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Adult Clinical Medicine > GI Diseases > Flashcards

GI Diseases Flashcards

1
Q

causes of acute abdominal pain

A
  1. appendicitis
  2. cholecystitis
  3. pancreatitis
  4. perforation
  5. obstruction
  6. infarction

*usually requires prompt attention

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2
Q

Causes of GI hemorrhage

A
  1. Inflammatory bowel disease (Ulcerative colitis, Chron’s)
  2. Diverticulitis/diverticular disease
  3. Ano-recal hemorrhoids
  4. Ano-recal fissures
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3
Q

causes of chronic abdominal pain

A
  1. esophagitis
  2. peptic ulcer
  3. dyspepsia
  4. IBS
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4
Q

ddx for abdominal pain at periumbilical

A
  1. obstruction
  2. infarction
  3. pancreatitis- also epigastric pain
  4. appendicitis- also RLQ
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5
Q

ddx for epigastric pain

A
  1. cholecystisis- also RUQ
  2. pancreatitis- also periumbilical
  3. perforation
  4. peptic ulcer
  5. dyspepsia
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6
Q

ddx for retrosternal pain

A

esophagitis

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7
Q

The acute abdomen is a challenging condition in medical practice, The first question to be answered is ____

A

whether immediate surgery is needed

*Early surgical consultation should be attained, even in doubtful cases, rather than awaiting for confirmation via laboratory radiologic studies

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8
Q

Necessary lab components of abdominal pain

A
  1. CBC w/ differential
  2. UA
  3. serum lipase
  4. amylase
  5. bilirubin
  6. electrolytes
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9
Q

radiographic imaging for abdominal pain

A
  1. Abdominal xray- reveals the intra-abdominal gas pattern
  2. Upright film includes diaphragm
  3. Left lateral decubitis- ID intra-abdominal air
  4. US- dx acute cholecysitis or appendicitis
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10
Q

the presence of postprandial nausea and vomiting suggests:

A
  1. chronic peptic ulcer
  2. disorders of gastric emptying
  3. outlet obstruction.
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11
Q

The documentation of weight loss mandates to search for ____.

If anorexia accompanies weight loss, particularly in elderly patients, __ must be excluded.

A

mechanic costs, such as inflammatory bowel disease or celiac disease

cancer

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12
Q

The most frequent causes of chronic of the abdominal pain are __

A

functional

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13
Q

Dyspepsia is characterized by:

A
  1. chronic intermittent gastric discomfort
  2. sometimes accompanied by nausea or bloating

*The symptoms are not always relieved by acid suppression and may be the result of the underlying motor disorder

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14
Q

Estimates are that ___% of Americans suffer from IBS on a regular basis and ___% of referrals to gastroentorologists are related to IBS.

A

15%

40 to 50%

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15
Q

characteristics of IBS

A
  1. abdominal distension
  2. flatulence
  3. disordered bowel function
  4. LLQ pain- but can be located elsewhere or more generalized
  5. sx usually begin in late teens to early 20s
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16
Q

Rome criteria for IBS dx

A

Recurrent abdominal pain or discomfort** at least 3 days/month in the last 3 months associated with two or more of the following:

  1. Improvement with defecation
  2. Onset associated with a change in frequency of stool
  3. Onset associated with a change in form (appearance) of stool
  • Criterion fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis
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17
Q

IBS clinical features

A
  1. Pain-not interfering with sleep and may be relieved by bowel movement–can be crampy or sharp, dull, gas-like and mild to severe
  2. Constipation, diarrhea or alternating constipation with diarrhea
  3. Feeling of incomplete evacuation
  4. Explosive defecation (20%)
  5. Mucus possible coating stools
  6. Bloating, flatulence
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18
Q

The patient should be asked about ____ that suggested diagnoses other than IBS and warrant further investigation.

A

“alarm symptoms”

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19
Q

Acute onset of symptoms raises the likelihood of ___ disease, especially in patients over 40 to 50 years old.

A

organic

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20
Q

example of “alarm sx”

A
  1. Nocturnal diarrhea
  2. severe constipation or diarrhea
  3. hematochezia
  4. Weight loss
  5. fever

*incompatible with the diagnosis of IBS and warrant further investigation of underlying disease.

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21
Q

In patient whose symptoms fulfill the diagnostic criteria for IBS and who have no alarm symptoms, evidence-based consensus guidelines:

A

do not support further diagnostic testing, As they likely have serious organic diseases did not appear to be increased.

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22
Q

Stool specimen examinations for open parasite should be attained only in patients with increased likelihood for __

A

infection

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23
Q

As with other functional disorders, the most important intervention that the clinician can offer for IBS is:

A

our reassurance, education, and support

*This includes identifying responding to the patient’s concerns, careful explanation without the disorder, Setting realistic treatment goals, And involving patient and the treatment process

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24
Q

____ of patients with IBS have mild symptoms that respond broadly to education reinsurance and dietary interventions.

A

More than two thirds

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25
Q

In discussing with the patient importance of the mind gut interaction with IBS, it maybe helpful to explain the alterations in visceral motility and sensitivity maybe exacerbated by:

A
  1. environmental
  2. social
  3. psychological factors

such as foods, medications, hormones, and stress.
*Moderate exercise is beneficial

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26
Q

Drug therapy for IBS should be reserved for patients with:

A

moderate to severe symptoms that do not respond conservative measures

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27
Q

IBS Management

A
  1. Reassurance
  2. Avoidance of irritants–beans, cabbage, brussels sprouts, raisins, coffee, red wine, beer
  3. Trial of high fiber diet–water soluble fiber
  4. Antispasmodics–dicyclomine
  5. Psychotropic agents–amitriptyline, SSRIs now being used
  6. Imodium for diarrhea–beware of cycle of constipation and diarrhea
  7. Do not encourage laxative use
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28
Q

what is celiac sprue characterized by?

A
  • inability to absorb gluten protein foods containing wheat, rye, oats and barley rice, potatoes , corn and cornmeal are allowed
  • intestinal mucosal injury resulting from immunologic damage from gluten in persons genetically predisposed to this condition
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29
Q

The prevalence of celiac among relatives of patients with celiac sprue is approximately __%

A

10%

*More common than we thought 1/133; if first degree relative, 1/22

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30
Q

Results from investigation suggests that an enzyme, ____, may be the autoantigen of celiac sprue

A

Tissue Transglutaminase

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31
Q

signs of celiac sprue

A

classic signs of malabsorption syndrome:

  1. bloating
  2. chronic diarrhea,
  3. flatulence
  4. lactose intolerance
  5. deficiencies of a single micronutrient (ie. iron deficiency anemia)

or asymptomatic

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32
Q

dx of celiac sprue

A
  • Intestinal biopsy is the most valuable test though a clinical response to the gluten-free diet establishes the diagnosis and precludes that needs to document healing by repeated biopsies.
  • positive TTG in a patient who is currently eating gluten
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33
Q

treatment of celiac sprue

A

-following gluten free diet

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34
Q

UC is characterized by

A

-by inflammatory changes that involve the colonic mucosa in a CONTINUOUS superficial fashion, generally starting in the rectum and extending proximately

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35
Q

Crohn’s disease is characterized by

A
  • any segment of GI system
  • often in a DISCONTINUOUS fashion
  • transmural inflammation, which results in significant complications such as abscesses, fistulas, and strictures.
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36
Q

transmural inflammation with Crohns disease but you at risk for what significant complications

A

abscesses, fistulas, and strictures

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37
Q

IBD includes what disease?

A

UC

Crohns

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38
Q

describe the onset of IBD

A
  • Onset at any age but may be bimodal with peak incidence age 10-30 as well as sixth and seventh decades (smaller peak)
  • 1/3 of cases of IBD present in 20s
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39
Q

what group of people are at higher risk for IBD

A

Ashkenazi Jews

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40
Q

Currently, the main theory regarding IBD pathogenesis involves:

A
  • a dysregulation of the normal intestinal immune process.
  • This dysregulation results in an overaggressive response, Most likely to the individuals own intestinal microbial flora or some other unidentified environmental component
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41
Q

describe the genetic predisposition of IBD

A
  • If both parents have IBD the risk of an offspring having IBD is 50%
  • Risk of disease is highest among twins–60% in CD and 20% for UC

*Approximately 10% of patients with IBD have a first degree relative with the disease, and first degree relatives of IBD patients have approximately a 10 to 15 fold increased risk of developing IBD.

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42
Q

what is the etiology of IBD

A
  1. multifactorial

2. genetic predisposition

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43
Q

The majority of patients with IBD initially exhibit:

A
  1. diarrhea
  2. abdominal pain
  3. urgency to dedicate
  4. rectal bleeding, and the passage of mucus per rectum.
    - The typical clinical course is of chronic intermittent exacerbations, followed by periods of remission.
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44
Q

describe main differences between UC and Crohn’s

A

UC

  • involves colon and rectum
  • continous superficial involvement of mucosa only
  • blood diarrhea
  • rare abdominal pain
  • no perianal disease or fistula
  • smoking is protective

Crohns

  • involve any area of GI tract (rectum usually spared)
  • skipped lesion and transmural involvement
  • non-blood diarrhea
  • frequent abdominal pain
  • perianal disease and fistulas
  • worsens w/ smoking
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45
Q

Radiologic findings:

tubular appearance resulting from loss of haustral folds

A

UC

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46
Q

Radiologic findings:

string sing of terminal ileum, RLQ mass, fistulas, abscesses

A

Crohn’s disease

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47
Q

ddx of IBD

A
  1. infectious colitis
  2. ischemic colitis
  3. radiation enteritis
  4. enterocolitis induced by NSAID drugs, diverticulitis
  5. Appendicitis
  6. gastrointestinal malignancies
  7. irritable bowel syndrome
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48
Q

ddx of diarrhea or rectal bleeding

A
  1. IBD- UC
  2. bacterial infections:
    - C. diff
    - Yersinia enterocolitica
    - Salmonella
    - Shigella
    - Campylobacter
    - E. coli

*high fever= suspect abscess

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49
Q

TB in high risk pts. may affect ____

A

terminal ileum

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50
Q

Tx of IBD

A
  1. Anti-inflammatory medicines
    - Aminosalicylates
    - Corticosteriods
  2. Immunomodulatory Agents
    - Tysabri (integrin receptor antagonist)
    - 6- mercaptopurine
    - Imuran (Azathioprine)
  3. Biologic Agents– TNF-alpha blockers (remicade and Humira)
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51
Q

Patients with severe or fulminant IBD, as indicated by abdominal pain, fever, tachycardia, anemia and leukocytosis, require:

Because IBD is a chronic recurrent illness, treatment is centered on ____

A

hospital admission and multidisciplinary team management.

controlling the acute attack with induction of remission followed by maintenance of remission.

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52
Q

what indicates severe or fluminant IBD?

A
  1. abdominal pain
  2. fever
  3. tachycardia
  4. anemia
  5. leukocytosis
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53
Q

pros and cons of corticosteroids for IBD

A

Pros:

  • effective for controlling active disease
  • indicated in patients where aminosalicylates fail

Cons:

  • not useful for maintaining remission
  • not for long term use
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54
Q

what IBD meds are safe and effective in those refractory to other modes of therapy

A

biological agents

-TNF-alpha blockers (remicade and humira)

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55
Q

IBD complications

A
  1. Hemorrhage
  2. Stricture
    - More in CD
    - In UC dysplasia or malignancy
  3. Fistulas
  4. Toxic megacolon
  5. Neoplasia
  6. Eye–episcleritis or scleritis; iritis and uveitis (HLA-B27)
  7. Skin–erythema nodosum and pyoderma gangrenosum
  8. Arthralgias
  9. Gallstones–in CD where ileal resections
  10. Sclerosing cholangitis
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56
Q

when is surgery useful in IBD

A

In CD–for refractory disease, perforation, recurrent obstruction and toxic megacolon

In UC–curative

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57
Q

anal and rectal lesions that cause bleeding

A
  1. Hemorrhoids
  2. Anal fissures or tear
  3. Fistula
  4. Proctitis–idiopathic or related to HIV
    - CMV, Gonorrhea, Mycoplasma
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58
Q

what are the different types of diverticula?

A
  • Diverticular hemorrhage–maroon stools

- Meckel’s diverticulum–distal ileum

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59
Q

describe internal hemorrhoids

A
  1. located above the dentate line
  2. if extensive may cause feeling of incomplete evacuation
  3. may protrude externally
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60
Q

describe external hemorrhoids

A
  1. located below the dentate line

2. may become thrombosed

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61
Q

causes of hemorrhoids

A
  1. Dilated veins of the hemorrhoidal plexus
  2. Tight internal anal sphincter
  3. Modern European toilet – sitting versus squatting
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62
Q

how can you prevent hemorrhoids

A
  1. High fiber diet
  2. Avoid constipation
  3. Avoid straining
  4. Use soap and water for 5. cleanup after stooling
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63
Q

Due to the very high General population prevalence of hemorrhoids, Many Medical treatments are aimed at common symptoms. But few are curative. including:

A
  1. Sitz bath
  2. Pain - Anesthetic sprays
  3. Puritis - Hydrocortisone (anusol)
  4. Bleeding Astringents (Preparation H), Hydrocortisone.
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64
Q

indications for hemorrhoid surgery

A
  1. Persistent bleeding
  2. Poor hygiene secondary to the hemorrhoids
  3. Persistent pain
  4. Prolapsed internal hemorrhoids
  5. Severe pain
  6. Incision of thrombosed hemorrhoids
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65
Q

surgical measurements for hemorrhoids

A
  1. injection
  2. banding
  3. cryo, or coagulation.

*Surgical resection in severe cases. All require surgical referral.

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66
Q

goals of rectal bleeding

A

1st goal: stabilize

  1. hemodynamics
  2. vital signs
  3. type and cross
  4. large bore IV

2nd goal:
1. discover cause frequently via endoscopy (EGD) or colonoscopy

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67
Q

colonic bleeding lesions

A
  1. CA
  2. colonic polyps
  3. angiodysplasia- ascending colon
  4. UC (more than CD)
  5. infectious Colitis (Campylobacter shigella, amebae, c. diff, salmonella)
  6. ischemic colitis- elderly or OCP/HRT users
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68
Q

Diverticuolosis is characterized by:

A
  1. Mucosal herniation through large bowel wall

2. Most in sigmoid colon; ~1/3 proximal colon

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69
Q

what people are most at risk for diverticulosis

A
  • Incidence increases with age
  • More common in low fiber Western diets
  • Inherited weakness in colonic wall
  • Almost unknown in Africa and Asia
  • People in Japan, Singapore and Thailand present with right sided disease
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70
Q

diagnostic studies for diverticulosis

A
  1. Plain films to r/o free air (perforation)
  2. CT to look for abscess
  3. Colonoscopy is contraindicated during acute diverticulitis (when inflammation occurs in and around the diverticular sac)
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71
Q

sx of diverticulosis

A
  • Usually asymptomatic

- Bleeding diverticula presents with acute painless large volume hematochezia

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72
Q

tx of diverticulosis

A
  • Massive bleed requires hospitalization
  • uncomplicated diverticulosis – is treated with a High fiber diet-10-25 grams daily
  • If hematochezia (erosion of fecalith in the diverticular sac) bed rest and support
  • Vasoconstrictive drugs after location determined

-Colonoscopy–in elderly never attribute bleeding to diverticula unless other conditions ruled out

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73
Q

sx of diverticulitis

A
  1. aching LLQ pain
  2. fever
  3. N/V
  4. constipation or loose stools
  5. hematochezia rare

*variable in severity

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74
Q

complications of diverticulitis

A
  1. perforation
  2. acute peritonitis
  3. sepsis and shock

*more common in elderly

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75
Q

tx of diverticulitis

A
  1. Bowel rest
  2. IV fluids
  3. Broad spectrum antibiotics (PO or IV)
  4. Repeated attacks or failure to respond to therapy may require surgical resection (make NPO)
  5. If peritoneal signs and abscess–resection or drainage

*-Abscess-IV abx and CT/US guided drainage before urgent surgery

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76
Q

To properly evaluate diarrhea complaint, clinician must determine:

A

the patient’s normal bowl pattern and the nature of the current symptoms.

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77
Q

Diarrhea of less than two weeks is most commonly caused by

A

invasive or noninvasive pathogens enterotoxin

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78
Q

describe acute non-inflammatory diarrhea

A
  1. watery
  2. nonbloody
  3. usually mild and self limited
  4. caused by a virus or non-invasive bacteria
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79
Q

treatment of diarrhea

A

-limited to hydration, as most diarrhea will not lead to dehydration provided to the patient takes adequate oral fluids containing carbohydrates and electrolytes

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80
Q

describe acute inflammatory diarrhea

A
  1. bloody
  2. pus in stool
  3. fever
  4. caused by invasive or toxin producing bacteria
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81
Q

dx studies of acute inflammatory diarrhea

and tx

A
  1. stool of cultures including equal AC death and over and parasites are warranted with empiric antibiotic or specific antimicrobial treatment warranted.
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82
Q

Chronic diarrhea is typically defined as

A

diarrhea present for over four weeks

*unlikely to be infectious

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83
Q

The presence of blood in diarrhea is also a useful clue because it suggests

A
  1. inflammation
  2. neoplasm
  3. ischemia or infection by invasive organisms
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84
Q

The social history in the evaluation of diarrhea should include:

A
  1. travel
  2. Source of drinking water
  3. consumption of raw milk
  4. sexual practices.
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85
Q

causes of chronic diarrhea maybe grouped into the following major pathophysiologic categories:

A
  1. medications
  2. osmotic diarrheas
  3. secretory conditions
  4. inflammatory conditions
  5. malabsorption conditions
  6. motility disorders
  7. chronic infections
  8. systemic disorders
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86
Q

chronic diarrhea w/ weight loss and evidence ofnutritional deficiencies suggest

A

malabsorption

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87
Q

Chronic bloody diarrhea is suggests

A

inflammatory bowel disease, particularly ulcerative colitis

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88
Q

Chronic diarrhea with no evidence of nutritional and metabolic derangements suggest

A

lactose intolerance (common)

89
Q

Diseases of the Esophagus

A
  1. GERD
  2. Barretts
  3. Dysphagia
  4. Mallory Weiss Tears
90
Q

what is GERD

A

GERD is defined as chronic symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus”

91
Q

the prevalence of GERD is - ___% in the adult population

Associated with ___

A

15-20%

significant health resource utilization

92
Q

2 main categories of GERD

A
  1. GERD with erosive esophagitis- defined by the presence of endoscopically visible damage to the esophageal mucosa
  2. NERD (non-erosive reflux disease) aka symptomatic GERD
93
Q

sx of GERD

A
  1. heartburn* (pivotal to the diagnosis of the condition)
  2. regurgitation
  3. dysphagia

*symptom patterns

94
Q

describe hearburn

A

a burning feeling rising from the stomach or lower chest up towards the neck”

*this description can help patients recognize this symptom

95
Q

___ is the effortless movement of stomach contents upward into the esophagus, throat, or mouth

A

Regurgitation

*It is often confused with vomiting, but is not accompanied by nausea.

96
Q
  • Patients may have a sensation that food is being hindered in passing from the mouth to the stomach
  • They may comment that the food seems to stick or stop or that it “doesn’t go down right.”
A

Dysphagia

97
Q

atypical sx of GERD

A
  1. CP (sometimes mistaken for angina)

2. Respiratory symptoms such as cough, sore throat, wheezing and laryngospasm

98
Q

GERD may be present in up to __% of patients with noncardiac chest pain and ___% of patients with chronic hoarseness

A

50%

78%

*Therefore, the possibility of GERD should always be considered in patients with these and other ‘atypical’ symptoms

99
Q

Reflux-related symptoms occur predominantly after ___ and are often trigged by:

A

after meals

  • triggered by
  • unusually large meals
  • fatty
  • spicy
  • acidic foods
  • bending, stooping, or lying down
  • lifting, straining, or other strenuous activities
100
Q

___% of patients undergoing cardiac catheterization for chest pain have normal angiography
__% of these have EGD or pH probe findings

A

30%

40-50%

101
Q
  • Most people with GERD show abnormal exposure of the esophagus to _____.
  • In most cases, this is due to ____
A

gastric acid and pepsin

-dysfunction of the lower esophageal sphincter (LES).

102
Q

abnormal exposure of gastric acid and pepsin to the esophagus can be increased as a result of:

A
  1. dysfxn of LES
  2. increased intra-abdominal pressure
  3. hiatal hernia
  4. inadequate clearance of refluxate from the esophagus
  5. delayed gastric emptying.
103
Q

what is a hiatal hernia and its complications

A

-occurs when the upper portion of the stomach moves up through the diaphragm

  1. can trap a portion of the gastric contents above the diaphragm, increasing the likelihood of reflux.
  2. The presence of a hiatal hernia can compromise the function of the LES, since the action of the sphincter is no longer reinforced by the diaphragm- This also increases the risk of reflux.
104
Q

Increases in esophageal exposure to acid and pepsin can also occur as a result of raised intra-abdominal pressure. This can occur during:

A
  1. pregnancy
  2. as a result of changes in posture (bending or straining)
  3. obesity
  4. coughing
  5. wearing tight clothes.
105
Q

Dietary factors that may aggravate GERD symptoms

A
  1. spicy foods
  2. fatty foods
  3. chocolate
  4. citrus fruits/juices
  5. alcohol
  6. peppermint
  7. caffeinated products
  8. tomato based products
106
Q

Medications that may aggravate GERD symptoms by:

A
  • impairing LES function

- or by damaging the esophageal mucosa.

107
Q

Medications that can impair LES function and aggravate GERD include

A
  1. beta-adrenergic agonists
  2. theophylline
  3. tricyclic antidepressants
  4. calcium channel blockers.
108
Q

diagnostic methods in GERD

A
  1. Most cases of GERD can be diagnosed on the basis of symptoms alone,
  2. techniques such as endoscopy (test of choice for alarm sx)
  3. pH monitoring
  4. or an empirical trial of PPI therapy, may be useful in some cases.
109
Q

____ is the primary diagnostic tool for GERD

A

A detailed history of the patient’s symptoms

*heartburn is the pivotal symptom for the diagnosis of this disease. Other typical symptoms include acid regurgitation and dysphagia.
Symptom analysis offers reasonable sensitivity and specificity for GERD.

110
Q

alarm symptoms of GERD

A
  1. Dysphagia
  2. Bleeding
  3. Anemia
  4. Weight loss
  5. Choking, chronic cough, 6. shortness of breath, or hoarseness
  6. Chest pain
111
Q

describe empiric therapy for GERD

A
  • trial of acid-suppressing therapy can be used in patients with suspected GERD to determine whether symptoms are acid-related
  • Either a standard treatment course or a short, high-dose course can be used–>The evidence currently available suggests that high doses provide the greatest diagnostic sensitivity
  • PPIs are the agents of choice for therapeutic trials, as studies have shown that these agents are significantly more effective in relieving GERD symptoms than other medical treatments
112
Q

EGD indications

A
  1. Heartburn and alarm symptoms
  2. When GERD symptoms persist despite 4-8 weeks of bid PPI therapy
  3. Severe erosive esophagitis after 2 months of PPI to assess healing and r/o Barrett esophagus
  4. In those with stricture in the past and now with recurrent symptoms
  5. In men older than 50 with chronic GERD and risk factors (elevated BMI, hiatal hernia, tobacco use, and intra-abdominal distribution of fat)
113
Q

describe pH monitoring

A

-involves the introduction of a pH probe into the esophagus via the nose. It allows investigation of the amount and timing of reflux, the correlation between reflux and symptoms, and the effect of therapy on reflux

114
Q

The AGC guidelines recommend that pH monitoring may be useful in patients with:

A
  1. persistent symptoms who do not have endoscopic evidence of erosive esophagitis
  2. patients with atypical symptoms such as chest pain or upper respiratory symptoms,
  3. patients with refractory symptoms
115
Q

what early work up should be done w/ someone who has alarm GERD symptoms

A

Additional diagnostic investigations, for example by endoscopy, are appropriate in patients with these symptoms in order to exclude complications of GERD such as esophageal stricture, peptic ulcer or carcinoma.

116
Q

Eosphageal complications of GERD

A
  1. Barrett’s esophagus (10-15%)–> adenocarcinoma
    - 6-10x more likely to get if GERD
  2. stricture (1%)
  3. esophageal CA
  4. ulceration
  5. bleeding
117
Q

treatment of GERD1

A
  1. lifestyle measures
  2. PPI
  3. H2 blockers
  4. Promotility drugs
  5. antireflux surgery
118
Q

lifestyle measures to help tx GERD

A
  1. Elevation of the head of the bed
  2. Avoidance of food or liquids 2 to 3 hours before bedtime
  3. Avoidance of fatty or spicy foods
  4. Avoidance of cigarettes, alcohol
  5. Weight loss
  6. Liquid antacid
119
Q

extra-esophageal complications of GERD

A
  1. asthma
  2. reflux laryngitis
  3. vocal cord ulcers
  4. subglottic stenosis
  5. tracheal stenosis
  • Caused by aspiration of refluxate into the trachea
  • These complications can lead to patients presenting initially to ear, nose and throat (ENT) or respiratory physicians.
120
Q

how do symptoms vary in patients with and without erosive esophagitis?

A
  • there are some differences between patients with and without erosive esophagitis with respect to patterns of heartburn severity and frequency, these differences are minor.
  • Therefore, it indicates that neither symptom severity nor symptom frequency can be used in isolation to differentiate between patients with erosive esophagitis and those without
121
Q

what is Barrett’s Esophagus?

A

a change in the esophageal epithelium of any length that can be recognized at endoscopy and is confirmed to have intestinal metaplasia by biopsy”

122
Q

describe the tissue change in barretts esophagus

A
  • Normally, the esophagus is lined with squamous epithelium. Chronic exposure to gastric refluxate may lead to transformation of areas of squamous epithelium into columnar epithelium. This tissue type is usually found in the lining of the stomach and intestine – hence the term ‘intestinal metaplasia’.
  • The change from squamous to columnar epithelium represents an adaptive response to the presence of acidic refluxate in the esophagus, as columnar epithelium is more resistant to acid than the squamous type
123
Q

Why is barretts esophagus of clinical importance

A
  • it is a premalignant lesion for esophageal adenocarcinoma.
  • Patients with Barrett’s esophagus may be 30 times more likely to develop this cancer than the general population.
  • Annually, 1 in 200 patients with Barrett’s esophagus develops esophageal cancer

*The prevalence of Barrett’s esophagus increases with the duration of reflux symptoms

124
Q

risk factors for Barrett’s Esophagus

A
  1. GERD
  2. smoking
  3. ETOH
  4. obesity
  5. 50-65y/o
  6. 80% white males
125
Q

tx of Barretts Esophagus

A

treatment will be under the supervision of a Gastroenterologist as the mainstay is regular surveillance via endoscopy and ablative therapy in addition to acid suppression.

126
Q

Evaluation of the patient complaining of difficulty swallowing begins with the discrimination between

A

oropharyngeal and true esophageal disease

127
Q

what is oropharyngeal dysphasia and what are diseases is it seen with?

A

Oropharyngeal dysphasia is a disorder of INITIATION of swallowing caused by a neurologic or muscular disease, including:

  1. Parkinson’s disease,
  2. stroke
  3. multiple sclerosis,
  4. myasthenia gravis,
  5. amyotrophic lateral sclerosis (Lou Gehrig’s disease).
128
Q

To differentiate between a neuromuscular disorder of the esophagus versus mechanical obstruction, you should question your patient

A

on rather liquid and/or solid foods are causing the problem.

solid food only= mechanical obstruction

solid or liquid= neuromuscular d

129
Q

A barium swallow is useful in ____, although endoscopy will then be necessary for purposes of ___

A

outlining lesions of the esophagus

biopsy and possible treatment via dilation.

  • Therefore many gastroenterologist evaluate dysphasia with an initial EGD to avoid numerous diagnostic tests.
130
Q

Esophageal manometry permits diagnoses of:

A

motility disorders such as achalasia and esophageal spasm.

131
Q

An esophageal stricture is defined

A

as a narrowing of the esophagus due to inflammation, scar formation, or both.

132
Q

Esophageal strictures occur in approximately __% of patients with GERD. GERD accounts for ___% of strictures.

A

1% to 2%

70-80%

133
Q

The use of ___ has dropped significantly incidence of erosive GERD and its sequela in patients with scleroderma.

A

PPI’s

134
Q

Aperistalsis and hypertonia of the LES resulting in

A

gradual dilation of the esophagus

135
Q

cause and associations of achalasia

A
  • Unknown etiology;

- associated with diminished or lack of neurons in the myenteric plexus of the esopageal muscle layers

136
Q

Dilation of the esophageal body and retention of barium above a tapered “bird’s beak

A

achalasia

137
Q

sx of achalasia

A
  1. fullness in chest during meals
  2. Chest pain precipitated by eating; heartburn
  3. Gradual progression to dysphagia
  4. Dysphagia is to both liquids and solids which may lead to wt. loss
  5. onset btw 25-60 y/o
  6. regurgitation 60-90% of pts
138
Q

tx of achalasia

A
  1. Balloon dilation or surgical esophagomyotomy to disrupt the sphincter muscle
  2. Medications: nifedipine (20-40 mg before meals),nitrates if tolerated
  3. Injection of botulinum toxin to induce paralysis; requires second treatment at about one yr.
139
Q

what is diffuse esophageal spasm and how is it diagnosed

A
  • A motility disorder of the esophagus that usually produces episodes of chest pain and intermittent dysphasia to both solids and liquids.
  • Manometry diagnoses the disorder.
140
Q

tx of diffuse esophageal spasm

A

Difficult to treat:

  1. Calcium channel blockers and nitrates
  2. balloon dilation
  3. Surgical myotomy
141
Q

what are esophageal rings

A

aka shot ski or B rings

- are rings of fibrous tissue that occur in the lower esophagus and cause intermittent dysphasia to solids.

142
Q

Classically patients experience dysphasia when eating a large piece of meat or soft bread (steakhouse syndrome).

A

esophageal rings

143
Q

what are esophageal rings associated w/

A

-with hiatal hernia and may be related to the ringlike strictures induced by reflux esophagitis

144
Q

what are Webs?

A
  • membranes of squamous mucosa that are usually found in the anterior wall of the cervical esophagus;
  • most asymptomatic with intermittant dysphagia being the presenting concern

*seen w/ esophageal rings

145
Q

tx of esophageal rings

A
  1. Pneumatic dilatation

2. PPI therapy to induce remission

146
Q

what are mallory-weis tear and how is it treated

A
  • a tear in the mucosal layer at the junction of the esophagus and the stomach
  • self limiting hematesis (usually)
  • associated w/ vomiting and retching

tx: as acute UGI bleed

147
Q

diseases of the stomach

A
  1. dyspepsia
  2. gastritis
  3. PUD
148
Q

what is dyspepsia

A
  1. Pain or discomfort centered in the upper abdomen

2. When heartburn is the dominant feature it is almost always associated with reflux

149
Q

what is dyspepsia characterized w/ or associated w/

A

fullness, satiety, burning, bloating, nausea, or vomiting

150
Q

Alarm features of dyspepsia which indicate an urgent evaluation include

A
  1. weight loss
  2. vomiting
  3. dysphagia
  4. evidence of anemia
  5. G.I. bleeding
  6. abdominal mass
  7. lymphadenopathy.
151
Q

a nonspecific inflammation of the mucosal surface of the stomach

A

gastritis

152
Q

Clinically, the three most common causes of gastritis are

A
  1. Heliobacter pylori,
  2. NSAIDs,
  3. stress related mucosal damages.
153
Q

how does erosion, ulceration, and bleeding occur w/ gastritis

A

During critical illness, events such as shock, hypotension, and catecholamine release are associated with reduced blood flow and mucosal ischemia. When blood flow to the mucosa is inadequate, the normal mucosal protective mechanisms are altered. In addition cytokines and oxygen free radicals are released. The combination of these events reduces the mucosal resistance to acid, causing erosions that may progress to ulceration and bleeding.

154
Q

major problem of stress gastritis

A
  • The major problem is blood loss, Which is occult in most instances.
  • Gross hemorrhage occurs in only 5%.
155
Q

tx of stress gastritis

A

Acid neutralization with H2RA or PPI are effective treatments

  • Prophylaxis with H2 blockers reduces bleeding 50%
  • If clinically significant bleeding consider IV PPI
156
Q

Mucosal erosions (in stress gastritis) develop with __ hours in critically ill patients

A

18 hrs

157
Q

__% of patients on NSAIDs have gastritis on biopsy

-Symptoms develop in ___%

A

50%

less than 25%

*Symptomatic patients should be endoscoped

158
Q

Endoscopic studies have shown a prevalence of gastroduodenal ulcers of __-% in patients with chronic arthritis treated with NSAIDs, which is ___ times the expected prevalence of age matched healthy populations.

A

10 to 25%

5 to 15

159
Q

tx of NSAID gastritis

A
  • removal of causal factors and acid protection treatment

- NSAID + PPI is as effective as COX-2 inhibitors

160
Q

what are peptic ulcers

A

mucosal defects of the G.I. mucosa of the stomach or the duodenum.

161
Q

The most important risk factors for the development of peptic ulcers is:

A

infection with H pylori and use of NSAIDs

162
Q

how do peptic ulcers present?

A

can present in a variety of forms ranging from:

  1. asymptomatic iron deficiency anemia to
  2. abdominal pain,
  3. obstruction
  4. perforation, and
  5. hemorrhage
  6. epigastirc pain- dull ache but may be sharp or burning
  7. N/V

It should be noted the symptoms may mimic those of other diseases, Including:

  1. cholecystitis,
  2. pancreatitis
  3. gastric cancer,
  4. GERD, and
  5. myocardial ischemia.
163
Q

imaging of peptic ulcers

A

Imaging studies of the G.I. tract are required to confirm the presence of peptic ulcers. Endoscopy is usually preferred because in addition to characterizing the ulcer, it allows tissue sampling to exclude malignancy, assessment of H. pylori infection, and in the cases of acute hemmorhage, deliver endoscopic therapy.

164
Q

what is the difference between a duodenal ulcer and a gastric ulcer

A

Duodenal Ulcer

  • most common
  • usually in duodenal bulb
  • pain improves w/ food*

Gastric Ulcer

  • less common
  • usually along the lesser curvature or prepyloric area
  • pain worsens w/ food*
165
Q

why is H. pylori testing essential in all patients w/ PUD?

A

the eradication of H. pylori infection is associated with significant reduction in ulcer

166
Q

gold standard for diagnosis of H pylori infection.

A

Gastric biopsy during EGD with histology

167
Q

describe H. Pylori testing during EGD

A
  • Histology–execllent sensitivity and specificity
  • Rapid urease testing–sensitivity reduced in posttreatment setting
  • Culture–excellent specificity; expensive
168
Q

describe nonendoscopic H. pylori testing

A
  1. Antibody testing-inexpensive; serology remains positive for years after treatment
    - Positive result of antibody testing may indicate past exposure but not necessarily current infection with H. pylori.
  2. Urea breath tests-useful before and after therapy;
    - costly
    - more accurate than serologic test
  3. Fecal antigen test-excellent positive and negative predictive values and useful before and after H.pylori therapy
169
Q

treatment goal of H. pylori in ulcers

A
  • Eradication of H. pylori should be attempted in all patients with evidence of infection.
  • Therapy must be of sufficient duration to ensure the small population of bacteria does not remain viable.
  • Combinations of two antibiotics, plus either a PPI or ranitidine, Are used to maximize the chance eradication.
170
Q

tx of H. pylori in ulcers

A

PPI bid plus 2 antibiotics and probiotics for 10-14 days

  • amoxicillin 1 g bid
  • levofloxacin 500 mg
  • omeprazole 20 mg bid
Can also use alternative antibiotics (based on resistance and allergies)
Clarithromycin
Metronidazole
Rifampin
Tetracycline

*Continue QD PPI therapy for 2 months to promote ulcer healing

171
Q

___ is one of the most lethal of all cancers.

-The_____ often results in advanced disease by the time of diagnosis

A

Carcinoma of the esophagus

lack of early symptoms as well as the bidirectional lymphatic flow

5 yr survival rates 9-13%

172
Q

risk factors for esophageal CA

A
  1. chronic GERD
  2. Barrett’s
  3. cig. smoking
  4. ETOH abuse
  5. achalasia
  6. Male
  7. AA– have 5 fold increased risk
  8. high fat diet
  9. obesity
  10. Usually occurs in 6th or 7th decade of life
    - Rare and individuals young than 40 years of age
173
Q

what is the most common presenting sx of esophageal CA?

A

dysphasia

*Patients with dysphagia should be in valued with upper G.I. study.

174
Q

___ one of the leading causes of cancer related deaths worldwide.

A

Gastric carcinomas

*mostly adenocarcinoma (95%)

175
Q

sx of gastric CA

A
  1. abdominal discomfort*
  2. early sateity (cannot ear a complete meal bc of a “full feeling”)
  3. N/V
  4. Majority of people have advanced disease by the time they are diagnosed b/c they often do not have sxs in the earlier phases

Advanced CA

  1. indigestion
  2. poor appetite
  3. wt. loss
  4. fluid in the abdomen
  5. blood in the stool
  6. anemia
176
Q

risk factors for gastric CA

A
  1. male: female 2:1
  2. rare before 40
  3. African-Americans, Hispanic Americans, and Native Americans, are 1.5 to 2.5 times more likely to develop gastric cancer
177
Q

how do you diagnose gastric CA and what is the survival rate?

A
  • Diagnosis is by upper G.I. radiology or endoscopy.

- Five year survival rates are less than 5-15%.

178
Q

Second only to lung cancer as a cancer cause of death in the U.S.

A

Colorectal cancer (CRC)

179
Q

3rd most common CA

A

colorectal CA (CRC)

180
Q

risk factors for colorectal cancer

A
  1. age- 90% of cases occur over 50
  2. personal or fhx of colorectal CA or IBD
  3. High risk conditions: alcohol use, tobacco use, and a high fat/low fiber diet, hereditary syndromes
181
Q

signs and symptoms of colorectal Ca

A
  1. the majority of colorectal neoplasms are asymptomatic until advanced.
  2. G.I. blood loss is the most common symptom and may show as a occult bleeding, Hematochezia, or unexplained iron deficiency anemia.
  3. abdominal pain from obstruction or invasion,
  4. change in bowel habits,
  5. unexplained anorexia or weight-loss.
  6. Palpable mass may present.
182
Q

lifetime risk of CRC is ___.

__% of patients w/ CRC have a fhx

A

1/20

25%

183
Q

Majority of colorectal cancer’s are believed to arise from ___

A

benign adenomatous polyps

*The length of time and adenoma takes to develop into an invasive cancer is unknown but data from multiple observational studies suggest at least 10 years.

184
Q

how do we screen for CRC?

A
  1. colonoscopy
  2. periodic screening by fecal occult blood testing

*recommended for asymptomatic average risk patients beginning at 50 years.

185
Q

what do you do if you find a colon polyp on a colonoscopy

A
  1. remove and send for pathology
186
Q

what are “Bad” polyp signs

A

adenomatous can progress

-hyperplastic are “ok”

187
Q

It takes about ___ for an adenomatous polyp to progress to a cancer

A

10 years

188
Q

what are high risk screening groups for CRC and how often should they be screened?

A
  1. IBD – every 1-2 years 8 years after diagnosis made
  2. Colon cancer – 3 yrs then every 5 years
  3. Adenomatous polyps – every 3-5 yrs depending on polyp type
  4. Hereditary Colon Cancer Syndromes variable timeline depending on syndrome and findings
189
Q

what are the two forms of familial cancer that account for approximately 4% of all colorectal cancer’s.

A
  1. Hereditary non-polyposis CRC (HNPCC)
    -aka Lynch syndrome
    2-3% of CRC
  2. Familial adenomatous polyp syndrome (FAP)
    - 1% of CRC

*All patients should be questioned on a family history of colon cancer.

190
Q

what is the cause of HNPCC and FAP?

A

HNPCC- mutation in genetic repair mechanism

FAP- defect in APC gene

191
Q

what are the screening recommendations for HNPCC/Lynch syndrome?

A
  • Screening every 1-2 years beginning at age 20-25 (or 10 yrs prior to youngest cancer case)
  • screen all family members

*Very high incidence of colon cancer (80% by age 50) with no surveillance

192
Q

what are the screening recommendations for FAP

A
  • Screening can start as young as 10 with screening every 1-2 yrs until age 40 then q3 yrs
  • Strongly consider genetic counseling
  • screen all family members
193
Q

Risk of colon cancer approaches 100% at age 50

A

FAP

194
Q

Other HNPCC associated tumors

A
  1. endometrial,
  2. stomach,
  3. ovarian,
  4. pancreas,
  5. ureter
  6. renal pelvis,
  7. biliary,
  8. brain,
  9. sebaceous gland adenomas
  10. small bowel
195
Q

associations of FAP

A
  1. Extra colonic tumors (gastric and duodenal)

2. 100-1000’s of polyps

196
Q

Colon CA Screening is key–more than __% of deaths from colon cancer could be avoided if people over 50 had regular screening tests.
-screening: only __% of those who are indicated

A

33%

40%

197
Q

key tips/points to colon CA screening

A
  1. ask about FH to assess need for earlier screening
  2. Blood may have a normal explanation but demands a workup
  3. Find the etiology of iron deficiency anemia
198
Q

Healthy adults pass flattus up to __ times daily and excrete up to ___.

A

20

1500 mL

199
Q

Flattus is derived from two sources:

A
  1. Swallowed air
  2. bacterial fermentation of undigested carbohydrate.

*Abnormal gas production may be caused by increased ingestion of these carbohydrates or, less commonly, by disorders of malabsorption.

200
Q

treatments of flattus

A
  1. dietary restriction to discover causes of flattus (e.g. Lactose intolerance).
  2. Nonprescription Beano or
  3. activated charcoal may aford relief.
  4. Simethicone is of no proven benefit.
  5. Many patients report reduced flattus with use of probiotics although there is Limited controlled studies of these agents for this purpose
201
Q

Virtually all stomach gas comes from ___

A

swallowed air

202
Q

With each swallow, ____ of air is ingested, and excessive amounts may result in:

A

2 to 5 mL

distension, flatulence and abdominal pain

203
Q

how can you ingest excessive air

A
  1. with rapid eating,
  2. gum chewing,
  3. smoking, and
  4. the ingestion of carbonated beverages
204
Q

who should you evaluate for “increased bleching”

A

Evaluation should be restricted to patients with other complaints such as dysphasia, heartburn, early satiety, or vomiting.

*Belching is a normal reflux and does not itself indicate gastrointestinal dysfunction

205
Q

sx: progressive dysphagia w/ solid or liquids and regurgitation of nonacidic material

Radiographic appearance:

  • dilated, fluid filled esophagus
  • distal bird beak stricture
A

Achalasia

206
Q

Manometric findings:
LES- high resting pressure, incomplete or abnormal relaxation w/ swallow

Body- low-amplitude, simultaneous contractions after swallowing

A

Achalasia

207
Q

sx: GERD, progressive dysphagia w/ solids and liquids, chronic heart burn

Radiographic appearance:
aperistaltic esophagus, free reflux, and peptic stricture

A

scleroderma

208
Q

Manometric findings:
LES- low resting pressure

Body- low amplitude peristaltic contractions or no peristalsis

A

scleroderma

209
Q

Sx: substernal CP (angina-like), intermittent dysphagia w/ pain w/ solids or liquids

Radiographic appearance:
simultaneous noncoordinated contractions

A

Diffuse esophageal spasm

210
Q

Maometric Findings:
LES- normal pressure

Body- Some peristalsis, diffuse and simulatneous nonperistaltic contractions, occasionally high amplitudee

A

Diffuse esophageal spasm

211
Q

problems swallowing solid food only suggests:

A

mechanical obstruction

  • carcinoma– over 50 w/ wt. loss
  • peptic stricture– chronic heartburn, no wt. loss
  • lower esophageal ring–bread/streak
212
Q

sx of oropharyngeal dysphagia

A
  1. coughing
  2. choking
  3. nasal regurgitation
213
Q

how do you screen someone for colorectal CA w/ average risk for colon CA

A
  1. anyone beginning at 50
  2. annual FOBT
  3. flexible sigmoidoscopy every 5 yrs
  4. annual FOBT plus flexible sigmoidoscopy every 5 yrs
  5. double contrast barium enema every 5 yrs
  6. colonoscopy every 10 yrs
214
Q

how should you screen someone for colorectal CA w/ 1 or 2 first degree relatives with CRC at any age or one or more adenomas at age less than 60

A
  1. colonoscopy every 5 yrs beginning at age 40 or 10 yrs younger than earliest diagnosis, which ever comes first
215
Q

how should you screen someone for colorectal CA w/ herediatry nonpolyposis colorectal CA

A
  1. genetic counseling/screening

2. colonoscopy every 1-2 yrs at age 25 and then yearly after age 40

216
Q

how should you screen someone for colorectal CA w/ FAP and variants

A
  1. genetic counseling/testing

2. flexible sigmoidoscopy yearly beginning at puberty

217
Q

how should you screen someone for colorectal CA w/ personal hx of CRC

A
  1. colonoscopy within1 yr of curative resection

2. repeat at 3 yr and then every 5 yrs if normal

218
Q

how should you screen someone for colorectal CA w/ personal hx of one or more colorectal adenomas

A
  1. colonoscopy every 3-5 yrs after removal of all index polyps
219
Q

how should you screen someone for colorectal CA w/ IBS for

A

colonoscopy every 1-2 yrs beginning after 8 yrs of pancolitis or after 15 yrs if only left sided disease

Adult Clinical Medicine (26 decks)

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