Dr.Merter Gulen Flashcards

1
Q

Right colon tumors:

A

-its contents are liquid
-More ulcerated type on the right
-The most common symptoms are blunt, persistent
-lower quadrant pain and anemia
(Iron deficiency anemia due to occult bleeding, weakness, weight loss Mass in the right lower quadrant)

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2
Q

Left colon tumors:

A

-the content is solid
-Left colon cancers are of the scirous and annular type.
-obstructive symptoms **
-change in bowel habits,progressive decrease in stool diameter

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3
Q

Rectal tumors:

A

Bloody – mucous stool, tenesmus, feeling of tightness Obstruction may be late

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4
Q

What is hartmann procedure?

A

A type of colectomy that removes part of the colon and sometimes rectum.

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5
Q

What are the differences between colostomy and colectomy ?

A

A colectomy can also be called a large bowel resection. A colostomy may be needed after colectomy.A colostomy is an opening to the outside of your body that lets stool exit into a bag.

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6
Q

Where are the high risk of colon tumors risk?

A

Rectum>sigmoid >cecum> ascending colon

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7
Q

What are the inflammatory bowel disease

A

ulcerative colitis, Crohn’s disease

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8
Q

The development of CRC relatively increased 3.5-6.5 in which patients?

A

Adenomatous polyp larger than 1 cm
Villous or tubulovillose polyp
high-grade dysplasia

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9
Q

What can increase the risk of CRC?

A

-Consumption of red and processed meat; long-term consumption
-Smoking-Cigaret
-Alcohol
-Androgen therapy;
-who have undergone a GnRH agonist or orchiectomy for prostate cancer (SEER database).
-BRCA gene mutations

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10
Q

Types of COLUMN POLYPS

A

a-Inflammatory, b- Hamartomatosis, c- Neoplastic (Adenamatous polyp): ,d- Hyperplastic polyps

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11
Q

HYPERPLASTIC POLYPS

A

*They are usually less than 5 mm in diameter
* Can be found in 50% of adults The most common are colonic polyps
* Dysplasia is not seen
* has no symptoms
* It is only removed for histological diagnosis.

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12
Q

JUVENILE POLYPS

A

*It is most common in children.
*It peaks at 5 years old
*70% solitary
*Most commonly found in the rectum
*The most common symptom is bloody stool and rarely rectal bleeding. Invagination, colic pains

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13
Q

Familial juvenile polyposis:

A

*Autosomal dominant. T
*here are hundreds of polyps in the colon.
* They can transform into adenoma and carcinoma. *Prophylactic colectomy is recommended
(Solitary juvenile polyps have no malignant potential)

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14
Q

Peutz-Jegher Syndrome

A

*Autosomal dominant (Serine-threonine kinase 11 gene defect)
*Hyperpigmentation and hamartomatous polyps in the mucocutaneous regions
* Polyps are mostly in the small intestine but can be found in the colon and rectum.

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15
Q

Cronkheit-Canada Syndrome

A

*Generalized hamartomatous polyposis *hyperpigmentation,
*alopecia
*onychodystrophy
*It does not show inheritance.
*There is no risk of malignancy.
*Diarrhea, enteropathy, and malabsorption may develop.

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16
Q

Is every polyp cancer?

A

Degree of dysplasia type of polyp
, Tubular Adenoma: 5% cancer risk Tubulovillous adenoma: 22% cancer risk
Villous adenoma: has a 40% cancer risk
Polyp size:
<1 cm = <1% cancer risk
1 cm = 10% risk of cancer
2 cm = 15% cancer risk
If the normal adenomatous polyp is larger than 0.5 cm, it should be treated.

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17
Q

What are Hereditary CRC syndromes?

A

 FAP (Familial Adenomatous Polyposis)
 Atenue FAP
 HNPCC/Lynch syndrome
 familial colorectal cancer
 MUTYH-associated polyposis (MAP)

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18
Q

FAP (Familial Adenomatous Polyposis)

A

-Gardner syndrome, Turcot syndrome, and attenuated variants of FAP
-From childhood, there are a large number of adenomatous polyps.
- It becomes symptomatic at about 16 years of age and if left untreated, 90% develops CRC by the age of 45, the lifetime risk is 100%. Thousands of polyps.
-Chromosome 5q, (75%)APC germline mutation (+)
-Colonoscopic screening is performed at the age of 10-15 for first-degree family members of an individual with FAP.
-If the APC gene is negative, it is taken into general screening after the age of 50.

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19
Q

FAP extra GIS involvement;

A

-retinal pigment epithelial hypertrophy
-Desmoid tumor Osteomas of the mandible (gardner)
-CNS tumors (turcot)

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20
Q

Atenue FAP

A

-There are mutations at the 3rd and 5th ends of the APC gene
-10-100 polyps present
-APC 60%
-Screening colonoscopy at age 15 if APC positive
-Surgical treatment is like FAP.

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21
Q

MUTYH-associated polyposis (MAP

A

-autosomal recessive
-It occurs as a result of biallelic mutation in the mutY homolog (MUTYH) gene.
-There are less than 500 polyps.

22
Q

Lynch syndrome (HNPCC)

A

*Autosomal dominant syndrome. RER pathway, DNA mismatch repair gene defect (hMLH1, hMSH2)
*It constitutes 3% of CRCs.
* It is frequently seen in extra colonic cancers such as endometrial, ovarian, hepatobiliary, gastric cancer. *Younger age 40-45 years,
* the prognosis is better 40% risk of synchronous-metachronous cancer *Colonoscopic screening 20-25 years or 10 years before first diagnosis

23
Q

Amsterdam criteria for HNPCC diagnosis

A

*3 relatives with colorectal cancer , where one is 1st degree relative of other two
*2 generations of colorectal cancer
*1 colorectal cancer before age 50
* FAP is excluded

24
Q

Bethesda Criteria

A

Amsterdam criteria or one of the following;
*Two cases of HNPCC-related cancer in one patient,
* including synchronous and metachronous cancers
*First-degree relative with HNPCC-associated cancer and/or colon adenoma (up to 45 percent of cancer cases) age,
*adenoma diagnosed before age 40) and colon cancer
* Colon or endometrial cancer diagnosed before age 45
*Signet ring cell or undifferentiated right colon cancer before age 45 *Diagnosed with adenoma before age 40

25
Q

familial colorectal cancer

A

*15% of CRCs
* If a family member younger than 50 has CRC, the risk increases.
*The risk is 6% if there is no family history of CRC
* CRC risk is 12% if a first-degree relative has 35% if near 2 relatives have Screening should begin at age 40

26
Q

colorectal cancer staging

A

*I/A confined to MUCOSA (T1) or muscular propria (T2)
no nodal involvement
no distant metastases
*II/B tumor penetrates muscularis (T3) or invades adjacent organs or structure (T4)
no nodal involvement
no distant metastases
*III/D any tumor stage
any nodal status
distant metastases

27
Q

TNM (tumor, lymph node , metastases) staging

A

Tis: carcinoma in situ
T1: Tumor has invaded the submucosa
T2:the tumor has invaded the muscularis proprietary
T3:tumor has spread to the serosa
T4:tumor has spread beyond the visceral peritoneum and has spread to adjacent organs
N1: 1-3 pericolic or perirectal lymph node involvement
N2:4 pericolic or ……
N3:vascular pedicle lymph node involvement
M0:no metastases
M1:there is metastases

28
Q

rectal cancer

A

*TEM (transanal endoscopic excision) in T1N0 patient.
*1 cm surgical margin should be (-). *Low-anterior resection APR(miles) *TME (total mesorectal excision)

29
Q

Poor prognostic factors in colorectal cancers

A

Young age (< 40)
Colon obstruction, tumor perforation Vascular, nerve and lymphatic invasion
High preoperative CEA level Aneuploidy, poor differentiation of tumor, mucinous and signet ring cell tumors, infiltrative (linitis plastica) and ulcerative cancers The most important prognostic factor in colorectal cancer is lymph node involvement.

30
Q

Adjuan – neoadjuan therapy

A

Radiotherapy can be used preoperatively or postoperatively in rectal tumors. Resectability can be achieved after radiation in unresectable rectal tumors.

31
Q
A
32
Q

what is indeterminated colitis

A

in 10-15% of patients with IBD confined to the colon, a clear distinction can not be made and it is called as Indeterminated Colitis.

33
Q

Ulcerative colitis

A

UC is confined to the colon mucosa and submucosa. Rectum is always involved with the inflammatory process and extends in a continuous fashion proximally.
can be seen at any age
males and females are effected equally
etiology:
*Environmental factors
*Genetic predisposition (family history of IBD)
*Altered immunologic response to antigens
*High fat diet

_most common and sever in rectum(start from rectum and spread)
_left colon involvement is more than right
_pancolitis is present in 30-50 % of patients
_terminal ileum involvement 10%
_continuous
_no solid areas are specific in the diagnose
_**cryptic abscesses are specific in the diagnosis
_column and meso shorten , haustra disappear

34
Q

what are the type of inflammatory polyps

A

Mucosa granular, edematous, fragile, ulcerated Pseudopolyps

35
Q

types of ulcerative colitis

A

proctitis , proctosigmoiditis , distal colitis , extensive colitis , pan colitis

36
Q
A
37
Q

what is the clinic features of ulcerative colitis

A

abdominal discomfort
pain
chronic bloody diarrhea
mucus discharge

38
Q

Extraintestinal manifestations of ulcerative colitis

A

Arthritis
Ankylosing spondylitis
Isolated sacroileitis
Erythema nodosum
Pyoderma gangrenosum
Primary sclerosing cholangitis
Uveitis

39
Q

what is the diagnosis of ulcerative colitis?

A

*Routine lab tests (leucocytosis, CRP ↑, sedim↑)
*Colonoscopy with multiple mucosal bx
*Stool samples (for infectious colitis) *Perinuclear antineutrophil cytoplasmic antibody (p-ANCA); ASCA (anti-S cerevisae antibody) USG

40
Q

what’s endoscopy of ulcerative colitis ?

A

Fragile mucosa Bleeding No vascularisation

41
Q

what are the complications of ulcerative colitis ?

A

*Fissure, fistula, abscess, incontinence
*Colon perforation due to fulminant colitis
*Massive bleeding
*Development of stenosis
*Dysplasia and Colon Ca: It can also develop in asymptomatic patients. Increases by 3% for the first 10 years, 2-3% for each year after 10 years It is more common in those who start UC at a young age.

42
Q

when does toxic megacolon occur

A

occur when swelling and inf spread into the deep layers of ur colon

43
Q

toxic megacolon :

A

*It is seen in 4-11% of fulminant colitis, mortality is up to 40%
*Fever, peritonitis, distension and toxemia develop.
*Transverse colon diameter increased in direct abdominal X- ray *In acute attack in patients with active colitis, toxic megacolon should be considered if diarrhea suddenly ceases without signs of improvement.
*Treatment: IV fluid management, antibiotics, steroids, surgery if perforation develops

44
Q

what is the medical therapy of ulcerative colitis ?

A

Induce remission
Maintain remission
Prevent and treat complications
Aminosalicylates Corticosteroids Immunomodulatory drugs Antibiotics (metronidazole, ciprofloxacin) Antidiarrheal agents (loperamide, diphenoxylate)

45
Q

what is the surgical therapy of ulcerative colitis

A

Fulminant colitis (toxic megacolon) Massive bleeding
Intractable disease
Colonic strictures (5-12%)
Dysplasia or carcinoma
1.Total proctocolectomy with end ileostomy 2.Total proctocolectomy with continent ileostomy 3.Total proctocolectomy with ileal pouch anal anastomosis (IPAA)

46
Q

crowns disease

A

*Transmural inflammation of the bowel characterized by a thickened wall.
*CD may affect any part of the gastrointestinal tract from mouth to anus. Most located at the terminal ileum.

47
Q

WHAT is the etiology of crohns disease ?

A

*Smoking
*Living in urban areas
*Genetic predisposition (family history of IBD)
*Altered immunologic response to antigens

48
Q

what is the epidemiology of crohns disease ?

A

*More common in urban areas *Relatively unusual in Asia, Africa, and S. America
*Incidence 4-5 cases per 100.000 *Common between 15-35 and 60-70 yrs (Bimodal)
*Frequency similar between males and females

49
Q

what is the clinic of crohns disease ?

A

Abdominal pain
Diarrhea (sometimes bleeding) Anemia
Malnutrition, vitamin deficiencies Weight loss
Growth failure
Perianal abscess/fistula

50
Q

what is the diagnosis of crohns disease?

A

*Clinic findings
* Routine lab and serologic tests, stool studies
*Imaging studies : Plain X-ray Barium contrast studies (colon, enteroclysis) CT, MRI, USG *Endoscopic Gastroscopy, colonoscopy with bx

51
Q
A