Colorectal Disorders Flashcards

1
Q

Colon CA is the ____ most common cause of CA death in the US. what is the 5 yr survival rate. MC site of metastasis?

A

3rd; 64%

metastasis: LIVER (usually goes to regional lymph nodes prior to liver)

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2
Q

what’s the biggest risk factor for colon cancer? other risk factors?

A

AGE: risk doubles each decade after 50 yr old
**other risk factors: family history, genetics (FAP, Lynch syndrome), hx of IBD, Hx of prior polyps, behavioral things (obesity/DM, ETOH, smoking, high fat diet)

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3
Q

what % of colon rectal cancer occurs after age 50?

A

90%

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4
Q

having a first degree relative with colon CA _________ the risk of you having it

A

doubles

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5
Q

what are two genetic conditions that put people at risk for colon CA?

A

1) . familial adenomatous polyposis (FAP) = adenomas begin in childhood, almost all will get CA, tx by proph colectomy
2) . hereditary non polyposis coli (HNPCC)- LYNCH SYNDROME = AD inheritance

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6
Q

what does most CRC come from?

A

adenomatous polyps that progress into adenocarcinoma (larger polyps more likely to contain neoplastic cells)

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7
Q

what type of polyps have a higher risk for invasive carcinoma?

A

villous polyps

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8
Q

what are screening recommendations for CRC for average risk patients? what tool and how often?

A

1) . Colonoscopy every 10 years starting at age 50 through 75 yo (individualized after age 75) BEST
2) . Flex sig every 5 years with fecal occult blood testing every 3 years
3) . high sensitivity fecal occult testing annually: if results are positive, NEED to do colonoscopy

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9
Q

for people with a prior adenoma or a previous resection of cancer, what screening test should be done?

A

colonoscopy

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10
Q

what are the screening guidelines for a person with a 1st degree relative with colon CA?

A

start screening that person at 40 years old OR 10 yrs before their family member was diagnosed with CA
*usually colonoscopy every 5 years, or annual FOBT if pt declines colonoscopy

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11
Q

how do you dx CRC? common lab finding?

A

TEST OF CHOICE: colonoscopy w biopsy
*see “apple core lesion” on barium enema = needs colonoscopy after
Labs: usually iron deficiency anemia

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12
Q

what is carcinoembryonic antigen monitoring (CEA)? what two things can it be used for? is increased or decreased levels better?

A

its a marker for CRC (not only specific for this type of CA) that can be used to monitor success of tx or recurrence; don’t want an inc in this

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13
Q

what is usual tx for CRC?

A

surgical based on staging and metastasis (radiation maybe for rectal CA)

  • localized = surgical resection followed by postop chemo
  • metastatic = palliative chemotherapy
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14
Q

what is the recurrence rate at 5 yrs for people with localized colon CA?

A

1.5% (considered “curative”)

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15
Q

what is a potential problem with using only a flex sig for CRC screening?

A

unable to assess for proximal lesions for which women are more susceptible to

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16
Q

what are five risk factors for rectal cancer? what is the best way to prevent this cancer?

A

HPV infection, MSM, Age > 50 yo, anal fistula hx, smoking

**prevention is best with HPV vaccine

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17
Q

CP, Dx, and Tx for rectal cancer

A

CP: rectal bleeding, change in bowel habits, abdominal pain, maybe urinary or low back sxs (rectal - tenesmus, keep pooping) and small caliber stool)
Dx: DRE/protoscopy, biopsy used for staging
Labs = CBC, CEA/19-9 for monitoring
Tx: surgical resection +/- chemo/radiation

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18
Q

what are the four types of colon polyps?

A

1) . pseudopolyps “inflammatory”: due to inflammatory bowel disease NON-CANCEROUS
2) . Hyperplastic: low risk of malignancy
3) . Hamartomatous “hereditary”: Juvenile (AD inheritance, inc risk of malignancy), FAP, Peutz-Jegher’s (can turn malignant so usually resected, starts with freckles and turns into numerous polyps)
4) . Adenomatous polyps: MC NEOPLASTIC polyp

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19
Q

3 types of adenomatous polyps

A

1) . Tubular: MC type, non-pedunculated, least risk of malignancy
2) . Tubulovillous: mixture of types, intermediate risk
3) . Villous: HIGHEST risk of becoming cancer, tends to be immobile

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20
Q

what are anal fissures and what are the most commonly caused by?

A

painful linear cracks in the distal anal canal

etiologies: constipation, hard stools, low fiber diets

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21
Q

CP, PE finding, and tx for anal fissures

A

CP: SEVERE rectal pain and painful BMs causing the patient to refrain from defecating
PE: longitudinal tear in anoderm that usually doesn’t cross dentate line
Tx: supportive measures bc most heal spontaneously (warm water sitz baths, analegics, high fiber diet), 2nd line is topical vasodilators, surgery if refractory

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22
Q

how does an anal abscess form? most common bug and site?

A

often results from bacterial infection of anal ducts or glands (anal ducts at dentate line)
S. Aureus MC, E. coli, proteus
posterior rectal wall MC site

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23
Q

how does an anal fistula form? common CP and Tx for it

A

its an open tract between two epithelium lined areas, usually seen with deeper abscesses
CP: may cause discharge and pain
Tx: colorectal specialist

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24
Q

common CP and Tx for anal abscess?

A

CP: deep dull pain worse with sitting, coughing and defecation, anorectal swelling, febrile, edema, induration, fluctuance just like typical abscess (think pain out of proportion to exam)
*may not be able to palpate if deeper abscess
Tx: I&D first and then WASH (warm water, analgesia, sitz bath, high fiber diet)
*ABX (vanc or bactrim) only needed for sepsis, extensive cellulitis, immunocompromised- DM!

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25
Q

definition of constipation. definition of chronic constipation

A
infrequent BM (<2/wk), straining, hard stool, incomplete evacuation
chronic: > 12 weeks (more likely to have complications)
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26
Q

management of constipation

A

Fiber: retains water and improves GI transit
bulk forming laxative (Metamucil): absorbs water and increases fecal mass
osmotic laxatives (miralax): causes water retention in stool (pulls water into the gut)
Stimulant laxative (colace): increases ACh regulated GI motility and alters electrolyte transport
If severe or chronic constipation: manual disimpaction followed by transrectal enemas

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27
Q

what is fecal impaction? what is it usually due to?

A

copious amount of immovable solid bulk of stool in the rectum due to decreased motility and inability to sense/respond to stool in the rectum

28
Q

dx and management of fecal impaction

A

Dx: DRE shows a lot of stool, do KUB if DRE is not diagnostic
Tx: digital disimpaction followed by warm water enema with mineral oil, can use miralax after disimpaction, patient education on reducing future constipation

29
Q

what are hemorrhoids and what are common risk factors?

A

engorgement of venous plexus originating from either the superior hemorrhoid vein (internal) prox to dentate line OR inferior hemorrhoid vein (external) distal to dentate line
RF: increased venous pressure (straining), pregnancy, obesity, prolonged sitting, cirrhosis

30
Q

CP of hemorrhoids

A

internal: painless intermittent rectal bleeding (bright red) when defecating
* uncomplicated internal are nontender and nonpalpable
external: perianal PAIN worsened by defecation, tender skin around area, palpable mass, usually DO NOT bleed

31
Q

Dx and Tx of hemorrhoids

A

Dx: visual inspection, DRE, or FOBT, Anoscopy helps with visualization of internal
Tx: overall high fiber diet, increased fluids, warm sitz bath
external = preparation H (vasoconstrict), sitz bath, mild corticosteroids
internal = hydrocortisone or suppositories
Procedures if = failed medical therapy, debilitating pain, or strangulation (rubber band ligation MC)
Hemorrhoidectomy for stage 4 internal or severe external

32
Q

what is the difference between diverticulosis and diverticulitis?

A

diverticulosis: outpouchings of colon due to herniation of the wall mucosa along natural openings of the vasa recta
Diverticulitis: perforation of diverticulum leads to inflammation and focal necrosis (fecaliths get trapped)

33
Q

diverticulosis: MC location, 3 RFs, CP, Dx, and Tx

A

MC location: right colon
RFs: low fiber diet, constipation, obesity
CP: usually AS (incidental finding), BUT MC cause of acute lower GI bleed
Dx: colonoscopy is test of choice
Tx: most cases the bleeding stops on own and management is based on preventing diverticulitis
*if active bleed, resuscitation of patient and endoscopic therapy to stop bleed

34
Q

diverticulitis: 4 complications, MC location, CP, Dx, and Tx

A

complications: fistula, bowel perforation, abscess, or bowl obstruction
MC location: sigmoid colon
CP: LLQ pain (MC) which transitions to diffuse pain with time (peritonitis), N/V, gas, bloating, maybe fever
Dx: CT scan is initial test of choice (“focal thickening of colonic wall and pericolonic fat stranding”, diverticula not always seen), NO barium enema or colonoscopy during acute attack
Tx: uncomplicated is tx output with clear liquid diet and ABX (cipro or bactrim + flaygl) 7-10 d
Pts with complicated diverticulitis are admitted
*pts refractory to med therapy, reoccurances, perforation or strictures = surgery

35
Q

which patients are considered “complicated diverticulitis” and what is the tx?

A

ANY pt with one of the 4 complications

*hospital admission with IV ABX, abcesses > 3cm may need percutaneous drainage

36
Q

toxic megacolon: what is it? 5 common causes

A

NONOBSTRUCTIVE extreme colon dilation (>6cm) with signs of systemic toxicity
causes: complications of IBD (UC), infectious colitis (c. Diff), ischemic colitis, recent travel or ABX use

37
Q

CP for toxic megacolon

A

CP: PROFOUND, BLOODY diarrhea, abd pain, NV distension + signs of toxicity (AMS, fever, tachy, hypotensive, dehydrated, peritonitis)

38
Q

Dx and Tx for toxic megacolon

A

Dx: Imaging + 3 (fever > 100.4, pulse > 120, WBC >10.5, or anemia) + 1 (hypotensive, dehydrated, electrolyte prob, AMS)
**KUB/abd XR usually first imaging (“dilated colon >6cm), CT can be used to assess for complications
Tx: SUPPORTIVE (bowel rest, NG tube bowel decompression, broad spectrum ABX- Ceft + Flaygl, IV fluids) + manage underlying cause

39
Q

what is Hirschsprung disease? MC location? MC gender? PP?

A

congenital megacolon due to absence of ganglion cells leading to FUNCTIONAL obstruction
MC in distal colon and rectum
MC males
PP: failure of complete neural crest migration leads to absence on enteric ganglion cells

40
Q

CP of Hirschsprung dz

A

1) . neonatal intestinal obstruction: meconium ileus (failure of meconium to pass for more than 48 hrs), bilious vomiting, abd distension, NO STOOL IN VAULT
2) . older children have more chronic constipation picture

41
Q

how to dx and tx hirshsprung disease

A
dx: anorectal manometry for screening (shows increased pressure and failure of sphincter relaxation), 
contrast enema (see transition zone between normal and affected bowel), rectal biopsy is definitive, abd xr shows dilated bowel loops but decreased air in rectum
tx: resection of affected bowel
42
Q

two types of inflammatory bowel disease and the difference between the two

A

UC: limited to colon, begins in rectum and ascends; involves only mucosa and submucosa
Crohn’s: can involve ANY segment of the GI system (MC starts at distal ileum); it is transmural which means it penetrates all mucosal layers

43
Q

CP of UC (hallmark clinical finding), mild-severe classifications

A

bloody diarrhea, crampy abdominal pain (LLQ) and tenesmus
can have mild fever, malaise, weight loss and extraintestinal manifestations (joints, liver, eyes, urinary, skin)
mild: <4 loose stools/day
moderate: >4/day
severe: 6/day

44
Q

how to dx UC? imaging and labs

A

labs: positive P-ANCA, increased ESR/CRP, anemia of chronic disease
Flexible sigmoidoscopy is imaging of choice in acute dz (pseudopolyps, uniform erythema and ulceration)
Barium enema: stovepipe or lead pipe sign (loss of haustral markings)
colonoscopy: NOT DONE IN ACUTE DISEASE

45
Q

Tx of mild-mod UC, mild-mod pancolitis, severe

A

mild to moderate: 1st line is topical 5-aminosalicylic acid (ASA)
mild-mod pancolitis: oral and topical 5-ASA plus steroids
severe: oral glucocorticoids, high dose 5-ASA, and topical ASA
surgical resection in some cases

46
Q

maintenance therapy options for UC and CD

A

6-MP and azathioprine, methotrexate, cyclosporine, tacrolimus, anti-TNF agents

47
Q

CP of Crohn’s Dz (ileocolitis, jejunocolitis, colitis/perianal dz)

A

ileocolitis: crampy RLQ abdominal pain, non bloody diarrhea and weight loss
jejunocolitis: malabsorption, steatorrhea, nutritional or electrolyte disorders
colitis and perianal dz: diarrhea, perirectal abscess, fistula or fissure formation
+ extra-intestinal manifestations could occur (rheum, derm, eye, liver, heme)

48
Q

dx and labs of crohn’s disease

A

upper GI series: initial test (string sign: barium flowing through narrowed/inflamed areas)
endoscopy/colonoscopy: “skip areas”, cobblestoning of mucosa
biopsy: transmural inflammation, noncaseating granulomas, creeping fat
labs: + anti-saccharomyces cerevisiae antibodies (ASCA), iron and b12 deficiency if severe

49
Q

tx for crohn’s disease (limited ileocolonic, ileal and proximal colon dz, severe and refractory)

A

limited ileocolonic: 5-ASA (mesalamine) or oral GCs
ileal and prox colon: GCs
severe and refractory: maintenance meds (azathioprine, 6MP, methotrexate, anti TNF)

50
Q

complications for crohn’s vs UC

A

crohn’s: perianal dz (fistulas, strictures, abscesses, granulomas), Fe and B12 deficiency
UC: primary sclerosing choleangitis, colon ca, toxic megacolon

51
Q

what is chronic mesenteric ischemia due to? compare this to acute mesenteric ischemia

A

1) . Chronic = ischemic bowel disease due to mesenteric artery atherosclerosis (decreased supply during increased demand such as eating)
* most patients have atherosclerotic disease
2) . Acute = abrupt onset of small bowel hypoperfusion MC due to acute arterial occlusion

52
Q

CP of chronic vs acute mesenteric ischemia

A
Chronic = dull abdominal pain worse after meals (intestinal angina) which leads to anorexia and weight loss
Acute = severe abdominal pain out of proportion to physical findings, may have NV/diarrhea, advanced disease can have signs of peritonitis
53
Q

3 different causes of acute mesenteric ischemia

A

1) . acute arterial embolism (MC) = superior mesenteric artery MC, embolism from A-fib MC, can also be thrombotic
2) . nonocclusive arterial ischemia = hypoperfusion due to shock, vasopressors, cocaine
3) . venous thrombosis = obstruction of intestinal venous outflow

54
Q

how to dx acute vs chronic mesenteric ischemia

A
acute = CT angiography often initial test, conventional arteriography definitive diagnosis
chronic = angiography definitive diagnostic test
55
Q

what are two elevated labs in acute mesenteric ischemia?

A

leukocytosis (elevated WBC) and lactic acid

56
Q

tx of acute and chronic mesenteric ischemia

A
acute = depends on cause but MC tx is surgical revascularization (embolectomy, angioplasty with stenting, bypass), surgical resection of bowel if non salvageble, anticoagulation in patients with a-fib
chronic = revascularization is definitive
57
Q

what is irritable bowel syndrome and PP theories behind it?

A

chronic, functional idiopathic pain disorder with NO organic cause, often late teens/early 20s

  • abnormal motility = chemical imbalance in the intestine causing motility and spasm problems
  • visceral hypersensitivity = lowered pain threshold to intestinal distention
  • psychosocial interactions and altered CNS processing
58
Q

common CP of IBS and three main alarm sxs

A

abdominal pain with bouts of constipation and diarrhea, pain often relieved with defecation, may have bloating, nausea, interefere with ADLs
*alarm sxs = evidence of GI bleed, anorexia/weight loss, persistent diarrhea causing dehydration

59
Q

how do you diagnose IBS?

A

DIAGNOSIS OF EXCLUSION
Rome criteria can help: recurrent abd pain at least 1 d/wk in the last 3 months with at least 2:
a). related to defecation
b). onset associated with change in stool frequency
c). onset associated with change in stool form (appearance)

60
Q

how to manage IBS?

A

lifestyle and dietary changes 1st line (low fat, high fiber, unprocessed food diet), avoid beverages containing sorbitol or fructose and gas-producing foods, sleep, smoking cessation, exercise

  • constipation sxs = prokinetics (fiber, psyllium, miralax after fiber), lubiprostone and linaclotide if prokinetics don’t work
  • diarrhea sxs = loperamide, rifaximin, eluxadoline, anticholinergics (dicyclomine, hyoscyamine)
61
Q

ischemic colitis: what is it, what is it normally due to, and where does it normally occur?

A

decreased colonic perfusion which leads to inflammation

  • MC due to transient systemic hypotension or atherosclerosis involving mesenteric arteries
  • MC at splenic flexure and rectosigmoid junction
62
Q

CP for ischemic colitis

A

LLQ, crampy abd pain with tenderness, bloody diarrhea or hematochezia (pain not as severe as acute mesenteric ischemia)

63
Q

Dx and Tx for ischemic colitis

A
Dx = CT of abdomen often first imaging ("thumbprinting" seen, segmental wall thickening), colonoscopy afterwards if no bowel perf pr peritonitis
Tx = mostly supportive care (restore perfusion, bowel rest, IV fluids), ABX in some pts
64
Q

sxs for colon cancer ascending vs decending colon

A
ascending/right = iron deficiency anemia (fatigue/pallor) plus anorexia, malaise, weight loss
descending/left = change in bowel habits (constipation) and more likely obstruction signs (abd pain, distention, nausea)
65
Q

what is the most common cause of large bowel obstruction?

A

adenocarcinoma