Lecture 7.1 MJ slides Flashcards
1) What is the most common fungal infection of the oral cavity?
2) What 2 groups of individuals does it occur freq. in?
1) Candida albicans
2) Immunosuppression
-Microbiota disrupted (i.e. antibiotic use)
Define Esophagitis
Result of chemical or infections (immunocompromised) mucosal injury
1) Define GERD
2) Define eosinophilic esophagitis and what it’s associated with
1) Most common cause of esophagitis; involving reflux of gastric acid in the lower esophagus
2) Chronic, immunologically mediated esophagitis with marked eosinophil superficial epithelium
1) Rings can be visualized on endoscopy of what esophageal condition? What is this condition associated with?
2) Describe the mechanisms and causes of this condition
1) Esophagitis; other signs of atopy.
2) ↓ LES tone
↑ abdominal pressure
Other causes: ETOH, smoking, obesity, pregnancy, hiatal hernia
Barrett Espohagus:
1) What is it?
2) What does it confer an increased risk of?
3) Occurs in ___% of people w/ GERD
4) What is the rate of change?
1) Intestinal metaplasia in the esophageal squamous mucosa
2) Confers and ↑ risk of esophageal adenocarcinoma
3) 10%
4) Dysplasia @ rate of 0.2-1% per year (considered pre-invasive lesion)
List 2 types of esophageal tumors
Squamous cell and adenocarcinoma
Squamous cell [of esophagus]:
1) What is it the most common cause of worldwide? What are the majority of these resultant from? (in US & Europe)
2) What is another risk of this cancer? What is critical, and what is the pathogenesis?
3) How does it present? (3 Sx)
1) Esophageal cancer; use of ETOH and tobacco.
2) HPV; early detection; molecular pathogenesis is poorly understood
3) Dysphagia, odynophagia (difficulty swallowing) and obstruction
Adenocarcinoma:
1) How common is it?
2) What does it arise from? Explain the progression
3) How does it present? Does it usually present early or late?
1) “On the rise”
2) From the background of Barrett’s and GERD; progression from Barrett’s to adenocarcinoma is through the stepwise progression of genetic and epigenetic changes
3) Pain, difficulty swallowing, progressive weight loss.
-Usually advanced at diagnosis
Define gastritis
A mucosal inflammatory process
What are the two types of gastritis? What can cause each?
1) Acute: Anything that interferes with gastric mucosal protection
2) Chronic: Most common cause is H. pylori.
→ MALT? (mucosa-associated lymphoid tissue) that can give rise to B-cell lymphoma
Chronic gastritis:
1) Describe how it can have an autoimmune cause.
2) What are 2 other causes?
1) Autoimmune: causes damaged to gastric body oxyntic glands
Frequently seen with anti-parietal cell and anti-intrinsic factor antibodies
2) NSAID’s & ETOH
Acute gastritis:
1) What are the Sx?
2) What may it progress to?
1) Range from asymptomatic → epigastric pain, N/V
2) Ulceration
List some causes of Hyperacidity in PUD
1) H. pylori infection: Causes hyperchlorhydria
2) Parietal cell hyperplasia
3) Excessive secretory function
4) Insufficient inhibitions of stimulatory mechanisms such as gastrin
-Zollinger Ellison syndrome: multiple ulcers caused gastrin-producing tumors
ABD pain/distention, vomiting, +/- constipation are the Sx of what?
Bowel obstructions
Hirschsprung Disease (congenital aganglionic megacolon):
1) Epidemiology
2) It’s a congenital defect in colonic innervation; how does this happen?
3) What kind of obstruction does it cause?
4) What is the Tx?
1) Occurs in 1 of 5000 live births
2) Mutations if the receptor tyrosine kinase RET most common
-Defective neural crest cell migration from cecum to rectum → lack of Meissner plexus (submucosal) and Auerbach plexus (myenteric) responsible for coordinated peristalsis
3) Functional obstruction (ex: Neonates present as failure to pass meconium)
4) Surgical resection of aganglionic segment with re-anastomosis of colon to rectum
Diverticulitis:
1) What are diverticula?
2) What is diverticulitis? What may it lead to?
3) What are the Sx?
1) Acquired outpouchings of the colonic mucosa and submucosa. (60+ y/o usually)
-Develop under conditions of elevated intraluminal pressure in the sigmoid colon.
2) Diverticulitis: obstruction of diverticula , stasis of contents, and inflammatory change
-Perforation
3) Cramping, LLQ pain and tenderness,, Constipation/ diarrhea
1) What do bowel obstructions present with?
2) What do they usually require?
3) What is the most common cause of obstruction in kids <2? How is this treated?
1) ABD pain/distention, Vomiting, +/- Constipation
2) NG tube/ surgery
3) Intussusception; air or barium enema.
What is the most common cause of most small bowel obstructions in adults?
Adhesions
List some causes of bowl obstructions
1) Herniation (incarceration leads to strangulation)
2) Adhesions
3) Volvulus (sigmoid colon)
4) Intussusception (kids)
Malabsorption Syndromes:
1) Define these
2) What are the clinical manifestations?
3) What are 3 examples?
1) Defective absorption of fats, vitamins, proteins, carbohydrates, electrolytes, minerals, and water
2) Most common presentation: chronic diarrhea
Hallmark: steatorrhea
3) **Celiac disease, Pancreatic insufficiency, Chron disease*
What are 4 causes of malabsorption syndromes? Explain each
1) Intraluminal digestion: macros broken down
2) Terminal digestion: hydrolysis of carbs and peptides
3) Transepithelial transport: nutrients, fluid, & electrolytes absorbed
4) Lymphatic transport: absorbed liquids
What are 2 common malabsorption syndromes?
1) Celiac disease
2) Lactase deficiency
Celiac:
1) Define it
2) What causes the malabsorptive diarrhea?
3) What two parts of digestion does it affect?
1) Celiac diseaseis an immune-mediated enteropathy triggered by the ingestion of gluten-containing grains.
2) Loss of brush border surface areaand, possibly, deficient enterocyte maturation.
3) Luminal and terminal digestion
Lactase deficiency:
1) What does it cause? Why?
2) Is it congenital or acquired?
1) Anosmotic diarrhea,owing to the inability to break down or absorb lactate
2) Either congenital or acquired
Infectious Enterocolitis: List the potential causes
1)Vibrio cholerae
2) Campylobacter jejuni
3) SalmonellaandShigella
4) Pseudomembranous colitis > allows C. difficile
5) Rotavirus
6) Parasiticandprotozoalinfections
Infective enterocolitis:
1) Vibrio choleraesecretes what? How does it cause secretory diarrhea?
2) Campylobacter jejuniis the most common bacterial enteric pathogen where? What else does it cause?
3) What two species are invasive and associated with exudative bloody diarrhea? (dysentery).
4) What else can each cause?
1) A preformed toxin that causes massive chloride secretion. Water follows the resulting osmotic gradient, leading to secretory diarrhea.
2)Campylobacter jejuniis the most common bacterial enteric pathogen in developed countries and also causes traveler’s diarrhea. Most isolates are noninvasive.GB
3) SalmonellaandShigellaspp.
4) Salmonellainfection is a common cause of food poisoning.
-S. typhican cause systemic disease (typhoid fever).
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Infective enterocolitis:
1) Pseudomembranous colitis is often triggered by what? What does it disrupt and allow to colonize and grow?
3) What is the result of this?
4) What is becoming more common as a therapeutic approach in individuals with recurrent disease?
1) Antibiotic therapy; disrupts normal microbiota + allowsC. difficile
2) The organism produces toxins that disrupt epithelial function.
3) Fecal microbial transplantation
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Infective enterocolitis:
1) What is the most common cause of severe childhood diarrhea and diarrheal mortality worldwide? What is the diarrhea secondary to?
2) What infections affect over half of the world’s population on a chronic or recurrent basis?
1)Rotavirus; secondary to loss of mature enterocytes, resulting in malabsorption as well as secretion.
2)Parasiticandprotozoal
Crohn disease, list the:
1) Site of origin
2) Pattern of progression
3) Thickness of inflammation
4) Sx
1) Terminal ileum
2) “Skip” lesions/ irregular
3) Transmural
4) Crampy abd. pain
Crohn disease, list the:
1) Complications
2) Radiographic findings
3) Risk of colon cancer
4) Surgery
1) Fistulas, abscess, obstruction
2) String sign on barium Xray
3) Slight increase
4) For complications (like stricture)
UIcerative colitis, list the:
1) Site of origin
2) Pattern of progression
3) Thickness of inflammation
4) Sx
1) Rectum
2) Proximally contiguous
3) Submucosa or mucosa
4) Bloody diarrhea
Ulcerative colitis, list the:
1) Complications
2) Radiographic findings
3) Risk of colon cancer
4) Surgery
1) Hemorrhagic, toxic megacolon
2) Lead pipe colon on barium Xray
3) Marked increase
4) Curative
Colon Cancer:
1) Etiology?
2) 2 genetic factors? (play impt role)
3) Dietary factors? (i.e. western diet)
4) What can interact with carcinogens?
1) Unknown in most cases
2) Familial adenomatous polyposis + Lynch syndrome (Hereditary non-polyposis colon cancer)
3) Low fiber, high carb, & high fat content
4) Oncogenes and tumor suppressor genes
