Hirschsprung’s Disease (congenital aganglionic megacolon)

28/01/2010

 

congenital condition in which a section the colon is aganglionic

there is little urge to defecate so the feces accumulate.

  • genetic defect on Chr 10
  • 1/5000 live births
  • Sigmoid colon typically affected

 

  Mechanism:

  • absence of ganglia in parts of the colon
  • no peristalsis occurs in affected region
  • contents accumulate
  • colon becomes distended, in turn results in distended abdomen
  • bowel obstruction may occur

 

Treatment:

  • Surgical exision of aganglionic region
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paralytic ileus or ileus

23/01/2010

A condition in which there is an absence of peristalsis in the intestine and contents are not moved along and eliminated.

1 mo old female with ileus below:

Etiology:

  • surgical physiological stress
  • abdominal infection
  • abdominal surgery
  • medications  – opiates
  • Peritonitis
  • Spinal cord injusry
  • electrolyte imbalance

Manifestations:

  • abdominal distension and discomfort
  • nausea
  • emesis
  • lack of bowel movement and flatulence
  • constipation

Treatment:

patient remains NPO status until GI and bowel sounds are heard.

Some types of laxatives (to be avoided in cases of bowel obstruction)

Surgery for bowel obstruction


Diverticulitis

17/01/2010

 

Diverticulitis: Inflammation, irritation or infection of existing diverticulosis in the colon.

Manifestations:

  • tenderness or pain in the lower left quadrant
  • nausea
  • vomiting
  • slight fever
  • elevated WBC

 

Diverticulitis: The diverticulosis complication

  1. inflammation with gross or microscopic perforation of the diverticulum.
  2. Perforation of the gut accompanied by peritonitis
  3. hemorrhage
  4. bowel obstruction

5. Fistulas formation:

  • usually involving the bladder
  • may involve skin
  • perianal area
  • small bowel
  • Permaturia (air in the urine) = a sign of vesicosigmoid fistula

 

diagnosis

  1. Hx
  2. CT
  3. Ultrasound
  4. Flat abdominal radiographs

 

treatment.

  1. symptoms and complication prevention
  2. increased bulk in diet to increase intracolonic pressure and promote defecation
  3. bowel retraining so the individual has at least one bowel movement per day
  4. Acute diverticulitis is treated by withholding solid food and administering a broad-spectrum antibiotic.
  5. IV fluids may be needed for those unable to tolerate oral fluids
  6. Sx reserved for complications

Martin, Glenn and Porth, Carol, Mattson. 2009. Pathophysiology Concepts of Altered Health States. 8th ed. Lippincott Williams and Wilkins. Philadelphia


Diverticulosis

09/01/2010

 

The condition of having diverticula in the colon, which are outpocketings of the colonic mucosa and submucosa through weaknesses of muscle layers in the colon wall.

 


Inflammatory Bowel Disease

08/01/2010

 

Two chronic disorders:


1.Crohn`s disease
2.Ulcerative Colitis

Etiology:

Genetic susceptibility (no gene yet identified): Intolerance of normal gut flora by the body`s immune system.
Immune response is unregulated.

  1. Ulcerative Colitis
  • Chronic inflammation of the colon that produces ulcers in its lining
  • region of affected gut is continuous

 2. Crohn`s Disease

  • A chronic form of inflammatory bowel disease that usually affects the lower small intestine (called the ileum) or the colon
  • skip lesions in small and large intestine

 

Differentiating Characteristics of Crohn`s Disease and Ulcerative Colitis

Characteristics Crohn`s Disease Ulcerative Colitis
Type of inflammation Granulomatous Ulcerative and exudative:
Level of involvement submucosa mucosa
Area of involvement Ileum, colon Rectum and left colon
Extent of Involvement skip lesions in small and large intestine region of affected gut is continuous
Diarrhea common common
Rectal bleeding rare common
Fistuals common rare
Stricture common rare
Perianal abscesses Common Rare
Development of cancer Uncommon Relatively Common

 

Martin, Glenn and Porth, Carol, Mattson. 2009. Pathophysiology Concepts of Altered Health States. 8th ed. Lippincott Williams and Wilkins. Philadelphia


Appendicitis

07/01/2010

Inflammation of the appendix, the blind ended vestigial tube connected to the cecum (proximal portion of the large intestine).

  • predominantly in those 20-30 years of age
  • can be seen in any age group

 

Etiology

  • idiopathic
  • obstruction of appendix lumen by fecal pellet
  • twisted, constricted area of appendix or adjoining bowel area

 

Pathophysiology

  • obstruction
  • mucus drainage and flow impeded
  • increased intraluminal pressure
  • perfusion impeded due to pressure
  • ischemia
  • tissue necrosis
  • bacterial invasion of appendix wall from appendix lumen
  • Complication: appendix rupture leading to peritonitis

\

Manifestation

  • Nausea
  • Vomiting

 

Pain Specifics

  • Pain commences in epigastric region or umbilical region
  • R lower quadrant pain later in progression (focused at appendix)
  • Pain terminates @ McBurney’s point – midpoint b/t iliac crest and umbilicus
  • Guarded, Rebound pain

 

McBurney’s point: point over the right side of the abdomen that is one-third of the distance from the ASIS (anterior superior iliac spine) to the umbilicus (the belly button). This point roughly corresponds to the most common location of the base of the appendix where it is attached to the cecum.

 

Diagnosis

  • Hx
  • Px – physical exam
  • Ultrasound
  • CT scan

 CT Scan below showing appendicitis:

Tx:

  • appendectomy within 24-48hrs of pain onset
  • delay may result in rupture and peritonitis

Martin, Glenn and Porth, Carol, Mattson. 2009. Pathophysiology Concepts of Altered Health States. 8th ed. Lippincott Williams and Wilkins. Philadelphia


Helicobacter pylori and stomach ulcers

29/10/2009

Stomach ulcers are caused by the gastric mucosa being infected with the bacterium Helicobacter pylori. Helicobacter pylori infects various areas of the stomach and duodenum causing inflammation and ulcers in the stomach.

There are two tests used to assay for the presence of H. pylori infection:

  1. Endoscopy where a tube with a camera is inserted down the esophagus into the duodenum to view the mucosal lining and obtain a tissue sample for assay.

2. The Ulcer Breath Test:

  • Carbon dioxide is exhale when we breath out
  • A breath sample is taken
  • Pranactin is then taken orally
  • A second breath sample is obtained once the Pranactin has been metabolised in the GI tract
  • The breath test is based on H. pylori’s ability to break down urea, the active ingredient in Pranactin.
  • H. pylori breaks down urea in a process that produces carbon dioxide.
  • The urea in Pranactin, however, is composed of a form of carbon called carbon 13, which is not found in high levels in breath.
  • When H. pylori breaks down the urea, carbon dioxide containing the carbon 13 is formed.
  • This carbon dioxide, containing carbon 13, enters the blood and travels to the lungs, where it is exhaled.
  • The test then compares first breath sample to the second sample and determines if a higher proportion of carbon dioxide (containing carbon 13) is present.
  • a higher level of carbon 13 in the second sample results in a positive H. pylori ulcer test.
  • Antibacterial medications to treat H. pylori infection can then be given

Martin, Glenn and Porth, Carol, Mattson. 2009. Pathophysiology Concepts of Altered Health States. 8th ed. Lippincott Williams and Wilkins. Philadelphia