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mechanism s of disease > Lecture 11: Oral Cavity and Digestive Tract (Exam 3) > Flashcards

Lecture 11: Oral Cavity and Digestive Tract (Exam 3) Flashcards

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1
Q

What Disorders were focused on in the oral cavity?

A

Cavities
Gingivitis
Xerostomia

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2
Q

What disorders were focused on in the esophagus?

A

Varices
Atresia/Fistulae
Reflux esophagitis
- Gastroesophageal reflux disease (GERD)
-Barrett’s Esophagus

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3
Q

What disorders were focused on in the stomach?

A

Gastritis (Acute v. Chronic)
-NSAIDS
-H. Pylori
-Autoimmune

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4
Q

What disorders were focused on in the intestines?

A

Duodenal Ulcer
Obstructions
Celiac disease
Inflammatory Bowel Disease
-Acute (infectionious)
-Chronic (Ulcerative Colitis, Crohn’s)
Hemorrhoids

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5
Q

What is Dental Caries?

A

Cavities
- oral bacteria convert sugar into acid
-S. mutans implicated in plaque formation
-Acids destroy the enamel and dentin of the teeth
-hydroxyapatite crystals are solubilized
-Fluorapatite crystals are more resistant

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6
Q

What is an example of a biofilm in the oral cavity?

A

plaque is a biofilm

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7
Q

What is the clinical perspective of cavities?

A

cells that make enamel are lost after the tooth erupts so enamel cannot be regenerated
-exposes pulp and nerves to cold/heat from food
-Treatment: fill
-Prevention: cleaning

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8
Q

What is gingivitis?

A

-Inflammation of the gingiva layer
- Gingiva is the oral mucosa (often parakeratized-keratinized)
-immediately around teeth

Caused by: oral bacteria forming a biofilm (plaque) on the teeth
-plaque beneath the gum line leads to gingival infections (gingivitis)

Consequences:
- gingival erythema and edema
-bleeding
-changes in contour
-loss of soft tissue around the teeth
-periodontitis (eventual loss of teeth)

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9
Q

What salivary glands were focused on?

A

Parotid (serous)
Submandibular (mixed gland)
-predominantly serous
-some mucous
Sublingual (mixed gland)
-under tongue
-predominantly mucous
-some serous

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10
Q

What proteins are found in saliva?

A

alpha-amylase to break down carbohydrates
-lysozyme to attack bacteria

Glycoproteins
-mucins (lubrication)
-conjugated antibodies

Ions/Water
-INcluding bicarbonate ion (buffering)

IgA
-polymerized

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11
Q

What is Xerostomia?

A

-dry mouth
-decrease in saliva production by salivary glands
-usually, side effects of medication
-a feature of autoimmune disorder Sjogren Syndrome
-Major complication of radiation therapy

Symptoms
Dry mouth atrophy of tongue papilla (with fissuring and ulcerations)

Complications:
increase rates of dental caries
increased risk of candidiasis (oral thrush)
Dysphagia (difficulty swelling )
Dysarthria (difficult speaking)

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12
Q

How is the esophagus developed?

A

Trachea and esophagus develop as one tube
-Trachea buds off foregut (lung buds)
-Must separate (failure=fistula)

During development, the esophagus fills in
-recanalizes to be an open tube
-Failure= atresia

Associated with defects in neighboring structures
-Heart defects
-genitourinary malformations
-neurologic disease

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13
Q

What is esophageal atresia?

A

-the lack or limitation of a space or lumen (usually. developmental)
-results in mechanical obstruction of the space or tube

-In the esophagus, most commonly associated with a fistula

-Symptoms:
-Regurgitation while feeding
-incompatible with life unless repaired (surgery

Treatment: surgery
-feeding tube will not be able to reach the stomach

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14
Q

What is an esophageal fistula?

A

-abnormal opening between tubes
Three types of fistula, but common is tracheal esophageal fistula with atresia

-Symptoms:
Aspiration, suffocation, pneumonia
-Severe fluid/electrolyte imbalances
-Struggling to breathe while eating

Treatment: surgery
-feeding tube may be able to reach the stomach (imaging may be required)

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15
Q

What is Cardiovascular esophageal disorder?

A

Portal Hypertension
-reduced/blocked blood flow in the liver increases pressure within the portal vein
-Portal vein drains from the GI tract

Increased pressure causes distension of blood vessels
-Channels form to relieve pressure
-Esophagus is the location of potential connection

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16
Q

What are esophageal Varices?

A

distention of blood vessels increases the likelihood of rupture
-Walls thin as pressure increases
-remember hypertension

Rupture can cause fatal hemorrhage
-Even if the patient survives, loss of liver perfusion will cause damage that can seriously compromise function

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17
Q

What are esophageal Varices?

A

distention of blood vessels increases the likelihood of rupture
-Walls thin as pressure increases
-remember hypertension

Rupture can cause fatal hemorrhage
-Even if the patient survives, loss of liver perfusion will cause damage that can seriously compromise function

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18
Q

What is Reflux esophagitis?

A

-also known as GERD (Gastroesophageal Reflux Disease)
-movement of stomach (or pancreatic) contents into the esophagus
-damage to the esophageal mucosa produces inflammation

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19
Q

What are the symptoms of GERD?

A

Heartburn: recurrent burning sensation in the chest due to mucosal injury
-worsens after ingestion of foods that decrease the tone of the lower esophageal sphincter (LES)
-Recurrence of disease produces additional damage
-Scarring affects the tonicity of LES

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20
Q

Describe the Lower Esophageal Sphincter?

A

tonically contracted smooth muscle ring
-prevents backflow of stomach contents
-relaxes during swallowing to allow food into the stomach

Responds to NT
-Nitric Oxide
-Vasoactive intestinal peptide (VIP)

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21
Q

What are the causes of Heartburn?

A

-foods and other factors (eg mint, coffee
-impaired reflexive esophageal contractions after LES relaxation
-increased gastric volume/pressure
-increased acid production
-gastric obstruction
-Alkaline injury
-Hiatal hernia

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22
Q

How does mucosal inflammation affect the esophagus?

A

-acid damages epithelium and underlying tissue
-infiltration of granulocytes
-intraepithelial eosinophils
-Neutrophils are signs of more advanced disease
-Development of bleeding ulcers and exudate
-Edema
-Hemorrhage

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23
Q

What is the progression of Heartburn

A

initial lesion produces scarring that increases the likelihood of additional reflux

Can produce:
-stricture
-pain
-obstruction
-perforation

or Barrett’s esophagus
-pre-cancerous

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24
Q

What is Barrett’s Esophagus?

Study These Flashcards
A

esophageal epithelium changes from stratified squamous to columnar

-substantial numbers of goblet cells

25
What are the treatments of GERD?
-limit factors that cause heartburn -take drugs to inhibit acid production -Used collapsed ballon to relieve pressure in the LES
26
What is gastritis?
-inflammation of the stomach -results from mucosal injury -Acute -neutrophils in lesion -Chronic -many different immune cells present Gastropathy -Limited immune response -visible injury and repair
27
What are the mucosal defenses in the stomach?
Defensive forces - surface mucus secretion Bicarbonate -secretion into the mucus -helps neutralize acid Mucosal blood flow Apical surface -membrane transport Epithelial regenerative capacity Elaboration of prostaglandins
28
What can compromise mucosal defenses?
Cells -damage directly by ingestion of strong acids or bases -toxicity of NSAIDs, alcohol, radiation, chemotherapeutic drugs Mucus production -decreased by age, damage to cells Bicarbonate secretion -Affected by NSAIDS, uremia, H. pylori
29
What happens when the mucosa is compromised?
-necrotic damage to the mucosa -leaving a gap in a protective barrier -inflammation occurs in mucosal CT and submucosa -Damage may perforate muscularis mucosae
30
What causes ulcers?
chemical - gastric acid -duodenal reflux Drugs -NSAIDS -aspirin Infection -H. pylori Lifestyle -alcohol -cigarette smoking
31
What are motility defects and how can they cause ulcers in stomach?
duodenal contents re-enter through the pyloric sphincter -contains bile acids Delayed emptying of gastric contents -increased acid exposure Food retention increases gastric production
32
What are NSAIDs and how can they cause ulcers?
Non-steroidal Anti-inflammatory drugs - prostaglandins -increase mucosal blood flow -promote bicarbonate and mucus secretion - stimulate mucosal repair and renewal NSAIDS inhibit prostaglandin production - deficiency predisposes to gastritis and ulcers
33
What are Helicobacter pylori?
-causes ulcers found in the mucus -causes neutrophil invasion and lymphatic nodules effects increase gastric acidity -through gastrin, somatostatin release compromised defenses -mucosal damage secondary to immune response -reduced bicarbonate secretion due to urease
34
What is stress-related gastritis?
-Ulcers secondary to stress -shallow ulcers (alcohol, drugs, stress) -including trauma surgery, or serious medical disease damage is most likely due to ischemic damage -systemic hypotension due to trauma -reduced gastric perfusion due to stress response -also role for systemic acidosis secondary to disease -lowers intracellular pH of mucosal cells
35
What is chronic gastritis?
-inflammatory infiltrates -gastric mucosal atrophy -of parietal cells, specifically Loss of glands -gastric acid secretion is reduced -serum gastrin levels increase Autoimmune (<10% of chronic) - Autoantibodies against parental cells, intrinsic factor, gastrin
36
What other diseases are associated with chronic gastritis?
results from: H. Pylori infection (most common) Autoimmune implicated in: -pernicious anemia -gastric adenocarcinoma (may see goblet cells metaplasia which is not normal) -GI endocrine hyperplasia
37
What is the pathology of Gastritis?
H. pylori infection -superficial plasma cells responding to the presence of bacteria Autoimmune -response is to parietal cells -deeper lesions near the base of the gland -Gland Atrophy
38
What is Pernicious Anemia?
-Vitamin B12 is required for thymidine synthesis -failure of DNA synthesis affects hematopoiesis -Megaloblastic (abnormally large blood cells and precursors)
39
What are motility defects and how can they cause ulcers in the stomach?
duodenal contents re-enter through the pyloric sphincter -contains bile acids Delayed emptying of gastric contents -increased acid exposure Food retention increases gastric production
40
What is a duodenal Ulcer?
more common than gastric ulcers -Results of H. pylori infection -altered mucosal immune response -excess acid Risk factors -diet (no specific associations) -smoking -excessive alcohol consumption
41
What is Volvulus?
intestinal obstruction -caused by twisting of the bowel -rotates around mesenteric contact point Also causes vascular blockage -Therefore obstruction and infarction Symptoms: obstruction/infarction -Obstruction: abdominal pain and distension, vomiting, constipation -Infarction: abdominal pain and tenderness, nausea, vomiting, bloody diarrhea, melanotic stool
42
What is intussuception?
-a most common cause of intestinal obstruction in children younger than 2 years -a segment of intestines slides into the next segment -Usually happens during constriction due to peristalsis -segment becomes trapped; will drag mesentery in -May develop into obstruction, mesenteric vessel constriction, possible infarction -Treatment: contrast/air enemas may reverse it If not, surgery required
43
What is malabsorption?
-most common clinical symptom is chronic diarrhea - defective absorption of food nutrients -Vitamins (lipids or water-soluble) -Proteins, carbohydrates -Electrolytes, minerals, water Common causes -Celiac disease (not autoimmune) -Pancreatitis -Cystic fibrosis -Inflammatory bowel disease
44
What is Celiac disease?
-immune-mediated enteropathy -Triggered by ingestion of gluten-containing grains -not autoimmune -Damage from immune response -Loss of brush border -Loss of Villi -Reduced surface for absorption=malabsorption Immune cells recruited -Natural killer cells (CD8+ T lymphocytes) - APCS will recruit CD4+ lymphocytes -Additional cells required
45
What is inflammatory Bowel Disease?
Infectious (acute) is excluded by: -examining stool for infectious organisms (if none, it is chronic) -lack of responsiveness to antibiotics Chronic (non-infectious) is characterized by flare-ups and remissions -Not autoimmune -spontaneous remissions
46
What is Acute IBD?
Infectious Enterocolitis -infection may be viral, bacterial, or parasitic -common infectious Agents -Vibrio Cholera - bacteria -Campylobacter jejuni (travelers diarrhea)-bacteria -Salmonella enteritidis (nontyphoid)-bacilli -Salmonella enterica (typhoid fever)-bacilli -Clostridium difficile (Pseudomembranous colitis)-bacteria -E. Coli (multiple)- bacilli
47
What is Cholera?
vibrio cholera produces a toxin affects cystic fibrosis regulator -causes excessive Cl- in lumen and affect water uptake causing diarhea - actual bacteria are non-invasive but do not colonize epithelium Limited histological changes to tissue
48
What is Traveler's Diarrhea?
residents are generally resistant Campylobacter jejuni -associated with ingestion of undercooked chicken, unpasteurized milk, contaminated water colonize mucosa
49
What is the pathology of campylobacter jejuni?
mucosal and intraepithelial neuroepithelial invasion, including in the crypts -crypt abscesses: neutrophil accumulation in the crypt -Maintenance pf crypt architecture (similar to EIEC)
50
What are the three types of E. coli?
E. coli (normal microbiota) are not pathogenic -ETEC (Enterotoxigenic E. coli) - principal cause of traveler's diarrhea -Produce two toxins (heat labile and heat stable) -Labile is similar to cholera -Stable is similar but through cGMP -EHEC (enterohemorrhagic E. coli) -cows are reservoirs (associated with contaminated beef -toxins cause dysentery (bloody diarrhea) -like disease EIEC (Enteroinvasive E. coli) - similar to Shigella; resistant to acid -Proliferate intracellularly in the M cells overlying Peyer's patches
51
What do EHEC and EIEC cause in acute IBD?
EHEC; Ischemia type morphology (surface atrophy and erosion) EIEC: Mucosal and intraepithelial neutrophil invasion, including in the crypts -Maintenance of crypt architecture (similar to campylobacter)
52
What is Typhoid fever?
-Caused by Salmonella enterica -two subtypes: typhi and paratyphi -also nontyphoid salmonella bacteria (does not cause typhoid) -Affect Peyer patches in the ileum -increases their size dramatically -enlarged mesenteric lymph nodes -Also debris-filled macrophages, lymphocytes, and plasma cells in the lamina propria. -will cause ulceration and possible perforation damage to spleen
53
What is Pseudomembranous colitis?
-antibiotic-associated colitis (eruption of neutrophils from crypt) -Clostridium difficile (C. difficile) overgrowth - normal component of intestinal microbiota -Also caused by immunosuppression C. difficile releases a toxin -Binds to small GTPase like Rho -Disrupts epithelial cytoskeleton (tight junctions) -Also induces cytokine release and apoptosis
54
What diseases are associated with Chronic IBD?
Crohn's disease -occurs anywhere along the GI tract -transmural -granulomatous Ulcerative colitis (rectum to large intestine) -superficial -limited to colon mucosa
55
What causes Chronic IBD?
Genetics mucosal immune response -immunosuppressive therapy Epithelial abnormalities -Cell-cell junctions -Transepithelial transport Microbiota -likely difference between UC and Crohn's
56
What is Crohn's disease?
Ulceration and inflammation are: -discontinuous -involve the entire thickness of the wall -can involve adjacent mesentery and lymph nodes Results in nutrient deficiency Initial clinical presentation includes mild diarrhea, fever, and abdominal pain Granulomas: macrophage clusters wall of threat mucosal, submucosal, and serousal granulomas
57
What is Ulcerative Colitis?
-inflammation is limited to the mucosa -begins at the anorectal junction and extends proximally -Characteristics of necrotic lesions in the Crypts of Lieberkuhn -NO granulomas
58
What are the similarities and differnces between UC and crohn's?
-10% of patients have lesions characteristic of both -Presentation is similar -bloody diarrhea -malabsorption Differences: in UC, there is no obstruction, perforation, or fistula formation
59
What are hemorrhoids?
Caused by: -Straining at defecation due to constipation -venous stasis due to pregnancy -portal hypertension (similar to esophageal varices Treatment: -Anti-inflammatory to reduce swelling -stool softener to prevent constipation -surgical removal Pathology -thin-walled, dilated, submucosal vessels that protrude beneath the mucosa -tend to become inflamed and develop thromboses -may lead to superficial ulceration Symptoms: pain and rectal bleeding

mechanism s of disease (4 decks)

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