GI to Appendicitis Flashcards
4 main layers of intestine
1) Serosa
2) Muscularis externa (composed of longitudinal and circular muscle)
3) Submucosa
4) Mucosa (composed of epithelium, lamina propria, and muscularis mucosa)
Fx of submucosa
The submucosa is the layer of dense irregular connective tissue or loose connective tissue that supports the mucosa, as well as joins the mucosa to the bulk of underlying smooth muscle.
Fx of mucosa
The mucosa is the innermost tissue layer of the small intestines, and is a mucous membrane that secretes digestive enzymes and hormones. The intestinal villi are part of the mucosa.
Review structural organization of alimentary canal
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What is diverticular disease?
How does its incidence relate to age?
- Multiple diverticula (an “out-pouching” of the wall of the digestive tract – pouching away from the lumen
- Prevalence = 5-10% of individuals > 45yrs
• 80% > 85yrs
*Strong correlation between age and prevalence!!
Etiology/risks for diverticular disease?
1) Poor DIET (low fibre) → constipation causes accumulation in lumen, pressure on lumen increases (which has already been weakened by process of aging), causing out-pouchings
2) With AGE, diet becomes imbalanced because of changed dentition, cannot be hard things, degenerative changes of tissue
3) INACTIVITY – activity enhances perfusion of GI tract
4) POOR BOWEL HABITS (constipation) – does not as regularly evacuate bowels will contribute to constipation
Patho of Diverticular Disease
- Normal weak points for vessel entry (Are entry points for blood vessels entering wall of intestines…the openings by which these enter are usually tight, will loosen with age)
- Intraluminal pressure inc → mucosa herniates through muscularis externa → bowel protrusion (wall pushes out through itself)
Where (in the GI tract) do the out-pouchings in diverticular disease usually occur? Just one or multiple?
Mostly within sigmoid colon (but can occur in most places in digestive tract) – mostly in large intestine because this is where problem of constipation is
• Multiple sites (usually have several outpouchings…not one single)
2 types of diverticular disease?
1) Diverticulosis
2) Diverticulitis
Difference between two types of diverticular disease?
1) Diverticulosis = non-inflamed out-pouchings (d/t injury or infection)
- Asymptomatic
2) Diverticulitis = inflamed out-pouchings
- Symptomatic
Symptoms of diverticulitis?
o Dull pain, nausea, vomiting, low grade fever
o Aching type of pain
Tx of diverticular disease?
- Address etiology/risks
* Address complications → sx for obstruction or perforation
Why does fever occur in absence of infection?
Damaged cells produce endogenous pyrogens
rest of mechanism is the same
What is IBS?
What is the problem?
- GI Mobility disorder
- Almost everyone has some level of it (is spectrum)
- No obvious abnormality in structure or function, pathology unclear
Etiology of IBS?
- Unclear (but are risk factors)
* Linked to diet, stress, smoking, lactose intolerance
Why is smoking associated with IBS?
Smoking has series of noxious components that circulate within body, can cause intestinal cancers, etc….
What is thought to be the pathology of IBS?
Patho not apparent but are speculated ideas:
1) Malabsorption of fermentable CHO and polyols- suggests we have fermentable CHOs (ex: fructose) and polyols (sugar alcohols, ex: sorbitol) then when ingested by those with IBS, are not properly processed (in small intestine or stomach?) - in colon the bacteria process these sugars and produced gas → end up with flatulence → Gas distends the intestine, presents with pain
2) Altered CNS regulation of GI motor and sensory fx?
know CNS innervates digestive tract and is largely involved in regulating motility of the gut (also perfusion, secretion, etc.)…suggestion of theory is that there’s a problem either in CNS or where neurons meet digestive tract (such as synapse) that effects
3) Molecular signaling defect of serotonin
(is produced in mucosa of gut…thought that process of synthesis, release, storage, action, and/or degredation is defective
Functions of Serotonin:
1) Mediates motility in the gut
2) Involved in sensation/pain
3) Involved in secretion
4) Involved in perfusion (vasodilation/constriction)
What main pieces of evidence show that a seronin defect may be involved in IBS?
1) Site of synthesis - produced in mucosa
2) Serotonin action & IBS manifestations
- Fxs of serotonin very much linked to symptoms of IBS
- If serotonin is functioning normally, should not feel sensation/pain of peristalsis…IBS do
Symptoms of IBS
- Abdominal discomfort & pain
- Constipation &/or diarrhea – can occur in same person; depends on what person is eating (food is trigger for one of these issues)
- Flatulence, nausea
- Mucoid stool (with excessive mucous secretion)
Dx of IBS?
• Problem because no obvious pathology
• Work through process of exclusion (excluding organic disease…such as infection of the gut, which would present with very similar symptoms)
o Various labs (cbc, stool exam looking for ova of parasites, likely barium swallow [to see structural defects such as ulcers]
• Scopes: endoscopy, colonoscopy
• Presentation: what food causes it, how it presents
What prep does endoscopy and colonoscopy require?
- endoscopy requires overnight fasting
- prep for colonoscopy is over 2 days, need clean lower bowel)
Tx of IBS?
• Very difficult • Based on severity and type • Avoid offending foods • Reduce stress • Drugs (if moderate to severe) --> Often have sposmatic pain → antispasmodics prn (reduce motility), ex: modulon --> Antidiarrheals ---> Constipation drugs ---> Antibiotics used with caution → to maintain normal flora in check
What is peritonitis?
What is the peritoneum?
Inflm of peritoneum
The peritoneum is a membrane made up of two layers. One layer lines the cavity and the other layer lines the organs. The peritoneum helps support the organs in the abdominal cavity and also allows nerves, blood vessels, and lymph vessels to pass through to the organs. The parietal peritoneum lines the abdominal wall and extends to the organs, whereas the visceral peritoneum covers the organs. The peritoneal cavity lies between these two peritoneal layers. It contains a thin layer of fluid that lubricates the peritoneal surfaces.
Etiology of peritonitis?
- Bacterial (esp E. Coli) or chemical irritation (bact moves out from gut into body cavity)
- Offending agent enters abdm cavity via: Perforated ulcer or ruptured appendix
- PID (pelvic inflammatory disease) is important risk
- Several other conditions can lead to peritonitis
- Spread of bacteria d/t perforation of wall of colon possible with colonoscopy
Why is PID (pelvic inflm disease) an important risk factor for peritonitis?
infection ascends into reproductive tract, infundibulum open to body cavity so bacteria can exit here (from filopian tube)
What bacteria are normally found in the body cavity?
None - is normally sterile!
Patho of peritonitis
1) Agent impacts peritoneum –> inflm
2) Easy spread (because is large structure) and rapid absorption of toxins into bloodstream (Blood vessels extensively spread through mesenteries, if bacteria enter here, becomes systemic)
3) Thick exudate forms (sticky)
How is the thick exudate that forms during peritonitis advantageous?
it localizes infection by preventing it from spreading to rest of peritoneum and can plug the hole that allowed the infection to occur → seals perforation and localizes infection
Body’s compensatory response to peritonitis?
SNS limits GI motility → why? so gut content is not propelled, limiting movement of material out of the perforation
Manifestations of peritonitis
- Severe (have systemic systems coming from localized problem which is usually sever problem)
- Fluid shifts (formation of exudate draws fluid in)
- Reduced gut motility –> as result, ileus, fluid and air retained, inc in pressure, inc in fluid secretion –> increases intraluminal pressure in the gut –> Potential distension and rupture of colon
- Altered perfusion: blood shunted to site of inflm (have hyperemia at site)
- Dyspnea
Ileus = ?
Cessation of peristalsis
Why does an increase in fluid secretion occur?
When gut is “upset” it will “cry”….increasing fluid secretion (largely mucous)
Outline why fluid shift occurs with peritonitis
** REVIEW: says to go back and look at look at inflm and vacular response
The resulting inflammatory response leads to massive fluid shifts (peritoneal edema) and adhesions as the body attempts to wall off the infection.
Why does dyspnea result in peritonitis?
Will avoid moving the diaphragm because it’s painful
Tx of peritonitis
- IV Abx
- Anti-inflm
- Fluids and electrolytes (to compensate for fluid shifts)
- Pain meds
- Sx if indicated (thick exudate needs removal or to correct perforated colon, etc.)
Fx on appendix
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What is appendicitis?
Incidence peaks at what age? Typically occurs in what range of ages?
- Acute inflm of appendix wall
- Peaks at 20-30 years of age (but possible at any age)
- Common between 5-30yrs – reason for this trend in prevalence is not known
Etiology of appendicitis:
- Idiopathic
- Two suggested theories: obstruction of appendix by hard fecal pellet (fecalith obstructs cecum) or twisted appendix or bowel
Explain how the proposed two causes of appendicitis come about?
- Appendix has mesentery coming from sides that attaches it to other parts of gut; If entry to appendix is blocked, will see accumulation of contents, increased pressure in lumen, inc secretion of mucous in the lumen (and therefore greater pressure)….this is one suggestion of what causes appendicitis
- Other suggestion is that appendix is twisted, or shifting and twisting of other connected parts (mesenteries) causes twisting of the appendix as well….is blocked off
Pathology of Appendicitis (if suggested etiology is true)
• Appendix lumen obstructed (either by fecal obstruction or twisting) → drainage into cecum blocked → inc luminal pressure (causing further secretion of mucus, which compounds this issue) → exceeds venous pressure → venous stasis (intraluminal pressure now greater than venous pressure)→ ischemia → necrosis of cells → bacteria invade wall (previously normal flora enter where cells have become necrotic)
Complication of appendicitis
perforation – leading to possible peritonitis
Manifestations of appendicitis
- Describe progression of pain
- PAIN
- Fever
- Nausea and vomiting
- Increased WBC on labs
Pattern of pain:
– has unique pattern acute onset without warning; originates in epigastric region or periumbilical pain (referred pain)
–> Pain increases
–> Then colicky over 12hr (colicky = spasmodic; waves of pain)
–> Then migrates to become localized to LRQ (rebound and gaurded pain
–> Ultimately pain focuses on McBurney’s Point (midpoint between umbilicus and iliac crest)
Why is pain in appendicitis described as rebound and guarded?
pain felt on release of palpation; also described as guarded pain → will go into fetal position (bring knees to chest) in order to relax muscles and minimize pain)
Why does nausea and vomiting result in appendicitis?
– is GI problem and this is manifestation of any GI problem; also d/t pain
Why fever in appendicitis?
d/t infection
Dx of appendicitis
- Hx and Px ESSENTIAL (follow pattern of pain)
- Ultrasound
- CT scan (if necessary)
Tx of appendicitis?
- IV Abx
- IV fluids
- Appendectomy within 24-48hrs (if delayed, possible perforation and peritonitis)
Why are IV fluids administered for appendicit?
will see fluid shifts here with perforated appendix → with exudate formation, have fluid following out
What causes diverticulosis?
d/t injury or infection
