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

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?

A

esophageal epithelium changes from stratified squamous to columnar

-substantial numbers of goblet cells

25
Q

What are the treatments of GERD?

A

-limit factors that cause heartburn
-take drugs to inhibit acid production
-Used collapsed ballon to relieve pressure in the LES

26
Q

What is gastritis?

A

-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
Q

What are the mucosal defenses in the stomach?

A

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
Q

What can compromise mucosal defenses?

A

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
Q

What happens when the mucosa is compromised?

A

-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
Q

What causes ulcers?

A

chemical
- gastric acid
-duodenal reflux

Drugs
-NSAIDS
-aspirin

Infection
-H. pylori

Lifestyle
-alcohol
-cigarette smoking

31
Q

What are motility defects and how can they cause ulcers in stomach?

A

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
Q

What are NSAIDs and how can they cause ulcers?

A

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
Q

What are Helicobacter pylori?

A

-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
Q

What is stress-related gastritis?

A

-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
Q

What is chronic gastritis?

A

-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
Q

What other diseases are associated with chronic gastritis?

A

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
Q

What is the pathology of Gastritis?

A

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
Q

What is Pernicious Anemia?

A

-Vitamin B12 is required for thymidine synthesis
-failure of DNA synthesis affects hematopoiesis
-Megaloblastic (abnormally large blood cells and precursors)

39
Q

What are motility defects and how can they cause ulcers in the stomach?

A

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
Q

What is a duodenal Ulcer?

A

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
Q

What is Volvulus?

A

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
Q

What is intussuception?

A

-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
Q

What is malabsorption?

A

-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
Q

What is Celiac disease?

A

-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
Q

What is inflammatory Bowel Disease?

A

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
Q

What is Acute IBD?

A

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
Q

What is Cholera?

A

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
Q

What is Traveler’s Diarrhea?

A

residents are generally resistant

Campylobacter jejuni
-associated with ingestion of undercooked chicken, unpasteurized milk, contaminated water

colonize mucosa

49
Q

What is the pathology of campylobacter jejuni?

A

mucosal and intraepithelial neuroepithelial invasion, including in the crypts

-crypt abscesses: neutrophil accumulation in the crypt
-Maintenance pf crypt architecture (similar to EIEC)

50
Q

What are the three types of E. coli?

A

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
Q

What do EHEC and EIEC cause in acute IBD?

A

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
Q

What is Typhoid fever?

A

-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
Q

What is Pseudomembranous colitis?

A

-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
Q

What diseases are associated with Chronic IBD?

A

Crohn’s disease
-occurs anywhere along the GI tract
-transmural
-granulomatous

Ulcerative colitis (rectum to large intestine)
-superficial
-limited to colon mucosa

55
Q

What causes Chronic IBD?

A

Genetics

mucosal immune response
-immunosuppressive therapy

Epithelial abnormalities
-Cell-cell junctions
-Transepithelial transport

Microbiota
-likely difference between UC and Crohn’s

56
Q

What is Crohn’s disease?

A

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
Q

What is Ulcerative Colitis?

A

-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
Q

What are the similarities and differnces between UC and crohn’s?

A

-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
Q

What are hemorrhoids?

A

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