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GI > Nichols + ??? 3 > Flashcards

Nichols + ??? 3 Flashcards

1
Q

Constipation

A

-Infrequent BM <3/week for 12 months with straining/feeling of incomplete evacuation/hard stool at least 25% of time

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2
Q

Normal Colonic Motility

A
  • motor function depends on contraction of circular layer of smooth muscle
  • has 3 patterns of contractions
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3
Q

Short Duration Colonic Contractions

A

Stationary Motor Contractions

  • Present over short areas of colon
  • Causes mixing of fecal material and extraction of water
  • Persists for <15 seconds
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4
Q

Long Duration Colonic Contraction

A
  • may be stationary or propagate for short distances
  • may travel in orad or aboral direction
  • assists in mixing and local propulsion of feces
  • migrates toward rectum in distal colon
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5
Q

Giant Migrating Complexes of Colon

A
  • propagates aborally aver extended distances
  • causes mass movement of feces
  • normally occurs 1-2 times/day
  • may be precipitated by colonic distention
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6
Q

Food Intake & Colonic Motility

A
  • food causes increased segmental activity
  • gastrocolic reflux-may be mediated by CCK
  • response is proportional to caloric content of meal
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7
Q

Hormones & Colonic Motility

A

CCk causes increased frequency & amplitude of segmental contractions
PgF
PgE
Serotonin

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8
Q

PgF

A

stimulates longitudinal muscle contraction

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9
Q

PgE

A

inhibits circular muscle contraction

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10
Q

Serotonin

A

mediates intestinal peristalsis and secretion in GI tract as well as modulation of pain perception

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11
Q

Role of Serotonin

A
  • serotonin (5-HT) is an important neurotransmitter in the brain-gut interaction (released by enterochromaffin cells)
  • 80% of total body 5-HT located in GI tract
  • 5-HT3 receptor antagonists have offered some help in alleviating pain in IBS and functional dyspepsia
  • 5-HT4 receptor agonists have a prokinetic effect in humans
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12
Q

Epidemiology of Constipation

A
  • 12-19% of people
  • more common in individuals with little daily physical activity, low income, and poor education
  • in patients 65 years of age, especially more in women
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13
Q

Constipation: Pediatric Etiology

A 
95% functional 
5% organic 
-anatomic
-metabolic 
-neuropathic
-drugs
-endocrine connective tissue D/O
-lead intoxication or botulism
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14
Q

Functional Constipation

A
  • infants and pre-school

- 2 weeks duration Pebble-like, hard stools

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15
Q

Functional Fecal Retention

A
  • common cause of chronic constipation

- with fear and toilet refusal from infancy to 16 years old

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16
Q

Constipation: Elderly

A
  • endocrine and metabolic disease
  • neurologic disease
  • psychological conditions
  • structural abnormalities
  • lifestyle
  • iatrogenic (meds)
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17
Q

Constipation Diagnosis

A
  • H&P/other medical conditions
  • evaluate current meds
  • rule out thyroid disorders or electrolytes problem
  • colonoscopy or Barium Enema
  • colon transit of markers
  • anorectum manometry
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18
Q

Lab Data of Constipation

A

performed in patients with rectal bleeding, weight loss of >10lbs, a family history of colon cancer, IBD, anemia, positive fecal occult blood, short-term constipation

  • CBC
  • serum glucose, creatinine, calcium
  • TSH
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19
Q

Malabsorption

A
  • problem in GI lumen, Defects in epithelial absorptive surface, post-epithelum defect
  • steatorrhea, carbs, proteins
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20
Q

Steatorrhea

A

greater than 5% of dietary fat intake

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21
Q

Patients with steatorrhea?

A
  • weight loss
  • stool characteristics
  • osteomalacia
  • easy bruising
  • Fe deficiency anemia not due to blood loss
  • adult dev. of lactase insufficiency
  • gastric surgery, specially Billroth II
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22
Q

Steatorrhea Stool Characteristics?

A
  • floats
  • greasy
  • stinks
  • hard to flush
  • oil droplets with minimal stools
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23
Q

Mechanisms causing diarrhea in steatorrhea?

A
  • increase of osmotically active particles of mal-absorbed dietary constituents
  • hydroxylation of 10-hydroxy-oleate which acts as cathartic
  • fatty acids themselves impair fluid & electrolyte absorption
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24
Q

Diagnostic Studies with Steatorrhea?

A
  • chemical fat balance, D-xylose absorption, secretin test, X-ray (flat plate of abdomen, CT scan, barium)
  • hydrogen breath test, aspiration of duodenal content for giardia & quant
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25
Q

Stages of Malabsorption

A
  1. Intraluminal Stage
  2. Intestinal Stage
  3. Lymphatic Transport Stage
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26
Q

What Causes the most Steatorrhea?

A

pancreatic insufficiency

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27
Q

Intraluminal Stage

A

-chronic pancreatitis
-Zollinger-Ellison Syndrome
-Post-gastrectomy
-cystic fibrosis
Solubilization: bile acid insufficiency
-cholestatic liver disease, terminal lleum resection, bacterial overgrowth in small intestine, reduced CCK released

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28
Q

Effects of Impaired Circulation of Bile Salts

A
  • diarrhea and if severe steatorrhea
  • increased proportion of the bile acids pols conjugated with glycine vs. taurine
  • increased proportion of deoxycholate in bile
  • a reduced bile salt pool size
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29
Q

Intestinal Stage

A

Epithelial cell surface digestion

  • Disaccharidase Insufficiency
  • Stasis Syndrome
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30
Q

Intestinal Stage: Intestinal Cell Dysfunction

A
  • gluten sensitivity enteropathy
  • stasis syndrome
  • whipple’s disease
  • intestinal ischemia
  • radiation enteritis
  • tropical sprue
  • genetic disorders such as cystinuria
  • anderson’s disease
  • abetalipoproteinemia
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31
Q

Causes of Malabsorption of GSE

A
  • Cells at surface of intestine are immature:
  • intestine is in a secretory state (Na-Cl-water)
  • conc. of bile salts above their CMC is reduced
  • absorptive functions of mature enterocytes (disaccharidases, Fe, Ca) are reduced
  • complex lipid synthesis is reduced
  • Endocrine Cells that produce CCK are reduced
  • absorptive area of intestine is greatly reduced
32
Q

GSE Pathogenesis & Treatment

A
  • inciting agent is gluten in a person with the right genetic background
  • treatment: remove exposure to gluten foods
  • clinical response to the gluten exclusion diet is mandatory to sustain a diagnosis of GSE
  • If NO response: patient is exposed to hidden sources, patient has GSE plus pancreatic insufficiency or the stasis syndrome, patient has a cause of villous atrophy other than GSE
33
Q

Diagnosis of GSE

A

IgA antibody ELSIA in detection of GSE

sen. 95-98%
spec. 94-95%

34
Q

Unexplained Causes of Steatorrhea

A
  • giardiasis
  • adrenal insufficiency
  • amyloid
  • diabetes
  • hyperthyroidism
  • combined variable immunodeficiency
35
Q

Lymphatic Transport Stage

A

-lymphatic duct obstruction: lymphoma, Whipple, Intestinal lymphangectasia, TB, carcinoid

36
Q

Pathology: Celiac Sprue/Gluten Sensitive Enteropathy

A

villous blunting
CD8
-noninfectious cause

37
Q

Viral Gastroenteritis

A

temporary dissacharidase deficiency

38
Q

Whipple Disease

A
  • rare intestinal, lymph node, cerebral, cardiac and joint infection with Tropheryma whippelii
  • PAS stain-positive actinomycete
  • late middle age white males
39
Q

Radiography with Constipation

A
  • plain films of abdomen: megacolon, impaction
  • barium enema
  • colon transit study (sitz marker)
  • defecography
40
Q

Sitzmarks

A
  • different techniques
  • Pt takes 1 capsule on day 0, check X-ray day5
  • if over 80% of the marker are passed by day 5 than colon transit normal
41
Q

Severe idiopathic chronic constipation

A
  • mostly women

- complaints include infrequent defecation, excessive straining when defecating, or both

42
Q

Sitz marker study

A
  • Normal Colonic Transit
  • Colonic inertia: with delayed passage of marker through proximal colon and no increase in motor activity after meals or with the administration of laxatives
  • outlet delay: in which markers move normally through colon but stagnate in rectum (more common in pelvic floor dyssenergia)
43
Q

Pelvic Floor Dyssynergia

A

Defecation Normally: involves relaxation of puborectalis and external anal sphincter muscles, together with increased intraabdominal pressure and inhibition of colonic segmenting activity

In Dyssynergic Defecation: ineffective defecation is associated with a failure to relax, or inappropriate contraction of, the puborectals and external anal sphincter muscles

44
Q

Severe Idiopathic Constipation

A
  • in one study frequency of the different abnormalities that can produce severe idiopathic chronic constipation
  • slow transit constipation 11%
  • dyssynergic defecation 13%
  • combo 5%
  • IBS 71%
45
Q

Treatment of Constipation

A 
Education: increase fluid & fiber intake
Laxatives
Lubiprostone: Cl channel activator
5HT4 agonists: Prucalopride
Bio-feedback
Surgery: sub-total colectomy with ileorectal anastomosis 
Suppositories: glycerin or bisacodyl
Disimpaction: patients with fecal impaction
46
Q

Fiber & Laxatives

A

Fiber: improve symptoms, bulk forming laxatives, Metamucil, methylcellulose, Ca poycarbopphil
Stool softners: docusate sodium
Osmotic Agents: polethylene glycol, lactulose
Stimulant Laxatives: bisacodyl, senna

47
Q

Lubiprostone

A

-locally acting chloride channel activator that enhances chloride-rich intestinal fluid secretion (anticonstipation)

48
Q

Misoprostol

A

prostaglandin analog

49
Q

Prucalopride

A

5HT4 prokinetic agent

not in US

50
Q

Hirschsprung Disease

A

-congenital disorder: obstipation from birth and colonic dilatation proximal to a spastic, non-relaxing and nonpropulsive segment of distal bowel MEGA COLON

51
Q

Hirschsprung Disease: Pathogenesis

A

absence of ganglion cells in large bowel, functional obstruction and proximal dilatation

52
Q

Hirschsprung Disease: Epidemiology

A

1:5000-8000
males>females 4:1
10% of cases in Down’s Syndrome
most sporadic, few familial

53
Q

Hirschsprung Disease: Heterogeneous defects in genes regulating

A
  1. migration and survival of neuroblasts
  2. neurogenesis
  3. receptor tyrosine kinase activity
54
Q

Hirschsprung Disease: Presentation

A
  • failure to pass meconium
  • obstructive constipation, occasional passage of stool
  • bouts of diarrhea, abdominal distention
55
Q

Physiological Definition of Diarrhea?

A

> 200gm stool per day

56
Q

Normal stool frequency?

A

3 bm a week to 3 bm per day

57
Q

Fluid Input Into Gut?

A 
Ingestion 2L
Saliva 1.5L
Gastric Secretions 2L
Bile 0.5L
Pancreatic Secretions 1.5L
Small Intestinal Secretions  1L
58
Q

Function of Na+ in Fluid Absorption: Small Intestinal Villi

A
  • Na+/glucose co-transporter

- Na+/H+ exhanger

59
Q

Function of Na+ in Fluid Absorption: Large Intestinal Crypts

A

-epithelial Na+ channel (ENaC)

60
Q

Increased Intraluminal Fluid: Pathophysiological Mechanisms

A
  1. Decreased Absorption (osmotic)
    - ingestion of unabsorbable solute
    - osmotic draw of fluid into the gut lumen
  2. Increased Secretion
    - active secretion of electrolytes + fluid into lumen
    - electrolytes comprise most stool osmolality
  3. Inflammation
    - mediators stimulate secretion
    - epithelial barrier compromised by cell death
61
Q

Causes of Osmotic Diarrhea

A
  1. Non-absorbable carbohydrates
    - lactose (milk, yougert, cheese)
    - sorbitol, mannitol
    - lactulose
  2. Non-absorbable electrolytes (laxatives)
    - Mg2+ compounds
    - Golytely (PEG) prep for colonoscopy
    - fleet phoshphosoda prep
  3. Miscellaneous
62
Q

Key to Secretory Diarrhea?

A

-excessive Cl- secretion into the gut

63
Q

Osmotic VS Secretory

A

volume: moderate vs voluminous, watery
resolves w/fasting vs persists during fasting
much flatulence vs no flatulence
stool ph < 5.3 vs ph 6-7
osmolar gap > 125 vs <50

64
Q

Causes of Secretory Diarrhea

A
  1. Bacterial toxins (cholera, heat stable e.coli, yersinia)
  2. Laxatives: senna, phenolphthalein, bisacodyl, ricinoleic acid (caster oil)
  3. meds: cholinergics, prostaglandins
  4. Chemical irritants: bile, arsenic, caffeine, ETOH
  5. Neuroendocrine tumors: VIPoma, carcinoid, medullary carcinoma of thyroid
65
Q

Acute Diarrhea

A 
< 3 weeks
infectious
secretory or inflammatory
self-limited
supportive care (mostly)
66
Q

Most common cause of Diarrhea in US?

A
  • viral
  • E. coli
  • campylobacter (bloody)
  • salmonella, shigella (bloody)
  • giardia (bad water)
  • cryptosporidium (aids)
  • c. difficile (hospital)
67
Q

Diarrhea cause in third world?

A
  • viral
  • campylobacter
  • E. coli
  • vibrio cholerae
  • entameba histolytical
  • salmonella, shigella
  • cryptosporidium (infants)
68
Q

Traveler’s Diarrhea

A

20-60% of travelers to third world
Prophylaxis recommendations: cooked food only, bottled beverages, no ice, wash hands before meals, peptobismol
-if diarrhea: fluids, anti-diarrheals, ciprofloxacin if severe

69
Q

Traveler’s Diarrhea: most common cause

A

E. Coli (40%)

70
Q

C. Difficile Colitis

A

Risk factors: abx use, extremes of age, hospitalization, institutionalization
Cause: Cytotoxins A & B
Diagnosis: pseudomembranous colitis on endoscopy, stool assay
Treatment: stop abx, metronidazole or vancomycin po, cholestyramine to bind toxins

71
Q

Chronic Diarrhea

A 
> 3 week duration
-infectious, immune-mediated, malabsorption
-osmotic, secretory (no mucosal injury)
-inflammatory (mucosal injury)
variable prognosis 
-special interventions required
72
Q

Clinical Features of Lactase Deficiency

A
  1. osmotic diarrhea
  2. flatulence
  3. acidic stool pH
73
Q

Irritable Bowel Syndrome

A

-common cause of chronic diarrhea in US
-disorder of motility & pain perception
-Diagnosis-abdominal pain, bloating, symptoms associated with bowel functions, no weight loss, bleeding, malnutrition, or anemia
Treatment: anti-cholinergic meds (diarrhea), 5-HT receptor antagonists (constipation), reassurance

74
Q

Microscopic Colitis

A

2 Types
-Lymphocytic colitis
-Collagenous colitis
Chronic watery, non-bloody diarrhea in adults
Treat: bismuth, aminosalisylates, steroids

75
Q

Behcet’s Disease

A 
generalized vasculitis
-oral & genital aphthous ulcers
-uveitis
-GI tract ulcers
-non-erosive arthritis
Treatment: immunosuppressives

GI (19 decks)

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