Inflammatory Diseases Flashcards
What is diverticular disease?
- bowel protrusions called diverticula (sing: diverticulum)
- pressure pushes against wall, if wall is weakened it bulges out
- multiple sites, but mostly in sigmoid colon
Etiology of diverticular disease:
- aging (80% >85yr; 40% >45yr)
- poor diet (low fibre diet) causing constipation which increases intraluminal pressure
- inactivity/poor lifetsyle
- poor bowel habits (constipation causes increased intraluminal pressure)
Pathophysiology of diverticular disease?
- normal weak points for vessel entry (vessel entry points in GIT = weak points on bowel wall)k
- increased intraluminal pressure –> mucosa herniates through muscularis externa –> diverticula form
- diverticulosis
- diverticulitis
Diverticulitis
- inflamed, perforated diverticula caused by
=compression at point of entry
=strangulation
=increased pressure in pouch
=risk of perforation/rupture of diverticula leads to release of intestinal bacteria and wastes in the the body
=risk for further complication
Diverticulosis
- noninflamed
- asymptomatic
- low risk of obstruction within bowel
Two factors needed for diverticula to form?
1) increased intraluminal pressure
2) weakened bowel walls
Manifestations of diverticular disease?
dull pain, nausea & vomiting, low-grade fever
Dx & Tx of diverticular disease?
Dx: CT (identifies number and location of)
Tx: address etiology/risks (improve diet/lifestyle), surgery (for obstruction of perforation)
Irritable Bowel Syndrome?
- common motility/sensory distorder
- individuals with IBS detect peristalsis and experience pain
- no obvious pathology (no abnormal structure or biochemistry)
Etiology of IBS
- unclear
- proposed links: lactose intolerant, diet, stress, smoking
Patho of IBS
- malabsorption of polyps and fermentable CHO (e.g. ethanol, sorbitol)
= when digested by bacteria in lg int, gas is produced as a byproduct –> pain & flatulence (gut flora process cause flatulence) - altered regulation of GI motor and sensory function (CNS regulation)
- molecular signalling defective for serotonin (NT that activates neurons in the bowel)
= site of synthesis: gut mucosa is primary sight of synth
= function and IBS manifestations: function of serotonin affected by molecular signaling, resulting in manifestations of IBS: 1) alternating diarrhea and constipation (cx: gut motility/peristalsis) 2) secretion in gut = excess mucous in gut = mucoid stools 3) involved in perfusion of bowels –> decrease function 4) sensation in gut (peristalsis) causes pain 5) abdominal discomfort and pain 6) flatulence
Dx of IBS
- exclude organic pathology thru various labs (analyze stool for parasites or ova of parasites) and scopes (colonscopy, sigmoidoscopy, gastroscopy)
Manifestations of IBS
- varied severity
- alternating diarrhea and constipation
- abdominal discomfort and pain
- flatulence, nausea
- mucoid stools
Tx of IBS
- avoid offending foods
- decrease stress
- drugs prn
=antispasmodics (inhibit bowel spasms to relieve discomfort and pain)
=antidiarrheals
=laxatives
both help with alternating bowel pattern
=antibiotics (CAUTION!!! do not eliminate normal gut flora, just control overgrowth): manage the production of flatulence
Peritonitis
Inflammation of the Peritoneum
Etiology of peritonitis
1) Bacteria (mostly E. coli; even n. flora)
- exit normal niche –> infection –> inflammation
2) Chemical irritation
- HCl, bile, enzymes leak out of gut
3) Agent enters abdominal cavity
- perforating ulcer
- ruptured ulcer
- chemically burns a hole through the stomach or duodenum
4) PID (pelvic inflammatory disease)
- bacteria migrate up the reproductive tract up to the fallopian tubes, exit through the infundibulum into the body cavity
5) Others (less frequentely)
- trauma
- foreign objects move into the peritoneum
PID
Pelvic Inflammatory Disease:
- bacteria migrate up the reproductive tract up to the fallopian tubes, exit through the infundibulum into the body cavity
Pathophysiology of peritonitis
- Initially, an agent impacts the peritoneum –> inflm
- peritoneum = large structure = 2 disadvantages
1) highly vascularized: bacteria can enter the bloodstream and spread easily
2) rapid absorption: toxins produced by bacteria are rapidly absorbed; potential for systemic distribution - with inflm, production of purulent exudate
- localizes inflammation:
- contains fluid, defense cells, bacteria, proteins
giving it a thick consistency –> slows down
spread throughout body cavity; therefore,
limits spread of agent/bacteria; therefore,
localizes inflammation.
- seals perforation
- decreases/prevents content leaking out of
hole in gut
- NOT COMPENSATORY - SNS limits GI motility (compensatory)
- prevents gut content being pushed towards
perforation via ileus (cessation of peristalsis)
Manifestations of peritonitis
- Severity
- fluid shift into bowel and abdominal cavity
- with inflm there is vasodilation and hyperemia, so
capillary hydrostatic pressure increases in the
abundant vessels of the peritoneum. Fluid shifts
out of vasculature into the abdominal cavity. - blood shunted to site of inflm
- perfusion altered -> blood shunted to site of inflm - pain (symptom of inflm), vomiting (d/t severe pain
activating the vomit reflex centre) - dyspnea
- breathing irritates inflamed peritoneum when
diaphragm pushes on it, pt minimizes depth of
respiration
Tx of peritonitis
- IV Antibiotics
- Nasogastric suction: prevent content of stomach to move towards perforation.
- Fluids and Electrolytes: potential for hypervolemia and electrolyte imbalance.
- Anti-inflammatories
- Pain medications
- Surgery: if indicated
Appendicitis
Acute inflammation of the appendix
Peaks at 20-30 yrs
Appendix & Theories for its function
k
Etiology of appendicitis
Idiopathic
Two theories:
1) fecalith obstructing the cecum
2) twisted appendix or bowel (obstructs entrance and exit of secretions & blood flow.
Pathophysiology of appendicitis
Lumen obstruction –> drainage from the cecum blocked –> increased luminal pressure –> pressure pushes on highly vascularized wall –> blood vessels pinched shut –> exceeds venous pressure –> venous stasis –> ischemia and eventually infarction –> necrosis of the tissue wall –> bacteria invade appendix wall –> infection within wall of appendix –> leads to inflammation of appendix wall –> swelling and production of exudate.
Manifestations of appendicitis
- Epigastric pain or Periumbilical pain (referred pain)
- N & V (pain activates N&V reflex centre)
- Pain increases from an ache to colicky, spasmodic pain over the next 12 hrs
- Pain localizes to LRQ (localized pain)
- Rebound Pain (palpate & release –> pain on release)
- Guarded Pain
- Increased temperature & WBC (running a fever)
- Pain localizes to McBurney’s Point (located midway between the iliac crest and umbilicus; where the base of the appendix attaches to the cecum)
Dx, Tx, & Complx of appendicitis
Dx: Hx, Px, US (size to determine risk of rupture), CT
Tx: IV fluids, Abx, Appendectomy (24-48hrs)
Complx: perforation & peritonitis
IBD
Inflammatory Bowel Disease: chronic inflammation of the small and large intestine
Etiology of IBD
1) Genetic Susceptibility (HLA/MHC genes)
2) Immune Response against normal flora of GI tract (not classic autoimmunity because IR is not targetting intestinal wall, but the bacteria attached to the intestinal wall)
3) Environmental Trigger (complex train etiology always has environmental trigger)
Two conditions of IBD
1) Crohn’s disease
2) Ulcerative colitis
Differences between Crohn’s disease and ulcerative colitis
Crohn’s Disease Ulcerative Colitis
- Granulomatous - ulcerative & exudative
- primarily submucosal - primarily mucosal
- skip lesions - continuous
- primarily ileum, sm int, - primarily rectum & L. colon
secondarily colon
- diarrhea common - diarrhea common
- rectal bleeding common - rectal bleeding common
- fistulas common - fistulas rare
- strictures common - strictures rare
- Perianal abscesses - perianal abscesses rare
common
- CA uncommon - Ca relatively common
Crohn’s disease
- one of two conditions of Inflammatory Bowel Disease
- primarily affects submucosa (second layer; dense irreg. tissue) of the terminal ileum; other areas and all layers can be affected.
- type of inflammation: granulomatous (bumbs of scar tissue; cobblestone appearance seen in scope)
- Extent of inflammation: skip lesions
- Slowly progressive, non-aggressive
Manifestations of Crohn’s disease
- Intermittent diarrhea (d/t lining of the GI tract impacted by inflammation)
- abdominal pain (r/t inflammation; colicky, spasmodic pain)
- weight loss d/t decrease in absorptive surface area causing nutritional deficiency
- change to ileum’s absorptive s.a –> non-fx tissue
–> nutritional deficiency (diarrhea & loss of
appetite contribute also) - fluid-electrolyte imbalance (d/t diarrhea; monitor on an ongoing basis)
Ulcerative colitis
- one of two conditions of IBD
- primarily affects mucosa (inner lining of lumen) in colon and rectum
- progressive proximally from the rectum
- continuous lesions
=bleeding ulcers (a.k.a. lacerations: cut in tissue/open sore)
=thickened inflammation areas (tissue) (extensive inflammation and scarring causing substantial exudate in gut causing congestion in gut) - edema and congestion (from exudate)
- crypt abscess
=Crypts of Leiberkuhn (intestinal cript or intestinal gland that normally secrets digestive enzymes and regenerate new tissue when damaged; accumulation of pus in crypts prevents regrowth of new tissue (thought to lead to colorectal CA) - pseudopolyps
=polyps (invagination of granulation tissue into lumen)
=pseudopolyps have the appearance of polyps but have inflamed tissue; therefore substantial amt of exudate produced, which can result in edema, and fluid in the lumen can cause congestion
Manifestations of ulcerative colitis
- bloody diarrhea (d/t ulcers)
- abdominal cramping causing pain
Dx of IBD
- Hx, Px (to exclude appendicitis, peritonitis
- scoping (colonscopy, sigmoidoscopy, biopsy)
- labs to exclude GI infection
Tx of IBD
- anti-inflammatory (sulfasalazine)
=d/t targetting of normal flora causing inflammation of the gut
=not targeting self-tissue, but still autoimmunity (not classic) - steroids (short-term in non-responsive cases to bring down inflammation then try anti-inflammatories again)
- immunomodulator (methotrexate): IBD=immune problem by targeting normal gut flora cx inflm)
- Antibiotics (low dose to control growth of norm flora)
- Surgery
=repair fistulas (cause bowel obstruction)
=drain ulcers and/or abscesses
=bowel resection (remove a section/entire portion of bowel; possibly resulting in permanent ostomy if anal sphincter cannot be salvaged) - avoid: caffeine, spicy foods, dairy (aggravate sympt)
- lifestyle modifications
Complication of Appendicitis
perforation (d/t excessive pressure)
Complications of Crohn’s Disease
- Fistulas: abnormal passage between a hollow/tubular organ and the body surface, or between two hollow/tubular organs
- abscesses: swollen area of the body (in this case the perianal area), containing an accumulation of pus
- bowel obstruction (may require sx)
Herniation
- organ protrusion through retaining structure
- usually in abdominal cavity (abdominal organ moving out of a weakened area on body wall/projection from one organ cavity to another)
Pathophysiology of Herniation
- weakened retaining structure (e.g. muscle)
=acquired through injury, sx on abdominal cause weakened are at incision point
=aging (degenerative)
=congenital: born with weakened wall - increased intra-abdominal pressure (pressure within abdominal cavity)
=pregnancy or obesity –> herniation
Hiatal Hernia
- hiatus (a gap in sequence): the aperture/hole in the diaphragm for the esophagus
- hiatus enlarges (d/t age, injury, etc.)
- part of stomach protrudes into thoracic cavity (d/t increased pressure in abdominal cavity)
Two Types of Hiatal Hernia
1) Axial or Sliding Hiatal Hernia
2) Paraesophageal, Nonaxial, or Rolling Hiatal Hernia
Axial or Sliding Hiatal Hernia
- 95%
- Gastroesophageal Junction (GEJ) and upper part of stomach protrude into thoracic cavity
- bell-like protusion
- approx. 50% asymptomatic (no tx)
- approx. 50% symptomatic: gastric reflux & heartburn
Gastric Reflux
churning of food in stomach with acid –> hiatus squeezes on stomach –> cardiac sphincter cannot stay closed d/t increased pressure –> contents move up esophagus. Content contains HCl: pH 2
Heartburn
- pain from gastric reflux
- in vicinity of chest
- esophagus does not have protective epithelial lining like the stomach –> pain is from destruction of tissue.
Paraesophageal, Nonaxial, or Rolling Hiatal Hernia
- non- upper part of stomach enters thoracic cavity
- GEJ remains below diaphragm
- Symptoms: pain, dyspnea, fullness
=Pain: chest. Herniated fundus can compress esophagus and cause food to get stuck in the esophagus and impede passage into stomach
=Dyspnea: herniated fundus take space in thoracic cavity. may impede left lung expansion and cause difficulty breathing.
=Fullness: herniated portion of stomach forms a mini-stomach –> activates stretch receptors that signal brain –> pt has false sense of being full.
Dx of Hiatal Hernias
- scopes
- barium swallow: ingest barium –> take CXR to indicate changes in GIT
Tx of Hiatal Hernias
- modify lifestyle (least invasive first)
=modify diet: avoid foods that increase secretion of acid; smaller frequent meals.
=behavior: do not bend down abruptly, sleep with HOB elevated, avoid food and liquid before bedtime, avoid smoking and caffeine, no bending at the hip. - drugs:
>antacids
>proton pump inhibitors (PPIs): inhibit pumping of H+ ions
>H2 Receptor Antagonists (H2RA): block the H2 receptor and interfere with formation of HCl. - surgery (approx. 15%): if discomfort severe and function of heart and lungs impacted.
>fundoplication: fundus of stomach is wrapped around the GEJ and stomach –> GEJ made wider and unable to slip up through an enlarged hiatus
Inguinal Hernia
- abdominal organ protrudes via the inguinal canal
=requires: weakened aperture of inguinal canal and increased intra-abdominal pressure - peritoneum forms hernia sac (contains intestine and omentum)
-requires Sx (d/t pain)
Indirect Inguinal Hernia
the intestines enter the inguinal canal
Direct Inguinal Hernia
the intestines exit through the body wall
Peptic Ulcer Disease
- ulcerative disorder of the lining of the stomach (20%) and/or duodenum (80%)
- primarily affects mucosa
- pt will experience remissions and exacerbations
Etiology of Peptic Ulcer Disease
HCl NOT CAUSE
- infection by bacteria Helicobacter pylori (not part of body’s normal flora)
- site and adhesion
1) colonize in stomach or duodenum
2) produce adhesion proteins –> attach to endothelium lining
3) overcome acidic environment: enzymes (urease) produced by bacteria to break down urea —-> C02+NH3 –> ammonia neutralizes acid (neutralized area permits bacteria to survive
Risk Factors of Peptic Ulcer Disease
- HCl and bilary acid: damage tissue if escapes containment organ
- NSAIDS: unknown cause
- chronic gastritis: continuous tissue damage
- smoking, alcohol, caffeine: aggravated by
Pathology of Peptic Ulcer Disease
role of H. pylori unclear
- inflammation mediators: infection –> inflammation –> tissue damage –> lead to ulcers
- hypergastrinemia (triggered by mediators produced by bacteria) –> increase gastrin production –> increase acid secretion –> tissue damage
- risk factors impede defenses against gastric acid
Manifestations of Peptic Ulcer Disease
- abdominal pain, burning, cramping on an empty stomach
- nausea, vomiting (d/t pain)
Complication of Peptic Ulcer Disease
- ulcer perforates entire wall –> HCl spills out into abdominal cavity –> chemical peritonitis (some H. pylori spill out, killed immediately by HCl as it can no longer create its own buffer anymore)
- hemorrhaging in upper GI tract (detect as occult blood in feces)
- bowel obstruction d/t edema (et. inflm), spasm or scar tissue contraction (cx by spontaneous muscle contractions of stomach or duodenal wall attempting to bring edges back together)
Dx of Peptic Ulcer Disease
- Hx (narrow it down to when mnfts occur)
- Serology (test for Ab to particular bact in blood)
- Urine Breath Test (Urea contains 1 C atom
- Stool Sample: fecal Ag (look for antigens of H. pylori)
