intestine disease Flashcards by jouna alsaif

what is progressive small intestinal disorder that damages jejunum and illeum more

tropical sprue

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a patient came from puerto rico presenting with diharrea, steatohrea, and megaloblastic anemia

tropical sprue

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what is the tx of tropical sprue

folic acid and tetracycline for 3-6 months

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what is PAS +ve macrophages

whipples disease

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what is whipples disease

caused by bacteria tropheryma whipplei

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what is tx of whipple disease

cotrimoxazole for 1 yr

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how can u diagnose for bacterial overgrowth

-hydrogen breath test : abnormal early peak of hydrogen (early peak from small intestine bacterial overhrowth, normal late peak from colonic flora )

-small intestine aspirate and fluid culture: gold standard

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tx of bacterial overgrowth

antibiotics (tetracycline and metronidazole)

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adenocarcinoma is most common where?

duodenum -50% of small bowel malignancies

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what type of cancer increases incidence in crohns and celiac

adenocarcinoma

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most common location of lymphomas

ileum (lymphoid tissue in peyers patch )

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what is zollinger ellison syndrome

a rare condition caused by a gastrin-secreting tumor (gastrinoma), leading to excessive gastric acid production, severe peptic ulcers, and chronic diarrhea.

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how does ZES happen and causes

• Gastrinomas → Tumors that produce excess gastrin, stimulating parietal cells in the stomach to hypersecrete acid.
• Leads to multiple, refractory peptic ulcers in the stomach and duodenum.
• 20–30% of cases are associated with Multiple Endocrine Neoplasia type 1 (MEN-1).

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diagnosis of ZES

✅ Fasting Serum Gastrin (>1000 pg/mL is diagnostic)
• Must be measured after stopping PPIs for at least 1 week.
• If gastrin is high but <1000 pg/mL, confirm with a secretin stimulation test (ZES tumors paradoxically increase gastrin with secretin).

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tx of ZES medically

✅ High-dose Proton Pump Inhibitors (PPIs) (e.g., omeprazole, pantoprazole) and H2 blockers to control acid secretion.
✅ Octreotide (somatostatin analog) for patients with metastases. slow tumor growth

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where are tumors in ZES located mostly

in gastrinoma triangle

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Carcinoid tumors most commonly found where

illeum

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where do carcinoid tumors arise from

intestinal entero chromaffin cells (serotonin producing kulchitsky cells)

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carcinoid tumors features and symotoms pneumonic

Mnemonic: “CARC-I-NOID”

C – Chromogranin A & 5-HIAA (tumor markers)
A – Appendix is most common site (GI tract: appendix, ileum, rectum)
R – Right-sided heart disease (fibrosis due to serotonin) left side not affected has MOA breaks serotonin down
C – Cutaneous flushing (episodic flushing, triggered by stress, alcohol, food)
I – Intestinal (GI symptoms) (diarrhea, cramping, obstruction)
N – Niacin deficiency (pellagra) (tryptophan is used to make serotonin, reducing niacin)
O – obstruction most common presentation and Octreotide treatment (somatostatin analog to control symptoms)
I – Increased serotonin (5-HT) & 5-HIAA (urine test)
D – Diarrhea & wheezing (bronchospasm)

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IBS

IBS is not srs usually due to functional reasons like stress, diet, hormones
it is a syndrome that focuses on symptomatic releif
no inflam or tissue damage
involve bnormal gut brain interactions

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what symptoms are never part of IBS

blood in stool and wt loss

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IBD

D for danger
chronic inflam w damage to intestine wall
serious includes UC + CD
bowel perforation cancer
focus on reduce inflam

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what is the commonest region involved in crohns disease

ileocecal but can affect the whole gi tract (mouth to anus)
rectal sparing is typical

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what shows discontinuous involvement skip leasion and cobble stone appearance

crohns disease

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what does crohns disease show in microscopic pathology

transmural patchy inflam affecting all 3 layers non- caesating granulomas 50%

what type of disease mimcs the pain of appendicitis presenting with right illiac fossa pain

crohns

symotoms of crohns

diarrhea, abdo pain, wt loss, constitutional symptoms

what type of disease is manifested as FISTULA, abscesses, tags, fissures

crohns

what would pts with crohns present with in physical exam

aphthous ulcers in the mouth abdo tender anal tags

what disease affects the colon only starts from rectum and extend proximally in varying degrees

ulcerative colitis

ulcerative colitis differs from crohns in the case of macroscopic pathology how

continuous involvement red mucosa bleeds easily ulcers and pseudopolyps

ulcerative colitis in microscopy

no granulomota superficial limited to mucosa crypt abscesses

major symptom of ulcerative colitis

diharrea with blood and mucus +/- lower abdo pain

proctitis (rectum inflamed ) may manifest as what

tenesmus - feeling of wanting to use the bathroom but nothing in rectum with mucoid diharrea

what is a complication of ulcerative colitis

toxic megacolon ( risk of perforation)

management of crohns disease

immunosuppressants- azathioprine (AZA) mercaptopurine (6-MP) antibiotics budenoside (corticosteroids)

what do u give tx if immunosuppresants fail in crohns

biologic therapy - Anti- TNF agents (infliximab)

what tx is of benefit in illeocecal CD

budenoside

what is tx of UC

first line tx : 5-ASA (aminosalicylate) corticosteroids

if first line didnt work in UC

immunosuppressants and biologic therapy

extensive colitis in CD/UC more than 10yrs leads to what

colorectal cancer

what is colonoscopy indications in high and low risk individuals

high risk : further colonoscopy and another biopsy 1 yr later low risk: undergo colonoscopy 3-5yrs later

what is ischemic colitis

when blood flow to the colon is reduced secondary to low intestinal perfusiom or thromboembolism

what areas are more common for ischemic colitis

watershed areas which have dual blood supply the farthest away from arterial circulation so more likely to have hypoperfusion (splenic flexure or cecum)

what defines constipation time period

less than 3 passages per week , straining, hard stool, incomplete evacuation

what does xray in ischemic colitis show

thumb printing (submucosal edema)

what are alarm symptoms of constipation

rectal bleeding or anemia recent onset in middle age or elderly w sense of incomplete evacuation

what are tx of constipation

high fiber diet lots of liquid long term laxatives treat the cause

what defines chronic diharrea

> 4 weeks duration of loose stool

what are most common causes of chronic diharrea

IBS, IBD, malabsorption syndromes( lactose /celiac)

acute diharrea

less than 2 wks from infection or drug induced

what is fatty diharrea caused from

fat malabsorption

wattery diharrea is of two types

osmotic secretory

osmotic diharea

osmotic diharrea caused by large quantitis of non absorbable substances in the lumen draw water in and inc stool water content stool osmotic gap >150

secretory diharrea

active secretion of fluid and electrolytes as well as decreased absorption stool osmotic gap<50

risk of cancer is high in colorectal polyp if what

if polyp > 2cm , villous, severe atypia

what is follow up surveillance colonoscopy for adenomatous polyp

>2cm, >2polyps, villous component on histo--> 3yrs <2cm, 1 or 2 polyps, tubular histo--> 5yrs

what is features of hyperplastic polyp

overgrowth of normal tissue, benign epithelial dysplasia, no malignant potential, common in elderly

adenomatous polyp

pre- malignant villous 40% risk of cancer

what is the sequence of growth regulating genes that lead to colorectal cancer

normal ----> small adenoma (APC) small adenoma---> Large adenoma (K-RAS) large adenoma ---> adenocarcinoma (P53)

microsatellite instability from faulty DNA mismatch repair function example in what

lynch

symptoms and signs of CRC depend on tumor location

right masses: occult blood loss, IDA, advanced cases palpable mass left masses: obstruction and macroscopic bleeding rectal masses: rectal bleeding, obstruction, diharrea, constipation tenesmus

unusual presentations of CRC include

malignant fistula formstion fever of unknown origin sepsis from strep bovis amd clostridum

what is gold standard for CRC

colonoscopy

colonoscopy screening for adenomatous polyp and personal history of colon cancer

adenomatous polyp: colonoscopy every 3-5 yrs personal: 1 yr after removal, then 3 then 5

colonoscopy screening for lynch, fap, peutz jegher, IBD

lynch: at age 25, repeat every 1-2 yrs FAP: colonoscopy at age 12, repeat every yr peutz- jegher: every 3 yrs start age 8 IBD: 8-10 hrs after diagnosis

what is the recommende screening for colon cancwe

every 10 yrs from age 45

what is FAP

autosomal dominant mutation in APC gene chrom 5 by age 20 hundred to thousand polyps 100% life time risk of CRC inc risk of extra colonic malignancies

what are FAP variants

turcots syndrome: polyps involve CNS tumors (gliomas) gardner syndrome: polyps associated with epidermal cysts, osteomas, bromatosis attenuated polyp: fewer polyp at a later age z

HNPCC- lynch

mutation in DNA repair gene (MSH2, MSH6, MLH1) resilt in microsatellite genomic instabillity

what are diff btwn the two types of lynch syndrome

lynch syndrome 1: pts with multiple polyps who develop right sided colon cancer young age lynch 2: same as lynch 1 but additional extracolonic adenocarcinomas of uterus, cervix, ovary, breasst

peutz jeghers syndrome

-mutation in STK11 (LKB1) gene -multiple hamartomatous polyp anywhere in gi tract -fisrt decade of life can be symotomatic -mucocutaneous pigementatioj ppn on lips, perioral region , palms of hand -common site of gi malignancy: colon and pancreas