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Flashcards in GI ddx Deck (32)
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1
Q

MC outpatient GI/liver problems

A
o	Dyspepsia/GERD
o	Irritable Bowel syndrome/Chronic Pain
o	Colon Cancer Screening
o	Elevated Liver Enzymes
o	Viral Hepatitis
o	Diarrhea
o	“Gas”
o	Management Issues with Chronic Liver Disease
o	Constipation/Hemorrhoids
o	Evaluating Possible Emergencies
2
Q

Acute constipation

A

(less than three months)
 This is really more of a problem in children, not much of a medical issue in adults
 Think about drugs/meds, dietary changes, etc
• Usually a dietary issue
 Treat with fiber and/or bulk-forming laxatives, dietary changes, pt edu

3
Q

Chronic constipation

A

 IBS, iron, not drinking enough water, lack of activity, stress, diabetes, pregnant
 Constipation can cause hemorrhoids
 Functional constipation – some patients who are not elderly have slow GI (not as common as other causes which are diet and lack of fiber and water)
 Hypothyroidism (feeling cold, tired, weight gain, hair loss lateral 1/3 of eyebrows)
 Diabetes
 Gut neuropathy
 Obstruction/colon cancer
 IBS
 Medications/drugs

4
Q

Definition of constipation: Rome criteria

A

o The diagnosis should be based upon the presence of the following for at least three months (with symptom onset at least six months prior to diagnosis)
o Must include two or more of the following:
 Straining during at least 25 percent of defecations
 Lumpy or hard stools in at least 25 percent of defecations
 Sensation of incomplete evacuation for at least 25 percent of defecations
 Sensation of anorectal obstruction/blockage for at least 25 percent of defecations
 Manual maneuvers to facilitate at least 25 percent of defecations (eg, digital evacuation, support of the pelvic floor)
 Fewer than three defecations per week
o Loose stools are rarely present without the use of laxatives
o There are insufficient criteria for IBS

5
Q

Hemorrhoid management

A

o Soft stools, avoid straining and constipation
o Treat symptoms with topicals
 Topical pads, creams, suppositories, etc.  Preparation H, etc. These can also help with rectal itching
o Treat bleeding, chronic hemorrhoids with banding or other surgical tx.  refer to a rectal surgeon and they can band the hemorrhoid
o Bulk forming laxatives (Metamucil, etc.) are available over the counter
 These are helpful as long as the people are drinking water!!

6
Q

Constipation managment

A

o Initial management of chronic constipation includes patient education, behavior modification, dietary change, bulk-forming laxatives, and the use of non-bulk-forming laxatives or enemas as next line therapy
o Management of severe constipation and defecatory dysfunction may involve suppositories, biofeedback, botulinum toxin injections into the puborectalis muscle
o Various pharmacologic therapies have been used for severe constipation with limited success
o BULK FORMING LAXATIVES ARE FIRST LINE AGENTS. Stool softeners, osmotic agents, stimulant laxatives etc. are later down the line and are often dealt with by the GI specialist

7
Q

ddx acute diarrhea

A

 Inflammatory (shigella, salmonella, campylobacter, E.coli, C. diff
 Non inflammatory (viral (Norwalk, rotavirus), giardia, parasites, meds, IBD, IBS

8
Q

ddx chronic diarrhea

A

 Infectious (travel hx, immunocompromised) (chronic bacterial infection, parasite
 Malabsoprtion (celiac disease, lactose intolerance)
 IBD, IBS

9
Q

IBS

A

o At least 15% of population has Sx of IBS
o Rivals URI as cause of absenteeism
o Accounts for >50% of outpatient GI practice

10
Q

clinical patterns of IBS

A
o	Classical: abdominal pain plus constipation/diarrhea
o	Diarrhea only
o	“Gas”
o	Related non-IBS syndromes:
	Non-ulcer dyspepsia (NUD)
	Chronic pain syndrome
	Psychogenic vomiting  
	Pelvic floor dysfunction
11
Q

IBS ddx

A

o Inflammatory Bowel Disease
o Enteric infection: Protozoal or bacterial
o Celiac sprue
o Malabsorption
o Diverticular disease
o Substance abuse (Including alcohol, coffee)
o Idiosynchratic food/additive reaction
o Eating Disorder
o True psychogenic disorder, somatization

12
Q

IBS etiology

A

o Probably heterogenous pathways to common Sx
o Older theories:
 Psychogenic
 Primary motility disorder
o Currently favored: visceral hypersensitivity
o Strong association with previous diarrheal infection
o History of sexual/physical abuse
o Psych: very high prevalence of psych Dxs
 affects medical help-seeking behavior
 Almost all normal people have IBS Sx but “forget”
 Post infectious IBS much more frequent if psych disturbance or stress at time of infection

13
Q

Proposed mechanism for IBS

A

o CNS
 Persistent stress response–>release of stress hormones
 Altered pain processing
o Mucosal inflammation
 Release of inflammatory mediators from mast cells, etc.
 Altered permeability/ bacterial overgrowth
o Peripheral (enteric) nervous system
 Greater sensitivity of gut nerve endings
 Increased transmission of pain signals to brain
 Myenteric plexus dysfunction hypermotility, spasm
o Gas formation
 Bacterial overgrowth, gas forming species
 Lactose/fructose/sorbitol malabsorption

14
Q

post-infectious irritable bowel syndrome

A

o IBS follows 7-30% of bacterial dysentery cases (PI-IBS)
o PI-IBS accounts for up to 25% of all IBS cases
o PI-IBS is indistinguishable from other forms of IBS

15
Q

pathogenesis of visceral hypersensitivity in IBS

A

o Peripheral and CNS Factors
o Increased mast cells
o Inflammatory infiltration of myenteric plexus (seen on full-thickness Bx 1)
o Cytokines released by low level inflammation
o Similar inflammatory infiltrate in post-infectious and idiopathic IBD
o Increased sensitivity not directly related to perceived Sx.
o Illness perception and behavior more related to co-existing psychopathology

16
Q

can IBS be caused by stress?

A

o Patients with IBS are typically stressed or depressed
o Stress levels correlate with IBS symptoms
o The stress response can explain most or all of the features of IBS
 Effects of stress hormones (CRF, etc)
 Effects of the autonomic nervous system
o Childhood abuse and/or neglect are associated with lifelong activation of brain stress pathways
o Drugs that block stress hormones (e.g., CRF) block IBS-like symptoms in stressed animals

17
Q

IBS physical findings and lab

A

o Physical findings: normal except sigmoid loop sometimes tender and palpable LLQ (but this is nonspecific)
o Normal pelvic exam in females
o Laboratory and imaging: Normal by definition
o Baseline lab: CBC, thyroid, stool OB, O&P, and WBC, culture (recent diarrhea), TTG
o (+/-flex sigmo or colonoscopy)

18
Q

Features supporting Dx of IBS

A
o	Rome Criteria
o	Long history with relapse/remissions
o	Triggered by stress or life events
o	Variability of Sx
o	Multiple somatic complaints
o	Associated anxiety or depression
o	Sx provoked by eating
o	Distress “out of proportion” to Sx
o	Attachment to “trendy” explanations,  eg
	yeast, pollution, allergies
o	You are treating the SYMPTOMS for IBS!! There is no known cure or cause
	If they have a fever, anemia, blood in stool, its NOT IBS!!
19
Q

IBS diagnosis questionable: red flags

A
o	Recent onset, particularly over 40 yo
o	Blood or occult blood in stool
o	Anemia
o	Fever
o	Weight loss or anorexia
o	Progressive symptoms
o	Localized pain other than LLQ
o	Vomiting
o	Painless diarrhea
20
Q

IBS dx: rome criteria 1

A

o At least 3 month Hx of continuous or intermittent abdominal pain/discomfort AND
o At least 2 of 3 below:
 Relief with defecation
 Onset associated with change in frequency of stool
 Onset associated with change in form of stool
o Additional symptoms supporting Dx include: bloating, mucus, incomplete evacuation
o 100% specificity, 60% sensitivity
o Apply onty after other Dx ruled out
o Useful for selecting groups for studies
o Predicts benign outcome
o Durable diagnosis

21
Q

evaluation of suspected IBS

A

o All patients: Hx, PE, CBC, ESR, thyroid panel, glucose, TTG (looking for celiac dz), stool OB (looking for WBC, etc.), O&P, WBC (or Calprotectin – higher in IBD patients because of inflammation)
o If symptoms severe or predominantly diarrhea:
 sigmoidoscopy or colonoscopy
 serology for celiac sprue and/or malabsorption work-up
o Therapeutic trial of Metronidazole if Hx suggests infectious exposure and “recent” onset

22
Q

IBS: practical approach to amangement

A

o Careful history of dietary habits, concurrent Rx, OTC or self medicated drugs/supplements, coffee, chewing gum, milk products
o Inform patient of expected negative test results before testing
o Mandatory studies: stool OB/O&P/WBC, CBC, thyroid, TTG, colonoscopy in selected cases
o Review all test results with patient

23
Q

IBS managmenet

A

o Validate with patient that symptoms are “real” and consistent with a specific Dx
o Explicitly reassure that IBS symptoms, no matter how severe or persistent, do not predispose to any cancer or other organ injury or degeneration
o Reassure that your attention to patient will continue even if symptoms resolve
o Warn before starting Rx that symptoms will respond slowly, if at all, and will likely recur in future. There is no “cure.”
o Be prepared to re-evaluate from time to time.
o Dietary manipulation:
 One thing at a time
 Reduce coffee, alcohol, tobacco, gum
 List of “gassy’ foods
 Specific elimination of milk or
 Wheat products in selected patients
o Increase in physical activity
o “Antispasmodic” and anti-diarrheal drugs
o Stool bulking agents and other BM facilitators
o Tricyclics or SSRI’s in selected patients
o Newer agents:
 Tegaserod (Zelnorm) for constipation-predominant IBS in women (withdrawn)
 Amitiza (for constipation-type IBS)
o Peripherally active opioids – not yet approved
o “Complementary Rx”– unproven but helpful in selected patients (powerful placebo? )
o Rx small bowel bacterial overgrowth?
o Miralax, cytotec
o SSRI and tricyclic with chronic pain
o High placebo response – no controlled proof of complementary Rx benefits over placebo
o Hypnosis, biofeedback, probiotics better than placebo
o Psych/behavioral Rx: additional benefits in severe IBS
o Hypnosis provides some sustained improvement:
o Key to Rx: Education, validation, support, reassurance, continuity (Comprehensive Self-management Program)

24
Q

IBS pitfalls in managment

A

o Never imply that Sx are “in the head”
o Never suggest that diagnosis is based on the absence of positive lab results
o Extra vigilance in patients with new or progressive symptoms (esp. over 50 yo)
o !!! Weight loss, anemia, bleeding !!!
o High threshold for recommending surgery in IBS patients for apparent concurrent surgical conditions: eg gallstones, diverticulosis, fibroids, “adhesions,” GERD
o Though they may in fact be “in the head”
o Investment of provider’s time is always more productive than additional lab or imaging tests
o Avoid analgesics, especially opiates, in patients with chronic pain
o Problem of “latent “ Celiac Sprue:
 serology and/or small bowel biopsy

25
Q

Ddx epigastric pain

A

o Nonulcer dyspepsia (BY FAR THE MOST COMMON): postprandial fullness, early satiety, epigastric pain
o Typically in young otherwise healthy pts
o GERD: heartburn, regurgitation, dysphagia
o PUD: epigastric pain, worse on empty stomach or offending foods
 postprandial belching, epigastric fullness, early satiation, fatty food intolerance, nausea, and occasional vomiting
o NSAID use
o Gastric tumor (rare): epigastric pain, fatigue, wt loss, anemia; progressive symtpoms

26
Q

length of time for an adequate PPI trial

A

8 weeks

27
Q

dyspepsia etiologies

A
o	GERD >20%
o	Peptic Ulcer 10-20%
o	Non-ulcer dyspepsia (Irritable Bowel Syndrome variant) >60%
o	Cancer (esophagus, stomach) <2%
o	R/O biliary Sx and NSAID use!
28
Q

non-ulcer dyspepsia

A

most common in young adults and teenagers  can’t be proven without an endoscopy but endoscopy is not indicated for people under 55
o Conundrum: In young populations NUD is overwhelmingly the most common cause of dyspepsia, but the diagnosis cannot be proven without endoscopy, and even after endoscopy it is a diagnosis of exclusion and patients are rarely satisfied – especially since no adequate, reliable treatment exists.
o For people with functional dyspepsia with H pylori and GERD, if you treat the H pylori, this does not mean that you have treated the GERD!  they will probably still have dyspepsia

29
Q

initial management of dyspepsia

A

o Endoscopy recommended if:
 “warning signs” present
 new/progressive/refractory symptoms in patient >55 years of age
o All others test and treat for H. pylori*
 Empirical PPI Rx if H. pylori negative: may continue long term
 *No need for H. pylori testing in GERD patients
o Role and timing of GI consult or endoscopy
 Endoscopy rarely reveals anything significant after H. pylori and PPI Rx, and cost is high
 Need for education about “non-ulcer dyspepsia”
 Some patients will “demand” endoscopy

30
Q

nonulcer (functional) dyspepsia

A

o Most common cause of dyspepsia (>60%)
o Not related to H. pylori
o R/o NSAIDs and other drug related enteropathy
o Etiology unknown – ? upper GI variant of IBS?
o Variable pathophysiology: stasis, reduced gastric compliance, duodenal/gastric hypersensitivity
o Distinguish from chronic pain syndrome, psychogenic vomiting, cyclic vomiting, etc
o No reliable effective Rx
o Effective management requires good provider-patient relationship and lots of reassurance

31
Q

long term management of NUD

A

there’s not a lot of long term evidence for what to do with these patients
o Long term PPI or H2 Blocker
o Tricyclics or other antidepressants
o Prokinetic agents
o Biofeedback/stress reduction/psych support
o H. pylori eradication effective in only 5%-10% of patients with “presumed” NUD
o H. Pylori eradicated: 31% symptom-free
o H. Pylori persistent: 26% symptom free
o Conclusion:
 H. pylori treatment is ineffective for most patients with non-ulcer dyspepsia
 H. pylori is not the cause of symptoms in most patients with non-ulcer dyspepsia

32
Q

dyspepsia due to GERD

A

o Don’t expect any improvement with H. pylori eradication
o Lifelong treatment is usually necessary, but may be PRN/intermittent (but how do we treat lifelong? Still unclear)
o Endoscopy indicated after 5-10 years of disease to r/o Barrett’s esophagus
o Consider Surgical anti-reflux Rx (only) in young patients with severe persistent Sx