DIG Exam 3 Sos LI

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100 Terms

1
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Memorize images

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80% goblet cells

20% enterocytes

Crypts of Lieberkühn

Cell replaced every _ days

Large intestine

6

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Longitudinal smooth muscle arranged in three longitudinal bands

Taenia coli

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Large intestine

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Paneth and endocrine cells in crypt of Lieberkühn

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Large intestine

Test tubes in a rack

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Large intestine

Daisy fields

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___% of water and most nutrients have been absorbed by the small intestine

90

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Stores formed feces

Descending colon

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Microbiome fermentation in the colon produces vitamins __ and __ for absorption into the blood

K;B

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Most common site for colorectal cancer

Descending sigmoid colon

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Obstruction of the lumen of the appendix by fecalith or lymphoid hyperplasia (more common in children)

Acute appendicitis

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Fever

Nausea/Vomiting

Rebound tenderness

McBurney point tenderness

Clinical presentation of appendicitis

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Obstruction → trapped secretions → lumen expansion → wall ischemia → necrosis → inflammation → perforation (or fibrosis) → peritonitis

Pathophysiology of acute appendicitis

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Acute appendicitis

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Acute appendicitis

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Diverticulosis comes before

Diverticulitis

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Affects 50% of people over 60 years of age and nearly everyone at 80 years of age

Asymptomatic disease

Diverticulosis

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Pseudodiverticula throughout descending and sigmoid colon

Consist of mucosa and submucosa out patch

Diverticulosis

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Age, obesity, smoking, lack of exercise, and diet high in animal fat and low in fiber

Risk factors for diverticulosis and diverticulitis

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Diverticulosis

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Diverticulosis

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Diverticulosis

(no muscularis unlike with Meckel’s which is a true diverticulum)

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It is believed that diverticulosis track along _________

Blood vessels because of a created weakness in the wall

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When pouche/s become obstructed → edema → necrosis → inflammation → perforation (or fibrosis) → peritonitis

Pathophysiology of Diverticulitis

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Fever

Abdominal pain

Lower left side

Nausea/vomiting

constipation or diarrhea

Clinical presentation of Diverticulitis

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Diverticulitis

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C diff overgrowth within days after antibiotic treatment during hospitalization

Watery diarrhea

Abdominal cramps/pain

fever

nausea

dehydration

Pseudomembranous colitis

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Pseudomembranous colitis

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Pseudomembranous colitis

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Pseudomembranous colitis

(mushroom explosion)

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AAA can cause ____ obstruction or insufficiency

IMA

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Ischemic due to hypoperfusion or obstruction (CAD, HTN, etc) in the splenic flexure and rectosigmoid junction

Watershed ischemic bowel

(Ischemic colitis)

can perforate

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Watershed ischemic bowel

Wall is too thick

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Ischemic colitis

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Ischemic colitis

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Adhesions

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Fibrous bands that form after irritation of the peritoneal serous membrane often occurring after surgery

Adhesions

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Polyp types

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Hyperplastic polyps ______ progress to adenomas

Do not

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20% of colonic polyps

Most often found in rectosigmoid region

Lack of apoptosis of cells at the surface of glands with sawtooth pattern
Broad based polyp

Hyperplastic polyp

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Hyperplastic polyp

(sawtooth pattern)

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Hyperplastic polyp

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2% risk of malignancy

Mucosa adenoma

Forms from a stalk

APC mutation

Tubular adenoma

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APC mutation

Tubular adenoma

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Tubular dysplastic gland histology and low level of dysplasia

Tubular adenoma

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Tubular adenoma

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Tubular adenoma

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25% risk of malignancy

Tubulovillous adenoma

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Tubular and villous dysplastic glands

Tubulovillous adenoma

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Tubulovillous adenoma

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Tubulovillous adenoma

(can look like anything though)

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40% malignant potential

Can be polyps or sessile (85%)

Associated with larger masses

Villous adenoma

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Villous adenoma

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Villous adenoma

(sessile mass)

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3rd most common cancer diagnosed

85% chromosomal instability (adenoma to adenocarcinoma)

15% Microsatellite instability

Colorectal cancer

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APC mutation → KRAS, BRAF → p53

Colon carcinogenesis

small adenoma→ large adenoma → cancer

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Colon cancer progression

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100% risk of colon cancer with mean age of 40.

FAP

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Up to 80% risk of colon cancer with mean age of 40.

Lynch syndrome

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Commonly tested for colorectal cancer recurrence

Carcinoembryonic antigen (CEA)

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Elderly patient with iron deficiency anemia rule out ______

Colorectal carcinoma

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Colorectal cancer

Apple core sign

Napkin ring shape

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Colorectal carcinoma

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Colorectal carcinoma

pencil stool

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Colorectal carcinoma

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Colorectal carcinoma

Adenocarcinoma context will tell you where it is

Hyperchromatic, pleomorphic nuclei and cells

with high N:C ratio, abnormal mitotic figures

and desmoplastic stroma

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Neural invasion

Colorectal carcinoma

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Lymph node metastasis of colorectal carcinoma (adenocarcinoma)

Lymph nodes should not have cytokeratin

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No polyps present or polyps at early age before cancer

Hereditary nonpolyposis colorectal carcinoma (HNPCC)

AKA Lynch syndrome

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Autosomal dominant, family member with colon cancer before age 50

Mutations in DNA repair genes (microsatellite instability repeated sequences of noncoding DNA)

Increased risk of cancer of uterus and ovaries, GI tract, urinary tract, and kidneys

Hereditary nonpolyposis colorectal carcinoma (HNPCC)

AKA Lynch syndrome

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Uterine cancer 60% by age 70

Colorectal cancer 80%

Colonoscopy at 21

Hereditary nonpolyposis colorectal carcinoma (HNPCC)

AKA Lynch syndrome

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Autosomal dominant disorder

Colorectal cancer

APC mutation

1000s of polyps usually start to develop in teens
Whole colon is removed prophylactically or carcinoma will develop in 40s

Familial adenomatous polyposis (FAP)

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APC mutation

Familial adenomatous polyposis (FAP)

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Familial adenomatous polyposis (FAP)

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FAP + fibromatosis and osteomas, soft tissue tumors, supernumerary teeth and cysts

Gardner Syndrome

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Gardner syndrome

(has FAP + these type issues)

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APC, MLK1, PMS2 mutations

FAP + CNS tumors

Turcot Syndrome

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Turcot syndrome

(has FAP + CNS tumors)

Top medulloblastoma and bottom glioblastoma

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Autosomal dominant

Mutiple hamartomatous polyps in GI tract, hyperpigmented macules on the lips and oral mucosa (melanosis)

Increased risk of adenomas and carcinoma

Peutz-Jeghers syndrome

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Normal tissue in abnormal patterns

hamartomatous

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benign looks like a tree

Peutz-Jeghers syndrome

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Peutz-Jeghers syndrome

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Most common vascular malformation of the intestines

Often found in elderly

May lead to GI bleeding and most commonly found in the cecum, terminal ileum, and ascending colon

Fatigue, anemia

Angiodysplasia (not dysplasia)

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Angiodysplasia

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Angiodysplasia

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consists of smooth muscle from the circular layer of muscularis propria controlled by parasympathetic nerve which relaxes involuntarily

Internal anal sphincter

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consisting of skeletal muscle controlled by somatic nerve that relaxes with conscious control

External anal sphincter

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Inability to correctly tighten and relax _____ ____ muscles to have a bowel movement

Constipation, urine or stool leakage, frequent need to urinate

Age, enlarged prostate, uterine prolapse, multiple pregnancies, medications and trauma

Pelvic floor dysfunction

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Forms sling around the rectum

relaxes to allow fecal mass to pass

Contraction maintains fecal continence by creating anorectal angle 80 degree

Puborectalis (keep in mind with pelvic floor dysfunction)

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Swollen veins in anus often from increased venous pressure

Hemorrhoids

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Pain, itching, irritation, swelling around the anus and bleeding

External hemorrhoids

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Below pectinate line

External hemorrhoids

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Painless bleeding during bowel movements may prolapse through anus causing pain

Internal hemorrhoids

95
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Above pectinate line

Internal hemorrhoids

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Tear in mucosa of anus often caused by hard dry bowel movement

Anal fissures

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Common causes of blood in the stool and may be due to low fiber in diet

Internal hemorrhoids

External hemorrhoids

Anal fissures

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First Aid pectinate line

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Condyloma

HPV related

Anus SCC

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SCC anus