Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

UIDC > Problem 1 > Flashcards

Problem 1 Flashcards

1
Q

What ranking takes the colorectal cancer for most deadly cancer

A

4th

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Risk factors for colorectal cancer

A 
male sex
age
family history
obesity
lack of physical exercise
smoking
excessive alcohol intake
red and processed meat intake
Diabetes type 2
inflammatory bowel disease 
previous colorectal cancer or adenomas
hereditary colorectal cancer syndromes
infection with certain bacteria like Fusobacterium nucleatum and Bacteroides fragilis
(picture)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What percentage of total deaths and cancer diagnosis

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What rank for women and men for most common

A

2nd for women

3rd for men

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Highest rates in which countries

A

most developed countries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why is there a decrease in the incidence

A

screening programs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

There is a worrying increase of colorectal cancer for who

A

people younger than 50 years specifically rectal cancer and left-sided colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Based on twin studies, what percentage of heritability is colorectal cancer

A

12-35%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the 2 kinds of hereditary colorectal cancer syndromes

A

non-polyposis and polyposis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Examples of non-polyposis syndromes

A

Lynch and familial colorectal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why is the Lynch diagnosis frequently missed

A

few adenomas, and if present they can be mistaken for sporadic lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the solution for not missing the diagnosis of Lynch syndrome

A

Systemic molecular screening of the tumor for patients under 70

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cause du syndrome de Lynch

A

dysfunction of the DNA mismatch repair system
SO expansion or contraction of the microsatellite regions so microsatellite instability
+deficiency of mismatch repair proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Is microsatellite instability specific for Lynch syndrome

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Are Lynch patients at risk of other cancers

A

Yes, endometrial, small bowel, ovaries, hepatobiliary, stomach, ureter, renal pelvis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is advised for Lynch patients from 20 to 25 years

A

1-2 yearly colonoscopies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Most cancers arise from…

A

a polyp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

3 steps to cancer formation

A

aberrant crypt
polyp (neoplastic precursor lesion)
cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How long does it take for cancer to form

A

10-15 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the origin cell for colorectal cancers

A

stem cell or stem-like cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where do the stem cells reside (causing cancer)

A

base of the crypts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How many major precursor lesion pathways

A
  1. traditional adenoma-carcinoma pathway (chromosome instability process) 70-90% of colorectal cancers
  2. serrated neoplasia pathway 10-20%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What happens in the traditional adenoma-carcinoma pathway

A

initiated by APC mutation, followed by RAS activation or function loss of TP53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What happens in the serrated neoplasia pathway

A

RAS and RAF mutations and epigenetic instability characterized by the CpG island methylation phenotype leading to microsatellite stable and instable cancers
also, presence of polymerase-ε or POLE mutations or mismatch repair deficiency [dMMR]) leading to a hypermutated phenotype.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why is right/left sides important

A

metastasis settings and responsiveness to anti-EGFR drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the molecular subtypes of colorectal cancer

A

CMS 1 MSI immune
CMS 2 canonical
CMS 3 metabolic
CMS 4 mesenchymial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which subtypes are mostly common for the right side

A

MSI-immune and metabolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the symptoms

A

occult or overt blood
change in bowel habits
anemia
abdominal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Does bleeding always mean something malignant

A

no, could be benign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How do we diagnose colorectal cancer

A

Colonoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is a complementary method to diagnose

A

CT scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is very important to check in blood test to diagnose

A

CEA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What does a high concentration of CEA pre-operative and post indicate

A

pre: bad prognosis
post: residual disease

34
Q

Why do mismatch repair test

A

Lynch
adjuvant fluoropyrimidine based therapy
and identifying patients who can respond to immunotherapy

35
Q

What are RAF and RAS mutations implicated in

A

proliferation
apoptosis
angiogenesis

36
Q

Treatment for T1 cancers and techniques

A

Depending on its size, the endoscopic techniques are:
en-bloc endoscopic mucosal resection
endoscopic submucosal dissection
endoscopic full-thickness resection.
The last 2 should be considered when there is a high suspicion of superficial submucosal invasion.

37
Q

How has surgery been optimized

A

by the use of sharp dissection along the embryological planes within the mesofascial interface, according to the so-called complete mesocolic excision principle.

38
Q

Excision for rectal cancer surgery

A

Total mesorectal excision is the standard oncological

approach

39
Q

Laparoscopy for surgery ?

A

yes for colon cancer

debated for rectal cancer

40
Q

Can colorectal cancer be an emergency ?

A

yes if obstruction or perforation

41
Q

How can colonic obstruction be relieved

A

by a decompressing colostomy or endoscopic stenting.
Decision for stenting should be multidisciplinary since it can limit the later use of anti-VEGF
drugs due to risk of perforation.

42
Q

Benefit of preoperative radiotherapy

A

reduces risk of recurrence

43
Q

Most used therapy is

A

Chemoradiotherapy with a dose of 45–50 gray in 25–28 fractions, and with a fluoropyrimidine as radiation sensitiser.

44
Q

The preffered local ablative therapy for liver

A

Radiofrequency ablation
For larger lesions and those close to vascular structures, microwave ablation or stereotactic radiotherapy might be good alternatives.

45
Q

Local treatment of lung metastases

A

Resection, stereotactic radiotherapy and radiofrequency ablation

46
Q

Treatment of peritoneal metastases

A

Cytroreductive surgery and hyperthermic intraperitoneal chemotherapy

47
Q

What is the main drawback of oxaliplatin use

A

sensory neuropathy

48
Q

What component indicates a good prognostic when it is present

A

dMMR for stage II

49
Q

What does the systemic therapy for metastatic colorectal cancer include

A

a chemotherapy backbone (Fluoropyrimidines, oxaliplatin, and irinotecan) paired with a
biologic (anti-VEGF or anti-EGFR antibody).

50
Q

What is the anti-VEGF monoclonal antibody called

A

Bevacizumab

51
Q

What does the anti-VEGF antibody target

A

angiogenesis

52
Q

Other anti-VEGF agents are…

A

aflibercept and ramucirumab

53
Q

What therapy do right-sided tumors not benefit from

A

anti-EGFR

54
Q

What should we test before using anti-EGFR therapy

A

RAS and RAF mutations

55
Q

Which first line therapy to use for left-sided RAS and RAF-wild-type metastatic colorectal

A

anti-EGFR agents (cetuximab or panitumumab) or

anti-VEGF agents (bevacizumab) can be used

56
Q

Examples of anti-EGFR agents

A

cetuximab and panitumumab

57
Q

Which tumors do not respond well to systemic treatment

A

BRAF-V600E mutations

58
Q

Treatment for BRAF-V600E mutation tumors

A

Upfront triplet chemotherapy with bevacizumab is recommended. Combinatorial strategies (BRAF-inhibitors and anti-EGFR antibodies paired with
chemotherapy or MEK inhibitors)

59
Q

Treatment for patients with refractory metastatic colorectal cancer who have not responded to systemic therapies

A

Regorafenib (a so-called dirty tyrosine-kinase inhibitor) and TAS-102 (combination of trifluridine and tipiracil, an oral anti-metabolite)

60
Q

Treatment for the 4–5% of tumours with dMMR or high MSI (MSI-H)

A 
PD-1 blockade with immunotherapies such as nivolumab or pembrolizumab is now approved.
Combination immunotherapy (nivolumab and ipilimumab) is also approved.
61
Q

What is bowel dysfunction after restorative rectal cancer resection called

A

low anterior resection syndrome

62
Q

How to manage low anterior syndrome

A

by dietary changes, medication (eg, loperamide) and anal irrigation

63
Q

What can the rectal cancer treatment, particularly combined radiation and surgery, affect

A

bladder and sexual function

64
Q

Chemotherapy side effects

A

cumulative neuropathy (paraesthesia, numbness or tingling affecting activities of daily living from platinum chemotherapy), and liver toxicity

65
Q

What is the guaiac test

A

Screening for microscopic amounts of blood with the guaiac test (or guaiac-based faecal occult blood tests) reduced colorectal cancer mortality by approximately 16% more than a decade ago.

66
Q

Prevention for patients with Lynch Syndrome

A

colonoscopic surveillance should be performed at a 2 yearly interval for all LS patients.

67
Q

At what age should we start colonoscopies for Lynch

A

We recommend colonoscopy from age 25 years for

MLH1 and MSH2 mutation carriers and 35 years for MSH6 and PMS2 mutation carriers.

68
Q

What are tumeurs desmoides

A

tumeurs mésenchymateuses bénignes à agressivité locale sans potentiel métastatique. Les tumeurs desmoïdes proviennent d’une prolifération tumorale au dépend des fibroblastes et myofibroblastes du tissu conjonctif.
appartiennent au groupe des tumeurs conjonctives parmi lesquelles on distingue des tumeurs malignes (cancers type sarcomes ou tumeurs stromales gastro-intestinales. . .) et des tumeurs bénignes (lipomes, fibromes. . .).

69
Q

Physiopathologie d’une mutation APC

A

La mutation germinale du gène APC aboutit à une perte de la fonction de la protéine APC, ce qui conduit à l’instabilité et la dégradation du complexe Wnt/APC/b-caténine conduisant la libération de la b-caténine (facteur de transcription), dont l’accumulation au niveau nucléaire stimule la division cellulaire

70
Q

What is FAP

A

maladie à transmission autosomique dominante liée à une mutation germinale du gène APC

71
Q

What is the syndrome de Gardner

A

L’association d’une polypose colorectale et de tumeurs

desmoïdes

72
Q

La particularité des tumeurs desmoïdes associées à la PAF

A

localisation majoritairement intra-abdominale et risque de complication

73
Q

TD

A

Les tumeurs desmoïdes « TD » ou fibromatose agressive
ne présentent pas de risque de dissémination à distance
mais une agressivité locale qui peut entraîner des complications
graves

74
Q

FR des tumeurs desmoides

A

histoire familiale
chirurgie pendant l’ enfance (colo-protectomie)
mutation
grossesse

75
Q

Mutations associees au syndrome de Lynch

A

anomalie constitutionnelle touchant les gènes de réparation de l’ADN du système MMR à pénétrance incomplète.
soit MLH1, MSH2, MSH6 ou PMS2 ou du
gène EPCAM (situé en amont du promoteur du gène MSH2 et qui conduisant à l’inactivation
épigénétique du gène MSH2). Une inactivation somatique de l’autre copie du gène (par
mutation, perte d’hétérozygotie..) aboutit alors à l’inactivation du gène MMR, et à la perte de
fonction de la proteine.

76
Q

diagnostic syndrome de Lynch

A

-Critères d’Amsterdam II mais manque de sensibilité
-Critères d’Amsterdam élargis et des critères
de Bethesda II. Ils sont plus sensibles mais moins spécifiques
-Il existe 2 techniques pour identifier un phénotype MSI : la biologie moléculaire par PCR pour mise en evidence d’une MSI et l’immunohistochimie (IHC) qui permet de mettre en évidence la perte d’expression de protéines du système MMR (tumeurs MMR déficientes)

77
Q

les 2 formes du syndrome de Lynch

A

Il existe deux formes phénotypiques variantes du syndrome de Lynch :
-le syndrome de Muir Torre, dont le spectre est élargi aux tumeurs cutanées sébacées et aux kérato acanthomes
-le syndrome de Turcot, dont le spectre inclut le cancer du côlon et des tumeurs du système nerveux central
(glioblastome, médulloblastome, épendydome).

78
Q

What is Lynch-like syndrome

A

En cas d’absence d’identification de mutation constitutionnelle d’un gène MMR chez un patient porteur d’une tumeur MSI (en cohérence avec les résultats d’immunohistochimie), et d’absence de méthylation somatique du promoteur du gène MLH1, le syndrome de Lynch ne peut être exclu, portant le diagnostic de syndrome « Lynch Like »

79
Q

Physiopathologie du syndrome de Lynch (3 Hypothesis)

A
  1. l’altération tardive du système MMR au sein du polype colique évolué aboutissant à l’accumulation des mutations nécessaires au cancer
  2. perte bi-allélique précoce.
  3. l’absence de passage par le stade d’adénome colique.
80
Q

When do we use immunotherapy and examples of meds

A

MSI sont de mauvais pronostic
Efficacité de l’immunothérapie chez les patients avec un CCR MSI ayant résisté aux chimiothérapies cytotoxiques classiques.
Anticorps monoclonal anti PD-1, le pembrolizumab, Nivolumab.
Un traitement par nivolumab associé à un Ac anti-CTLA4, l’ipilimumab

81
Q

Effet de l’aspirine sur polypes

A

le taux de développement de polypes n’était pas diminué

UIDC (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions