2. Lapatinib
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70
Q

Disadvantage of Trastuzumab monotherapy in breats cancer?

A

66-88% will develop resistance, often within a year

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71
Q

Advantage of HER2 expressing breast tumor over one that doesn’t express HER2?

A

Breast cancers that overexpress HER2 can be properly monitored and better targeted than those that do not overexpress HER2

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72
Q

How can breast cancers become resistant to Trastuzumab?

A
  1. They can produce cytokines that impair stimulation of monocytes by the monoclonal antibody Trastuzumab
  2. They can lose the main domain that Trastuzumab binds to on the HER2 receptor
  3. They can produce substances like MUC4 that can cover and protect the HER2 receptor from Trastuzumab binding
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73
Q

Coley’s toxin - mechanism of action:

A

Induced infection with Strep.pyogenes –> increased expression of TNFa –>

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74
Q

Explain the logic behind immunosppressive therapy:

A

As the cancer grows and is more and more stimulated, itsIn immunosuppressive therapy we often give monoclonal antibodies to destroy immunosuppressive molecules in order to cause a stronger immune response in the body against cancer cells

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75
Q

Name 4 drugs that are commonly used in immunosupressive therapy, and what are they often called?

A

Often called check-point inhibitors, these include:

  1. Ipilimumab - Anti CTLA4
  2. Nivolumab - Anti PD1
  3. Pembrolizumab - Anti PD1
  4. Atezolizumab - Anti PDL1
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76
Q

What is Oncolytic Virus therapy based on?

A

Modifying viruses to target certain cancer cells, replicate within them and then cause them to burst to then go on to kill other cancer cells. When lysis of these tumor cells occur, the systemic of immune response of the body is also activated and assist in killing these cancerous cells as well as removing dead cell debris.

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77
Q

What is T-VEC?

A

A modified HSV that can be used un Oncolytic Virus therapy of melanoma.

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78
Q

What do most masses found in breasts turn out to be?

A

Fibroadenomas

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79
Q

List the factors that may increase risk of breast cancer: (16)

A
  1. Sex: female
  2. Age above 40
  3. Early menarche
  4. Late menopause
  5. Not having children
  6. Caucasian race above 40, or african race under 40
  7. First-degree relatives with breast cancer
  8. Second-degree relatives that got B.C before menopause
  9. BRCA1 or BRCA2
  10. Mutation of p53, CHEK2, Rb-1, C-Myc
  11. Having Li-Fraumeni or Cowden syndrome
  12. Benign Breast Disease
  13. Previous irradiation
  14. Previous breast cancer
  15. Contraceptives or postmenopausal hormone supplementation
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80
Q

What is the % of breast cancer patients with BRCA-1 or BRCA-2?

A

1%

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81
Q

What is Benign Breast Disease?

A

Ductal hyperplasia

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82
Q

Prognostic factors to consider when treating breast cancer:

A
  1. Resection margin status
  2. Vessel invasion
  3. HER2 overexpression
  4. Estrogen and prgesterone overexpression
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83
Q

Most common cancer in women?

A

Breast cancer

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84
Q

Current recommendation for screening of breast cancer:

A
  • Mammography very 2 years in women over 50
  • Annual MRI and mammography for women with a strong family history of breast cancer (BRCA doesn’t matter)
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85
Q

Which type of breast is easiest to detect a cancer in on a mammogram?

A

A fatty breast, meanwhile a dense breast is harder to detect a cancer in

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86
Q

What is BI-RADS scale?

A

A scale going from 0-6 grading suspectibility of malignency of breast cancer based on a mammogram. Also helps decide if patient needs additional imaging or biopsy. (4 or more = biopsy)

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87
Q

Breast examination signs of breast cancer: (9)

A
  1. Nipple discharge
  2. Lumping or thickening
  3. Skin texture change
  4. Armpit pain
  5. Change in the nipple morphology
  6. Visible lump
  7. Dimpling
  8. Breast or nipple is pulled to one side
  9. Skin irritation
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88
Q

How do you want to assess a breast cancer patient for primary tumor and regional lymph node involvement?

A
  1. Physical examination
  2. Mammography
  3. Breast and lymph node US
  4. Core biopsy of tumor and pathalogy determination based on histology, grade, HER2, KI67, estrogen and progesterone
  5. US-guided biopsy of regional lymph nodes
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89
Q

What can we do if the breasts are too dense for a mammography? Other indications?

A

Take an MRI instead.

Other indications:

  1. Familial breast cancer with BRCA mutations
  2. Lobular cancers
  3. Multifocal cancers
    4.
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90
Q

What are the 5 main intrinsic subtypes of breast cancer?

A
  1. Luminal A
  2. Luminal B (HER2 positive)
  3. Luminal B (HER2 negative)
  4. ErbB-2 overexpression
  5. Basal like (Tripple negative)
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91
Q

Luminal A, clinicopathologies and treatment:

A

Clinicopathologies:

  1. ER: positive
  2. PR: positive
  3. HER2: negative
  4. Ki-67: low
  5. Recurrence risk: low

Treatment:

*

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92
Q

Luminal B (HER2 positive), clinicopathologies and treatment:

A

Clinicopathologies (all are positive):

  1. ER: positive
  2. PR: positive
  3. HER2: positive
  4. Ki-67: positive
  5. Recurrence risk: NA

Treatment:

  • Endocrine therapy, cytotoxic therapy and anti-HER2
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93
Q

Luminal B (HER2 negative), clinicopathologies and treatment:

A

Clinicopathologies (HER2-neg, might also be PR neg):

  1. ER: positive
  2. PR: positive or negative
  3. HER2: negative
  4. Ki-67: positive
  5. Recurrence risk: high

Treatment:

  • Endocrine therapy and cytotoxic therapy
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94
Q

ErbB-2 overexpression subtype, clinicopathologies and treatment:

A

Clinicopathologies (only HER2 is positive):

  1. ER: negative
  2. PR: negative
  3. HER2: positive
  4. Ki-67: NA
  5. Recurrence risk: NA

Treatment:

  • Cytotoxic therapy and anti-HER2 therapy
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95
Q

Basal-like subtype, clinicopathologies and treatment:

A

Clinicopathologies (all are negative):

  1. ER: negative
  2. PR: negative
  3. HER2: negative
  4. Ki-67: NA
  5. Recurrence risk: NA

Treatment:

  • Cytotoxic therapy
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96
Q

TNM of breast cancer:

A
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97
Q

What is the preferred treatment in early breast cancer, and how is it done??

A

Breast Conserving Therapy. Local treatment of breast cancer by lumpectomy followed by moderate-dose radiation therapy.

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98
Q

What are the indications for a mastectomy?

A
  1. Large tumor size (relative to breast size)
  2. Tumor multicentricity
  3. Inabillity to achieve negative surgical margins after multiple resections
  4. Patients unable to get radiation
  5. Other contraindications of Breast Conserving Therapy
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99
Q

Chemotherapy for breast cancer:

  1. How long should it be administered?
  2. What do we use?
  3. What about patients with cardiac complications?
  4. What about highly proliferative tumors?
A
  1. 12-24 weeks (4-8 cycles)
  2. Anthracycline/Taxane-beased regimens (Doxorubicin is the gold standard anthracycline)
  3. Non-anthracycline regimens (doxocrubicin contraindicated, use taxanes instead)
  4. Dose-dense therapy + G-CSF support
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100
Q

When treating breast cancer, which therapies can be combine (done at the same time) and which therapies cannot? (we do not consider surgery when asking this question)

A

Yes:

  • Radiotherapy and endocrine therapy

No:

  • Chemotherapy (anthracycline) and radiotherapy
  • Chemotherapy (anthracycline) and endocrine therapy
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101
Q

Which type of endocrine therapy can be used with chemotherapy (anthracycline/taxane) when treating breast cancer?

A

Endocrine therapy with GNRH for protection of ovaries during chemo.

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102
Q

When combining chemotherapy (anthracycline/taxane) with radiotherapy in breast cancer, should chemo be adjuvant or neoadjuvant?

A

Neoadjuvant

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103
Q

What is Preoperative systemic treatment in breast cancer and what are the indications for it?

A
  • Chemotherapy (anthracycline/taxanes) implemented before surgery to reduce the extent of surgical incision in large operable cancers.
  • Indications: All patients with >2 cm tumor with a chemotherapy-indicated subtype like HER2-positive and Tripple negative subtype
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104
Q

Do you give adjuvant chemotherapy to a patient with breast cancer that has recieved PST before surgery?

A

No, all chemotherapy should then be given during PST as neoadjuvant treatment.

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105
Q

What can you add additionally to general PST for breast cancer patients with Tripple-negative subtype or BRCA1/2 subtypes?

A

Platinium compunds can be added to the general therapy with anthracycline/taxanes.

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106
Q

In high-risk Tripple-negative subtype breast cancer patients not achieving PST with normal neoadjuvant cht treatment regimen, whatt should you consider to add?

A

Capecitabine or Platinium compunds

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107
Q

In ER-negative/HER2-positive patients that cannot reciev general CHF as a PST, what can you give instead?

A

Endocrine therapy, which can be given both before and after surgery.

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108
Q

When dealing with HER2-positive cancers, which drug do we want to include in our treatment therapy, and is almost standard one year regimen in these cases?

A

Trastuzumab

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109
Q

What therapy do you NOT want to concomitantly give Trastuzumab with and why?

A

You should NOT give Trastuzumab at the same time you are giving Anthracycline as this may cause cardiotoxicity. Use non-anthracyclines instead like taxanes.

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110
Q

What can we use instead of Trastuzamab or Pertuzamab in HER2 positive therapies where these medications have not given enough HER2-blockade?

A

T-DM1 (Transtuzamab Emtansine) which block HER2 through a different mechanism.

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111
Q

Which drug is the standard used during adjuvant hormone therapy of premenopausal women with breast cancer? How long do we use it and why do we use it?

A

Tamoxifen for 5-10 years. It inhibits Estrogen receptors and also works as an OFS (Ovarian Function Suppression).

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112
Q

Why is OFS important when treating breast cancer?

A

It preserves fertility and protects ovaries from damage by the strong chemotherapeutic agents.

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113
Q

If endocrine therapy of breast cancer is still insufficient and patient recover menses within the first 1-2 years of treatment, what can we add to the typical Tamoxifen treatment

A

In addition to Tamoxifen, the patient starts with Ovarian Function Supression (OFS) therapy often using Gosarelin.

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114
Q

In a high-risk patient recieving Tamoxifen and Gasorelin during endocrine therapy for breast cancer, what can we replace it with for an even stronger OFS?

A

We can replace it with Aromatase-inhibitors as they achieve a stronger OFS.

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115
Q

Standard Endocrine therapy treatment for postmenopausal women with breast cancer?

A

Tamoxifen + Aromatase Inhibitor

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116
Q

If you have already started Tmoxifen therapy in a postmenopausal woman and want to switch to an aromatase inhibitor, when can you do that?

A
  • After 2-3 years if you want to switch to or add a non-steroidal Aromatase-inhibitors or Exemstane (steroidal)
  • After 5 years if you want to switch to Letrozole or Anastrozole instead
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117
Q

If we want to give Endocrine therapy as neoadjuvant, which drugtype whould we consider?

A

Aromatase Inhibitors (both steroidal or non-steroidal may be used)

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118
Q

Side-effects of Tamoxifen? (2)

A
  1. Increases risk of uterine cancer
  2. Risk of blood clot
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119
Q

Side effects of aromatas inhibitors: (9)

A
  1. Bone dimineralisation (Dexa scan regularly)
  2. Hot flushes
  3. GI problems
  4. Fatigue
  5. Myalgia
  6. Headache
  7. Depression
  8. Aloplecia
  9. Weight gain
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120
Q

Follow up procedure after breast cancer treatment:

A

Visit every 3-4 months in the first 2 years, then every 6-8 months for 3 years, and anually after the 5th year.

(Dexa scan follow-up for patients treated with AI’s)

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121
Q

Main 2 FIRST tests for testicular cancer?

A
  1. Testicular Sonography
  2. Tumor markers
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122
Q

3 main tumor markers for testicular cancer?

A
  1. AFP
  2. HCG
  3. LDH
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123
Q

Which tests do you may have to do after suspecting testicular cancer after positive markers and sonography? (2)

A
  1. Inguinal biopsy of contralateral testis or midline extragonadal tumor
  2. Ultrasound
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124
Q

What information can a histopathology report of a testicular cancer biopsy tell us:

A
  1. WHO classification
  2. Tumor size
  3. Multidiplicity
  4. Extension of tumor
  5. Vascular invasion
  6. Presence of synctiotropoblasts if it’s a seminoma
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125
Q

What kind of tumor is 98% of testicular cancers?

A

Germ Cell Tumors (GCT)

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126
Q

What is the cure % of stage 1 testicular cancers and % of metastatic testicular cancers?

A
  1. Stage 1 cure rate: 100%
  2. Metastatic cure rate: >80%
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127
Q

Where in the body are testicular cancers usally localised?

A
  • 95% are localized in the testicles
  • 5% are extratesticular (localized in retroperitoneum, mediastinum, cerebrum…etc)
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128
Q

Which 2 groups are germ cell tumors divided into?

A

Seminomas and non-seminomas (50/50)

129
Q

3 criterias to be met for a GCT to be a Seminoma:

A
  1. Histology of pure seminoma
  2. Normal AFP
  3. Elevated/Normal B-hCG
130
Q

What kind of non-seminoma GCTs may we find? (4)

A
  1. Embryonal cancers
  2. Yolk sac tumors
  3. Trophoblastic tumors
  4. Teratomas

….etc

131
Q

Diagnostic workup for checking if seminoma has metastasis? (3)

A
  1. Abdominal/pelvic CT with contrast
  2. Chest X-ray/CT
  3. repeat tumor marker test
132
Q

Indiactions for doing a brain MRI in a seminoma patient? (2)

A
  1. B-hCG >5000 IU/L
  2. Lung metastases
133
Q

Diagnostic workup for checking if non-seminoma has metastasized? (2)

A
  1. Chest/abdominal/pelvic CT
  2. Repeat tumor marker test
134
Q

Indications for brain MRI of a non-seminoma patient? (6)

A
  1. B-hCG >5000 UI/L
  2. AFP > 10 000 ng/mL
  3. Lung metastases
  4. Non-pulmonary visceral metastases
  5. Neurologic symptoms
  6. Choriocarcinoma
135
Q

TNM staging of testicular cancer?

136
Q

“N” of TNM staging of testicular cancer?

137
Q

S part of TNM staging of testicular cancer?

138
Q

Chemotherapy regimen of testicular cancer:

A

3 cycles of the following drugs:

  1. Cisplatin day 1-5
  2. Etoposide day 1-5
  3. Bleomycin day 1, 8, 15
139
Q

Post-chemotherapeutic managment of Seminoma:

A
  1. CT of chest, abdomen and pelvis to see if there’s complete response –> follow up
  2. If no complete response, do FDG-PET and take biopsy of the remaining tumor –> further treatment
140
Q

What is RPLND?

A

Retroperitoneal Lymph Node Dissection:

Surgical treatment option for low-grade Germ Cell Tumors

141
Q

In testicular cancer, what is a Late Relapse and how do we treat it?

A

It’s a relapsing tumor occurring >2 years after treatment. Do not respond well to chemo by itself so we need to start with surgery, then chemo.

142
Q

In testicular cancer, what is Late Toxicity, and what can occur? (6)

A

Late Toxicity are additional problems that may occur after treatment of testicular cancer due to the intense treatment regimen. This includes:

  1. Reduced fertility
  2. Hypogonadism
  3. Cardiovascular disorders
  4. Metabolic syndrome
  5. Toxicity of other organs
  6. Leukaemia (Etoposide)
143
Q

Most prevelant cancer worldwide?

A

Lung cancer

144
Q

Which cancer cause most cancer-related mortalities worldwide?

A

Lung Cancer

145
Q

Risk factors for Lung Cancer?

A
  1. Male
  2. Smoking 80% (also second hand smoking 30%)
  3. Asbestos (Mesothelioma)
  4. Radiotherapy 0.8%
  5. Radon gas 0.5%
146
Q

What kind of cancer is Paraneoplastic Syndrome?

A

SCLC - Small Cell Lung Carcinoma

147
Q

Symptoms of lung cancer? (13)

A
  1. Cough (80%)
  2. Dyspnea
  3. Stridor
  4. Hemoptysis
  5. Recurring pneumonia- bronchi obstruction
  6. Pleural effusion (exudate)
  7. Chest pain, shoulder and arm pain
  8. Horner´s syndrome
  9. Unilateral diaphragm paresis
  10. Weight loss
  11. SVC syndrome
  12. Clubbing
  13. Paraneoplastic syndrome
148
Q

Diagnosis methods for lung cancer:

A
  1. History and Examination
  2. X-Ray
  3. CT chest and abdomen
  4. PET (for distant metastases and lymph nodes)
  5. Biopsy (either through bronchoscopy or transthoracic needle biopsy)
149
Q

What is Mediastinoscopy? Any alternatives to it?

A

Involves making an incision 1cm above the sternal notch and guiding a scope down the pretracheal are to lymph nodes we want to biopsy in a lung cancer patient.

Alternatives, thoracoscopy or thoracentesis.

150
Q

Most common sites of lung cancer metastases?

A

BLAB:

  1. Bone
  2. Liver
  3. Adrenals
  4. Brain
151
Q

What does EBUS and EUS stand for? And what are they used for in lung cancer?

A
  • EBUS: Endobronchial ultrasound
  • EUS: Endoscopic ultrasound

Used for help in staging the lung cancer

152
Q

Rate of NSCLC compared to SCLC lung cancer? Which type is most severe?

A
  • NSCLC: 87%
  • SCLC: 13

SCLC is the most severe as surgery is usally contraindicated here.

153
Q

The 4 cancer types of NSCLC:

A
  1. Adenocarcinoma (the most common type)
  2. Squamous cell carcinoma
  3. Large cell carcinoma
  4. NOS carcinoma
154
Q

Two stagings of SCLC?

A
  • LS: Limited stage disease
  • ES: Extensive stage disease
155
Q

Which NSCLC stages is surgery indicated for?

A

Stage IA - IIIA

156
Q

Surgical options for NSCLC?

157
Q

Which surgical option is the most commonly done for NSCLC?

158
Q

What is VATS and what kind of NSCLC is it used for?

A

VATS - Video-assisted Thoracoscopic Surgery

  • Indicated for Lung Cancer with peripheral tumors upto 6cm without hilar adenopathy
159
Q

What is the indication for postop adjuvant therapy of NSCLC?

A

The tumor is >4cm or is in stage 2A - 3A

160
Q

Adjuvant therapy after NSCLC surgery?

A

Cisplatin + Vinorelbine every 3 weeks, 4 cycles

161
Q

Surgical protocol for NSCLC: (4)

A
  1. Is the tumor stage 1A -3A? Mainly lobectomy, unless it is very large or very small.
  2. Is the tumor <6cm without hilar adenopathy? VATS.
  3. Is the tumor >4cm or in stage 2A-3A? Adjuvent therapy of Cisplatin and Vinorelbin every 3 weeks, 4 cycles
  4. PET to check node and other metastases
162
Q

What is R1 resection?

A

Radiotherapy of macroscopic tumor margins that are left after a surgical removal of tumor.

163
Q

When is radiotherapy indicated in lung cancer? (4)

A
  1. As adjuvant after surgery (R1 resection)
  2. Patients that either can’t or don’t want to have surgery
  3. Small/peripheral tumors of T1-T2 N0 M0
  4. In palliation on local metastases to decrease hemoptysis or dyspnea + brain metastases
164
Q

What is a Hypofractionated schedule?

A

Instead of many weeks of small dose radiation, having a few weeks of high-dose radiation. Its safety is due to the radiation being precisely pointed on the tumor from different angles so sarrounding tissues will get less radiation (stereotactic).

165
Q

How is radiotherapy implemented?

A

Stereotactic radiation therapy where the radiation is coming from several angles causing a high-dose point on the tumor in a hypofractionated schedule.

166
Q

Indication for systemic (chemo) therapy of lung cancer?

A
  1. Metastases
  2. Mediastinal lymph node involvement
  3. Stage 3A N2 NSCLC as part of multidisiplinary (might also be considered as adjuvent for 2A-3A tumors)
  4. As part of radio-chemotherapy of stage 3B
  5. Stage 4 NSCLC palliative therapy
  6. SCLC treatment regimen
167
Q

2 different ways of organising radio-chemotherapy of stage 3B NSCLC:

A
  1. Concurrent: give chemo and radiation at the same time for stronger effect (although high toxicity)
  2. Sequential: give chemo and radio at seperate times for less toxicity (although weaker effect)
168
Q

3 options for palliative systemic therapy of stage 4 NSCLC:

A
  1. Tyrosine Kinase Inhibitors
  2. Immunosuppression
  3. Cytotoxic therapy
169
Q

How to decide which type of palliative systemic therapy to apply for stage 4 NSCLC?

A
  1. Check cell histology from the biopsy you took
  2. If adenocarcinoma, test for EGFR mut./ALK/ROS –> if positive give Tyrosine-Kinase Inhibitors, if negative see below
  3. Both adenocarcinoma and SCC can be checked for PDL1 expression –> if >50% start immunosuppressive therapy
  4. If all are negative go on to chemotherapy

(PS. if histology shows SCC, start from point 3)

170
Q

Palliative regimen for stage 4 NSCLC that is adenocarcinoma:

A

Cisplatin + one of the following:

  1. Pemetrexed (good combo)
  2. Afatynib (proven to increase overall survival well)
  3. Erlotinib
  4. Gefitinib
171
Q

Palliative regmien for stage 4 NSCLC that is SCC:

A

Cisplatin + Gemcitabine

172
Q

What is Crizotinib?

A

An oral ALK-inhibitor usefull in targeted palliative therapy of stage 4 NSCLC patients positive for the EML4-ALK gene.

173
Q

If Pembrolizumab doesn’t work in palliative immune therapy of stage 4 NSCLC, what can you use instead.

A

Nivolumab, which is also anti-PD1 and is used in 2nd line if Pembrolizumab doesn’t help.

174
Q

An important complication to consider when dealing with SCLC:

A

A lot of these tumors may become neuroendocrine tumors which may cause additonal paraneoplastic syndromes.

175
Q

How does SCLC usally present on imaging?

A

As a large mass with hilar or mediastinal adenopathy

176
Q

Treatment of Limited Stage (limited disease) SCLC?

A

Chemoradiotherapy with Cisplatin + Etoposide (can be given concurrently or sequentially)

177
Q

Which criteria must be fulfilled for surgery to be even considered in LS SCLC? (2)

A
  1. No invasion of vital structures
  2. No lymphnode metastasis

Often combined with adjuvant chemotherapy

178
Q

What is Prophylactic Cranial Irradiation, how and when is it implemented?

A

Prophylactic Cranial Irradiation is given to patients 3-5 weeks after chemoradiation therapy to make sure that there will not be a brain metastasis. It can only be done if the following criteria are met:

  1. Complete Response or Partial Response to chemoradiation
  2. There is no sign of brain metastasis occurring at the time
  3. PS0 - 1 on Zubrod Scale
179
Q

What type of SCLC is the most common?

A

Ekstensive Stage (Extensive Disease) SCLC is the most common (70%) because most SCLC patients are diagnosed late and by then they are already at ED.

180
Q

First-line treatment regimen for ED SCLC:

A
  • Cisplatin + Etoposide (+ limited radiotherapy)
  • If any response, also do a Prophylactic Cranial Irradiation
181
Q

2nd-line treatment of ED SCLC:

A

Topotecan or CAV (Cyclophosphamide, Doxorubicin, Vancristine)

182
Q

When is 2nd-line ED SCLC treatment indicated?

A

If patient has had his 1st-line treatment and the tumor progresses within 3 months after treatment, we try 2nd-line instead (but if the tumor progresses AFTER 3 months of 1st-line treatment, we try another round of 1st-line treatment

183
Q

Where can Upper GI cancers be found? (5)

A
  1. Stomach (Gastric)
  2. Pancreas
  3. Esophagus
  4. Biliary
  5. Liver (Hepatocellular)
184
Q

Deadliest and most common upper GI cancer?

A

Gastric cancer

185
Q

Risk factors of Gastric cancer?

A
  1. H. pylori
  2. Tobacco
  3. Nitrosamines
  4. Genetic Predisposition
  5. Male
  6. Alcohol
  7. Salty and “unhealthy” diet
186
Q

What is the % of gastric cancers with a genetic predisposition, and what can these predispositions be?

A

1-3%

  1. Hereditary diffuse gastric cancer
  2. Lynch syndrome / HNPCC (Hereditary Non-Poplyposis Volorectal Cancer)
  3. FAP (Familial Adenomatous Polyposis)
  4. Peutz Jegher’s Syndrome
187
Q

Where in the stomach are gastric cancers located? (4)

A
  1. Pylorus (>50%)
  2. Lesser curvature of the stomach (25%)
  3. Fundus and body of stomach (10%)
  4. Greater curvature of stomach (3-5%)
188
Q

Symptoms of Gastric cancer? (8)

A
  1. Discomfort
  2. Pain in stomach area
  3. Nausea and Vomiting
  4. Dysphagia and Odynophagia
  5. Hematemesis
  6. Melena
  7. Weight loss
  8. Feeling full/ bloated after a small meal
189
Q

Diagnostic workup of gastric cancer:

A
  1. Gastroscopy with biopsy
  2. CT to check for metastases and staging (in women, also do pelvic CT)
190
Q

What is the most common type of gastric cancer?

A

Adenocarcinoma (90%)

191
Q

What is ESDand what is it used for?

A

ESD - Endoscopic Submucosal Dissection

  • Used in surgical treatment of mild gastric cancers
192
Q

What is the D (D1, D2, D3 etc…) classification used for?

A

The D-classification represents the location of certain lymphnodes and is used for specification of certain lymph nodes that get removed during a lymphadenectomy.

193
Q

Treatment of Gastric cancer, stage 1A T1a N0?

194
Q

Treatment of Gastric cancer, stage 1A ,T >1a , N >0?

A

Gastrectomy with D1+ lymphadenectomy

195
Q

Treatment of Gastric cancer stage 1B - 3B?

A

Gastrectomy with D2 lymphadenectomy + adjuvant or neoadjuvant chemotherapy

196
Q

Chemotherapautic agents used for gastric cancer: (3)

A
  1. Fluoropyrimidines
  2. Platinum agents
  3. Anthracyclines
197
Q

If gastric cancer also exhibits HER2-expression, which agent do you wnat to add to the mix during chemo?

A

Trastuzamab

198
Q

When is radiotherapy indiciated when tretaing gastric cancer?

A

Indicated mainly for palliative treatment of metastases. Sometimes in combination with palliative systemic chemotherapy.

199
Q

Risk factors for Pancreatic cancer? (9)

A
  1. Cigarette smoking
  2. Obesity
  3. Chronic pancreatitis
  4. Alcohol
  5. Genetic predisposition
  6. HBV
  7. H. pylori
  8. Red processed meat
  9. High fruit and folate intake reduces risk
200
Q

What is the % of Pancreatic cancers with a genetic predisposition, and what can these predispositions be? (4)

A

10% (often due to germline mutations)

  1. Li Fraumeni
  2. HNPCC
  3. BRCA2 mutation
  4. Peutz-Jegher´s syndrome
201
Q

Most common locations of pancreatic cancer: (3)

A
  1. Head of pancreas 75%
  2. Body of pancreas 15%
  3. Tail of pancreas 10%
202
Q

Symptoms of Pancreatic cancer: (7)

A
  1. Jaundice
  2. Diabetes
  3. Abdominal and lower back pain (especially while eating or lying supine)
  4. Nausea and Vomiting
  5. Lack of appetite and weight loss (although patient is bloating)
  6. Light colored stool and dark urine
  7. Fatigue
203
Q

Most common type of pancreatic cancer?

A

Adenocarcinoma (95%) with an 80-85% chance of pancreatic ductal carcinoma

204
Q

Diagnostic workup of Pancreatic cancer?

A
  1. CT with contrast (gold standard)
  2. Esophageal USG (often for NETs in the right location)
  3. USG-guided biopsy for metastases
205
Q

Treatment protocolfor pancreatic tumor:

A
  1. Whipple procedure (gold standard)
  2. Pancreatosplenectomy (in sever cases)
  3. Lymphadenectomy (often of >15 nodes)
  4. Adjuvent chemotherapy after surgery
206
Q

Chemotherapeutic agent used in adjuvent therapy of pancreatic cancer:

A
  • Mainly Gemcitabine (altthough 5-Flu may also be used, but is more toxic)
  • For metastases: Folfirinox, or Gemcitabine + nab-Paclitaxel
207
Q

What type of pancreatic cancer has a better prognosis than the common adenocarcinoma and what type has a worse prognosis?

A
  • Better: Acinar cell carcinoma
  • Worse: Undifferentiated/ Adenosquamous Carcinoma
208
Q

Risk factors for Esophageal SCC? (2)

A
  1. Smoking and alcohol
  2. Old age
209
Q

Most common sites of esophageal SCC?

A

Proximal/middle part of esophagus

210
Q

Risk factors of Esophageal Adenocarcinoma?

A
  1. Obesity
  2. GERD
  3. Old age
  4. Male
  5. Barret´s esophagus
211
Q

Most common site of esophageal adenocarcinoma?

A

Distal part of esophagus

212
Q

Symptoms of esophageal cancer:

A
  1. Dysphagia and odynophagia
  2. Vomiting and weight loss
  3. GI bleeding
  4. Recurrent aspiration
213
Q

Diagnostic workup of esophageal cancer? (4)

A
  1. Endoscopy with biopsy (gold standard)
  2. Endoscopic ultrasound (very helpful)
  3. CT neck, chest and abdomen (for staging and metastasis)
  4. PET/CT if we still suspect undetected metastasis
214
Q

Treatment for early N(0) esophageal cancer?

A
  • Endoscopic resection (gold standard)
  • Eletromagnetic spectroscopy (EMR) or Electron spin resonance spectroscopy (ESR) are 2 radiation optioins that might also be considered
215
Q

What is Brachytherapy?

A

Placing a radioactive substance inside the patient to kill the cancer cells.

216
Q

Treatment for advanced esophageal cancer:

A
  1. Adenocarcinoma: always surgery + maybe adjuvent chemo or radiation (if tumor express HER2, also give Trastuzamab)
  2. SCC: always chemoradiation + maybe surgery
  • Metastasis: Chemotherapy or Brachytherapy
217
Q

Chemotherapeutic agents of choice when treating esophageal cancer: (2)

A

Carboplatin or Cisplatin

218
Q

Risk factors of melanoma? (3)

A
  1. UV exposure
  2. Genetic predisposition and family history
  3. Immune suppression
219
Q

Genetic predisposition to melanoma: (2)

A
  1. Dysplastic nevus syndrome
  2. BRAF mutation
220
Q

Explain the ABCDEs of detecting melanoma:

221
Q

Explain the Glasgow 7-point checklist of melanoma:

A

Suspect melanoma if 1 or more major signs:

  1. Change in size
  2. Change in shape
  3. Change in color

Suspect melanoma if 3 or 4 minor signs:

  1. Inflammation
  2. Crusting or bleeding
  3. Sensory change
  4. Diameter >7mm
222
Q

Explain the Breslow scale:

A

Breslow thickness is the measurement of the depth of the melanoma from the surface of your skin down through to the deepest point of the tumour.

223
Q

Diagnostic workup on melanoma: (3)

A
  1. Physical examination using ABCDE , 7-checkpoint list or Breslow scale
  2. Dermatoscopy and videodermatoscopy
  3. Tumor biopsy + lymph node biopsy for histopathology and staging
224
Q

Explain the staging of melanoma:

A
  • Stage 1+2 - no metastasis to regional or distal lymph nodes
  • Stage 3 - some involvement of regional lymph nodes
  • Stage 4 - disseminated disease
225
Q

Treatment of stage 1-3 melanoma?

A

Tumor excision + sentinel/regional lymphadenectomy

226
Q

Treatment of stage 4 melanoma:

A

Mainly systemic treatment

  1. Chemotherapy
  2. Surgery if patient is in good condition
  3. Radiotherapy if metastasis to bone or CNS
  4. Targeted therapy and imminotherapy if tumor has BRAF mutation
227
Q

Chemotherapautic agents used for melanoma: (4)

A

Multi-drug regimen:

  1. DTIC
  2. Temozolomide
  3. Paclitaxel
  4. Fotemustine
228
Q

Name 2 BRAF inhibitors:

A
  1. Vemurafenib
  2. Dabrafenib
229
Q

Name 2 MEK inhibitors:

A
  1. Cobimetinib
  2. Trametinib
230
Q

2 drug regimens that might be used in targeted therapy of BRAF positive melanoma:

A

One of the following regimens:

  1. Vemurafenib + Cobimetinib
  2. Dabrafenib + Trametinib
231
Q

2 drugs that might be used in immunotherapy of BRAF positive melanoma:

A
  1. Nivolumab
  2. Pembrolizumab
232
Q

2 alternative treatment options special for melanoma:

A
  1. T-VEC
  2. IL-2
233
Q

How can recurrence occur after melanoma treatment? (4)

A

It can occur either as:

  1. Satellite lesion (around primary site)
  2. Transit lesion (along lymphatic drainage)
  3. Nodal recurrence (in the lymph nodes)
  4. Metastasis (recurrence in other organs)
234
Q

Most common type of cancer in the urinary system?

A
  • Most common site of cancer: urinary bladder (>90%)
  • Most common type of urinary cancer: Urothelial cancer (90%)

So we often think of urothelial cancer of the bladder

235
Q

Risk factors of urinary bladder cancer:

A
  1. Smoking and chemichal compounds in air
  2. Cyclophosphamide
  3. Genetic predesposition
  4. Recurrent UTI and chronic irritation
  5. Catheters
  6. Previous irradiation
236
Q

What is TURBT?

A

Transuretheral Resection of a Bladder Tumor

237
Q

Diagnostic workup of bladder cancer: (3)

A
  1. USG bladder (gold standard)
  2. Cytoscopy with TURBT and biopsy for histopathology
  3. For staging and metastases: CT/MRI of chest, abdomen and pelvis
238
Q

Step by step treatment option for superficial tumors of TIS - T1?

A
  1. Cytoscopy with TURBT
  2. Local adjuvant therapy right afterwards
  3. Follow up cytoscopy 1-4 weeks after
239
Q

Chemotherapeutic agents used for adjuvant therapy in superficial bladder cancers?

A
  1. Doxorubicin
  2. Mitomycin C
  3. Bleomycin
  4. BCG (an immunomodulatory agent mainly for TIS tumors)
240
Q

Step by step treatment of locally invasive (T2-T3) urinary bladder cancer:

A
  1. Neoadjuvant chemotherapy before surgery
  2. Radical cystectomy (with DaVinci machine)+ lymphadenectomy
  3. Adjuvant chemotherapy or radiation after surgery
  4. Urinary diversion afterwards

*Trimodality therapy might be also be considered

241
Q

Why do we do both neoadjuvant and adjuvant chemotherapy in locally invasive (T2-T3) bladder cancer?

A

Because the cancer has a very strong tenedancy to metastasise, even after surgery.

242
Q

Why do we use a DaVinci machine during cystectomy and lymphadenectomy of bladder cancer, why do we have to be so precise?

A

Because the cancer can often lie close to the pudendal nerve, and we have to be carfeull so we don’t damage it, as this would cause sexual dysfunction in both male and female.

243
Q

What is Urinary Diversion? Why is it done?

A
  • A surgical procedure that reroutes the normal flow of urine out of the body when urine flow is blocked. It can either be rerouted to a urostomy that lies outside of the body (non-continent) or to a pouch wiithin the body with an artiaficially made sphincter (continent)
  • Done when there is a block in the urinary cystem (eg. after a radical cystectomy)
244
Q

Explain the Trimodality-therapy option for treatment of locally invasive urinary bladder cancer. How and why is it done?

A

Done to spare the bladder so the patient won’t need a urinary diversion.

  1. Radical cytoscopy with TURBT
  2. Then chemoradiation with Cisplatin and 66Gy radiation
  3. . Follow up with cystoscopy and radiation of 40 Gy.
  4. If there is still cancerous cells -> normal treatment with radical cystectomy and lymphadenectomy
245
Q

Common metastasis sites of urinary bladder cancer:

A
  1. Abdominal wall
  2. Lungs
  3. Liver
  4. Bones
  5. Lymph nodes
246
Q

How common is colorectal cancer?

A
  1. 3rd most common in men
  2. 2nd most common in women
  3. 90% of all colorectal cances cases occur >50yo
248
Q

Most common type of colorectal cancer?

A

Adenocarcinoma (90-95%)

249
Q

What is mucinous adenocarcinoma?

A
  • A type of colorectal adenocarcinoma
  • 10% of all adenocarcinoma
  • High mucin production –> fluid in abdomen
250
Q

What is Signet-ring cell carcinoma?

A
  • An aggressive type of colorectal adenocarcinoma
  • 1% of all colorectal adenocarcinoma
  • Also cause a mucin buildup
251
Q

Most common type of anal cancer?

A

Squamous Cell Carcinoma

252
Q

Risk factors of colorectal cancer: (7)

A
  1. >85 years of age
  2. Hereditary factors
  3. High fat, high protein, low fiber
  4. Red, processed meat
  5. Alcohol
  6. Cigarette smoking
  7. History of CRC, DM2, polyps, IBD
253
Q

Hereditery factors that may cause colorectal cancer: (2)

A
  1. Lynch Syndrome (HNPCC):
  • In 2-5% of cases of colorectal cancer
  • Early onset, more aggressive, right sided tumor
  • Increased risk of other tumors like endometrial
  1. Familial adenomatous polyposis (FAP)
  • Early onset
  • Recognised by a large amount of GI polyps in the small intestine and also in the stomach sometimes

+ family history of CRC or polyps may also increase risk

254
Q

Why is as much as 75-80% of colorectal cancer sporadic?

A

Because it is often a combination of aquired mutations occurring throughout life that give a late and sudden onset when the amount of mutations get high enough.

255
Q

Symptoms of colorectal cancer: (5)

A
  1. Abdominal pain
  2. Melena
  3. Microcytic anemia
  4. Change in bowel habits (obstructive symptoms, pencil stools)
  5. Anorexia and fatigue
256
Q

Diagnostic workup of colorectal cancer: (4)

A
  1. Medical examination of symptoms
  2. Colonoscopy with biopsy (gold standard), often of sigmoid or rectum
  3. Labtest: CEA, Ca19-9, membran glycoprotein
  4. Metastasis: USG, CT, PETCT CXR, TRUS, Dexa (depending on location)
257
Q

What is TRUS and what is it used for?

A
  • TRUS: Transrectal Ultrasound
  • Used for evaluation of prostate cancer and colorectal cancer
258
Q

Explain stage 1-4 of colorectal cancer:

A
  • Stage 1: TIS, submucosa invasion
  • Stage 2: Invasion of muscle layer
  • Stage 3: Involved regional Lymph nodes
  • Stage 4: Disseminated - 65% show + CEA
259
Q

Treatment for non-metastatic (stage 1-3) colorectal cancer of othe parts than the rectum:

A
  1. Surgery (right or left hemicolectomy, transverse resection, colostomy etc..)
  2. Adjuvant chemotehrapy if >12LN invasion or tumor is stage 3
  • Rectal tumors require both neoadjuvant and adjuvant therapy of either chemo or radiation
260
Q

Treatment option for metastatic (stage 4) colorectal cancer:

A
  • Mainly systemic chemotherapy (either traditional or HIPEC)
  • Surgery only indicated if there is bowel perforation or if metastasis are resectable
  • In case of non-resectable liver metastasis: neoadjuvent + surgery
261
Q

Chemotherapeutic agents used for in chemo of colorectal cancer:

A
  • Leucovorin + 5FLU (mainly)
  • Others: Capecitabine, Oxaliplatin or Irinotecan
  • If tumor is KRAS positive: anti-EGFR like Cetuximab or Pantumumab
262
Q

Biologic anti-VEGF agents helpfull in adjuvent therapy of colorectal cancer: (3)

A

Anti-VEGF:

  1. Bevacizumab
  2. Regorafenib
  3. Zib-aflibercept
263
Q

Follow-up after treatment of colorectal cancer:

A

Combination of colonoscopy and physical examination:

  • Physical examination everey 3-6m for 2 years, then every 6m forthe next 3 years
  • Colonoscopy after 1 year, if negative, do one more after 3-5 years
264
Q

Possible screening methods for colorectal cancer: (7)

A
  1. Colonoscopy - gold standard
  2. Sigmoidoscopy - max to splenic flexure, clonoscopy if polyps found
  3. Double-contrast barium enema - detect 50% of adenocarcinomas
  4. CT-colonography - colonoscopy if polyps found
  5. FOBT (Fecal Occult Blood Test)
  6. FIT (Fecal Immunochemical Test) - more sensitive than FOBT
  7. Fecal DNA - more sensitive than FIT
265
Q

Screening protocol for colorectal cancer:

A
  1. Adults age 50-75 (age 40 if familial history)
  2. Annual FOBT/FIT
  3. Sigmoidoscopy every 5 years or clonoscopy every 10 years
266
Q

Screening protocol for colorectal cancer in patient with FAP:

A
  • Start from age 10-12
  • Annual stool DNA
  • If positive, do a total colectomy
267
Q

Screening protocol for colorectal cancer in patient with HNPCC:

A
  • Screen from age 20-25
  • Colonoscopy every 1-2 years
268
Q

Screening protocol for colorectal cancer in patient with IBD:

A
  • Starts either 8 years after whole bowel onset, or 12-15 years after right-sided bowel onset
  • Colonoscopy every 1-2 years
269
Q

Cancers that require neoadjuvant therapy before resection due to their aggressiveness: (5)

A
  1. Esophageal
  2. Gastric
  3. Triple neg breast cancer
  4. Rectal cancer
  5. Urethral endothelium cancer
270
Q

2nd most common cancer in men?

A

Prostate cancer

271
Q

Most common type of prostate cancer?

A

Adenocarcinoma

272
Q

Risk factors of prostate cancer: (5)

A
  1. Old age
  2. Being african or scandinavian
  3. Family history of prostate cancer
  4. BRCA1 or BRCA2
  5. STDs
273
Q

Drugs that can be taken to decrease risk of postate cancer: (2)

A

5-alpha-reductase inhibitors:

  1. Finasteride
  2. Dutasteride
274
Q

Signs and symptoms of prostate cancer:

A

Early disease: asymptomatic

Locally advanced disease:

  • Bladder outlet obstruction (main symptom)
  • Other: UTI, hematuria, irritation during urination

Disseminated disease: depending on metastases location

275
Q

What do we screen for in prostate cancer, and when do we start?

A

We start screening for PSA at age 50, unless patient has risk factors like BRCA mutations or family history of prostate cancer, then screening should start at 40-45 years of age.

* Digital-Rectal Examination might also be added to the screening

276
Q

What is Gleason’s Pattern and how does it work?

A

Also known as Gleason’s grading system, is used for grading prostate cancer biopsies. Score is decided by adding together the two most prevalent differentiation patterns.

277
Q

Step-by-step diagnostic workup of prostate cancer:

A
  1. First do a Prostate exam and take PSA, refer patient to urologist if findings are abnormal
  2. Do a TRUS (Transrectal Ultrasound-guided Biopsy) and find Gleason Score
  3. Repeat biopsy if PSA keeps rising
278
Q

How do we decide if prostate cancer is low, moderate or hight risk?

279
Q

Treatment of low and intermediate risk prostate cancer?

A

Radical prostatectomy or radiotherapy. If asymptomatic or patient has <10 years to live, we might also consider active surveilance where we measure PSA every 3 months and biopsy after 1 year, to see if cancer progresses.

280
Q

Treatment of high-risk prostate cancer?

A
  • Radiotherapy: ERBT by itself, or combination of ERBT and Brachytherapy using radium-223
  • Radical prostatectomy might also be considered
281
Q

Additional management options of METASTATIC prostate cancer:

A
  • 1st-line: Androgen supression using LNRH or bilateral orchiectomy
  • 2nd-line: Mainly for CRPS
    • Antiandrogens (flutamid, bicalutamid)
    • Chemotherapy (Docetaxel)
    • New options: Abiraterone, SipuleucelT
282
Q

Abiraterone, mechanism of action and use:

A
  • CYP17 blocker –> decreased androgen synthesis
  • Treatment option for CRPC
283
Q

What is Sipuleucel T?

A

A cell-based cancer immunotherapy for prostate cancer. Mononuclear cells are taken from the patient, modified in a lab, then re-injected afterwards for a direct immunereaction against the cancer cells.

284
Q

What kind of precancerous lesions are there? (6)

A
  1. Keratosis acitinica (skin)
  2. Cornu cutaneoum (skin)
  3. Leukoplakia (mucousae)
  4. Polyps (GI)
  5. Barret esophagus
  6. Condylomas (warts, like we see with HPV)
285
Q

What are the hallmarks of cancers? (4 + 6)

A

Main:

  1. Deregulate cellular energetics
  2. Genome instability and mutation
  3. Tumor-promoting inflammation
  4. Avoiding immune destruction

Other:

  1. Sustained proliferative signaling
  2. Evading growth suppressors
  3. Activating invasion and metastasis
  4. Enabling replicative immortality
  5. Inducing angiogenesis
  6. Resisting cell death
286
Q

Difference between curative and palliative radiotherapy:

A
  • Curative: High total dose, low fraction dose (eg. 30 days daily irradiation with 2 Gy)
  • Palliative: Lower total dose, less need to keep fraction dose low (eg. only 8 Gy from one dose)
287
Q

Why can radiation cause tissue necrosis?

A

Because it has an antimetabolite and antiangiogenic effect.

288
Q

Organ-spesific side effects of radiotherapy: (10)

A
  1. Lung:
  • Radiation Pneumonitis
  • Lung fibrosis
  1. Heart Failure (dilated cardiomyopathy)
  2. Mucositis (death of mucosal stem cells)
  3. Salivary glands: Xerostemia
  4. Thyroid: Hypothyroidism
  5. Eyes: Retinal necrosis
  6. Skin:
  • Hair loss
  • Red swollen skin
  • Disqualification and infections
  1. Colon: irritation, perforation, bleeding
  2. Urinary: hematuria, and increased/decreased urination
  3. Bones: Osteoradionecrosis and loss of teeth
289
Q

Which chemotherapeutic agents cause diarrhea, and why?

A
  • Mechanism of action: Damage to mucosa cause decreased absorption and increased secretion, irritant causing decreased transit time, osmotic agents causing osmotic diarrhea.
  • Drugs:
    • 5-FU
    • Capecitabine
    • Irinotecan (Fluoropyrimidines)
    • TKI’s and Mab’s against EGFR
290
Q

Spesific side effect of Irinotecan (Fluoropyrimidines)?

A

Acute cholinergic crisis (cholinergic symptoms). Treated with atropine.

291
Q

Which chemotherapeutic drug is often linked with C.difficile infection?

A

Paclitaxel

292
Q

When is a patient undergoing chemotherapy at a risk of Neutropenic enterocolitis?

A

When PNM <500/uL and bowel wall-thickness is >4mm

293
Q

Why can chemotherapeutic agents cause nausea and vomiting?

A
  • Mechanism of action: stimulate chemoreceptor zones
  • Drugs:
    • Cisplatin (hight)
    • Carboplatin (moderate)
    • Cyclophosphamide (moderate)
    • Doxirubicin (low)
  • Treatment: Aprepitant
294
Q

Which chemotherapeutic agents might cause skin toxicity? Which symptoms and infections might they cause?

A

Occurs 60% of patients

  • Drugs:
  1. Anti EGFRs
  2. TKI’s
  3. Mabs
  • Symptoms:
  1. Acneiform rash that itch
  2. Teleangiectasis
  3. Hirsutism
  • Infections:
  1. S.aureus
  2. Bacteremia
295
Q

Cetuximab vs Panitumumab, which is chimeric and which is humalog?

A
  • Cetuximab = chimeric
  • Panitumumab = mouse
296
Q

Anastrozole («-zole»)

  • Target?
  • Application?
  • Side effects?
A
  • Type: Aromatase inhibitor
  • Application: Luminal A breast cancer
  • SE: Osteoporosis and musculoskeletal pain
297
Q

Bevacizumab

  • Target?
  • Application?
  • Side effects?
A
  • Target: Anti-VEGF
  • Application: Colon cancer
  • SE:
  1. Hypertension
  2. Thromboembolism
  3. Impaired wound healing, bleeding
  4. GI perforation
  5. Proteinuria
298
Q

Bleomycin

  • Application?
  • Side effects?
A
  • Application: Testicular cancer
  • SE: Lung fibrosis
299
Q

Capecitabine

  • Application?
  • Side effects?
A
  • Application: Colon cancer
  • SE:
  1. Hand-foot syndrome (rash)
  2. Cardiotoxicity
  3. Myelosuppression
300
Q

Cetruximab or Pantumumab

  • Target?
  • Application?
  • Side effects?
A
  • Target: Anti- EGFR
  • Application: KRAS wildtype
  • SE:
  1. Hypersensitivity
  2. Acne
  3. Diarrhea
301
Q

Cisplatin

  • Application?
  • Side effects?
A
  • Application:
  1. Lung cancer
  2. Esophageal cancer
  3. Testicular cancer
  4. Bladder cancer,
  • SE:
  1. Nausea and vomiting
  2. Cardiotoxicity
  3. Nephrotoxicity
  4. Nurotoxicity
  5. Myelosuppression
302
Q

Cobimetinib

  • Target?
  • Application?
A
  • Target: MEK inhibitor
  • Application: Melanoma
303
Q

Cyclophosphamide

  • Application?
  • Side effects?
A
  • Application: Sarcomas
  • SE:
  1. Nausea and vomiting
  2. Hemorrhagic cystitis
  3. Bladder cancer
304
Q

Dabrafenib

  • Target?
  • Application?
  • Side effects?
A
  • Target: BRAF inhibitor
  • Application: Melanoma
  • SE:
  1. Skin reaction
  2. Arthralgia
  3. Liver toxicity
305
Q

Denosumab

  • Target?
  • Application?
A
  • Target: Rank-ligand
  • Application: Osteoporosis
306
Q

Doxorubicin

  • Application?
  • Side effects?
A
  • Application:
    1. Breast
    2. hematologic
    3. Sarcomas
  • SE:
    • Cardiotoxicity
    • Vomiting
307
Q

Gemcitabine

  • Application?
A
  • Application: Pancreatic cancer
308
Q

Imatinib

  • Side effects?
A
  • SE:
    1. Congestive Heart Failure
    2. Nausea and Vomiting
    3. Headache
309
Q

Iphosphamide

  • Side effects?
A
  • SE:
    1. Hemorrhagic cystitis
    2. Encephalopathy
    3. Nausea and Vomiting
    4. Alopecia
310
Q

Ipilimumab

  • Target?
  • Application?
  • Side effects?
A
  • Target: anti-CTLA4 mAB
  • Application: Melanoma
  • SE:
    1. Hypersensitivity (autoimmunity, rash, pruritus etc…)
    2. Enterocolitis
    3. Hypophysitis
    4. Liver toxicity
311
Q

Irinotecan

  • Application?
  • Side effects?
A
  • Application: Coloncancer
  • SE:
    1. Diarrhea (tx. atropine)
    2. Neutropenia
312
Q

Nivolumumab

  • Target?
  • Side effects?
A
  • Target: PD1 inhibitors
  • SE:
    1. Diarrhea
    2. Organ-spesific infections (“-itis” infections, eg. thyroiditis)
313
Q

Paxlitaxel

  • Application?
  • Side effects?
A
  • Application: Breast cancer and Melanoma
  • SE:
    1. Nausea and vomiting
    2. Peripheral neuropathy
    3. Anemia and neutropenia
    4. Hypersensitivity
314
Q

Tamoxifen

  • Target?
  • Application?
  • Side effects?
A
  • Target: Anti -ER
  • Application: Breast cancer
  • SE:
    1. Thromboembolism
    2. Endometrial cancer
    3. Increased bone mass
    4. Hot flashes
    5. Vaginal bleeding
315
Q

Traetinib

  • Target?
  • Application?
A
  • Target: MEK inhibitor
  • Application: Melanoma
316
Q

Trastuzumab

  • Target?
  • Application?
  • Side effects?
A
  • Target: anti-HER2
  • Application:
    1. HER2-positive breast cancer
    2. Adenocarcinoma of esophagus
    3. Gastric cancer
  • SE:
    • Cardiotoxicity
    • Hypersensitivity
    • Pulmonary toxicity
    • Nausea and Vomiting
317
Q

Veramurafenib

  • Target?
  • Application?
  • Side effects?
A
  • Target: BRAF inhibitor
  • Application: Melanoma
  • SE:
    1. Skin reaction
    2. Arthralgia
    3. Liver toxicity
318
Q

5-FU

  • Application?
  • Side effects?
A
  • Application: Colon cancer
  • SE:
    1. Nausea and Vomiting
    2. Diarrhea
    3. Infections

5 MD (7 decks)

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