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Mechanisms of Disease > Week 11 Gastrointestinal Diseases > Flashcards

Week 11 Gastrointestinal Diseases Flashcards

1
Q

Name the oral cavity disorders.

A

Cavities
Gingivitis
Xerostomia

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2
Q

Esophageal disorders

A

Atresia/Fistula
Varices
Reflux Esophagitis
- Gastroesophageal reflux disease (GERD)
- Barrett’s Esophagus

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3
Q

Stomach disorders

A

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

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4
Q

Intestinal disorders

A

Duodenal ulcer
Obstructions
Celiac Disease
Inflammatory Bowel Disease
- Acute (infectious)
- Chronic (ulcerative colitis, Crohn’s disease)
Hemorrhoids

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5
Q

What are dental caries?

A

Cavities
- oral bacteria convert sugar to acid (S. mutans implicated in plaque formation)
- plaque on teeth is a biofilm
- acids destroy enamel and dentin of the teeth
- hydroxyapatite crystals are solubilized
- fluorapatite crystals are more resistant to solubilization by acid

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6
Q

Describe the clinical aspect of cavities.

A
  • cells that make enamel are lost after tooth erupts (enamel cannot be regenerated, but you can regenerate dentin)
  • exposes pulp and nerves to cold/heat from food
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7
Q

What is treatment and prevention for cavities

A

Treatment: fill cavity
Prevention: cleaning
- If cavity has progressed through dentin, it will expose pulp, which has lots of BVs and nerves

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8
Q

What is Gingivitis?

A

Inflammation of the gingiva
- oral mucosa immediately around teeth (often parakeratinized- keratinized)

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9
Q

What is the cause of gingivitis?

A

oral bacteria forming a biofilm (plaque) on the teeth
- plaque beneath the gum line leads to gingival infection (gingivitis)

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10
Q

What are the consequences of gingivitis?

A
  • gingival erythema and edema (redness and swelling)
  • bleeding
  • changes in contour
  • loss of soft tissue around teeth (soft tissue anchors it to bone)
  • periodontitis (eventual loss of teeth)
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11
Q

Name the 3 major salivary glands and their predominant type of gland.

A
  1. Parotid (serous)
    - in front of ears and along jaw line
  2. Submandibular (mixed gland)
    - along floor of mouth, but near jaw
    - predominantly serous
    - some mucous
  3. Sublingual (mixed gland)
    - immediately underneath tongue
    - predominantly mucous
    - some serous
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12
Q

Describe the components of saliva

A

Proteins
- alpha-amylase to break down carbs
- lysozyme to attack bacteria in the mouth
- saliva very important for protective function
Glycoproteins
- mucins (lubrication)
- conjugated antibodies
- released by mucus cells
Ions/Water
- including bicarbonate ion (buffering)
- buffer some of the acid in the mouth
IgA
- polymerized
- produced by plasma cells around the acini

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13
Q

What is Xerostomia?

A

Dry Mouth!
- decrease in saliva production by salivary glands
- usually side effect of medication
-feature of autoimmune disorder (Sjogren Syndrome)
-major complication of radiation therapy

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14
Q

What are the symptoms of Xerostomia?

A

Dry mouth
Atrophy of tongue papilla with fissuring and ulcerations

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15
Q

What are the complications of xerostomia?

A
  • increased rates of dental caries
  • increased risk of candidiasis (oral thrush)
  • dysphagia (difficulty swallowing)
  • dysarthria (difficulty speaking)
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16
Q

Treatment for xerostomia.

A
  • finish meds causing it or switch meds
  • address Sjogren syndrome
  • pylocarpine to stimulate saliva production through muscarinic chononergic receptors
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17
Q

Describe esophageal development.

A

Trachea and esophagus develop as one tube
- trachea buds off foregut (lung buds)
- must separate (failure = fistula)
During development, esophagus fills in
- recanalizes to be open tube
- failure = atresia
Associated with defects in neighboring structures
- heart defects
- genitourinary malformations
- neurologic disease
This is all relatively early in development

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18
Q

What is atresia?

A

Lack or limitation of space or lumen (usually developmental)
- results in mechanical obstruction of space or tube
In the esophagus, most commonly associated with fistula
Symptoms:
- regurgitation while feeding
- incompatible with life unless repaired (surgery)
Treatment: surgery
- feeding tube will not be able to reach stomach

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19
Q

What is fistula?

A

Abnormal opening between tubes (failure of separation)
Symptoms:
- aspiration, suffocation, pneumonia
- severe fluid/electrolyte imbalances
- struggling to breathe while eating
Treatment: surgery
- feeding tube may be able to reach stomach (make sure it is not placed in lungs)
Tracheoesophageal fistula with atresia is the most common congenital defect

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20
Q

Describe cardiovascular esophageal disorder.

A

Secondary to Portal Hypertension
- reduced/blocked blood flow in the liver increases pressure w/in portal vein
- portal vein drains from GI tract–> increased pressure along GI tract
Increased pressure causes distension of BVs
- channels form to relieve pressure
- esophagus is location of potential connection b/c highly vascular

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21
Q

What are esophageal varices?

A

Distension of BVs increases likelihood of rupture
- walls thin as pressure increases
- remember hypertension
Rupture can cause fatal hemorrhage–> patient will vomit massive amounts of blood
- even if patient survives, loss of liver function will cause damage that can seriously compromise function of the liver

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22
Q

Describe pathology of esophageal varices.

A
  • thinning of mucosa and thinning of BV walls that can rupture
  • upon endoscopy, walls of esophagus should be relatively smooth, but instead you see these vessels that are squiggly or you may see large pseudo-polyps forming
    - these are massively distended BVs
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23
Q

What is the treatment for esophageal varices?

A
  • trying to treat the liver disorder to reduce blood
  • surgically remove varices to reduce pressure
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24
Q

What is reflux esophagitis?

A
  • movement of stomach or pancreatic contents into esophagus
  • damage to esophageal mucosa produces inflammation
  • clinically known as GERD (gastroesophageal reflux disease)
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25
Q

Symptoms of GERD

A
  • heartburn: recurrent burning sensation in the chest due to mucosal injury
  • worsens after ingestion of foods that decrease tone of lower esophageal sphincter (LES)
  • recurrence of disease produces additional damage
  • scarring affects tonicity of LES- increases risk of further heartburn
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26
Q

What is the lower esophageal sphincter and what does it do?

A

Tonically contracted smooth muscle ring
- prevents backflow of stomach contents
- relaxes during swallowing to allow food into stomach
Responds to neurotransmitters
- nitric oxide
- vasoactive intestinal peptide (VIP)
- also controlled by vagus nerve, which participates in swallowing

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27
Q

What are the causes of reflux esophagitis or GERD?

A
  • foods (chocolate, coffee, peppermint) and other factors
  • impaired reflexive esophageal contractions after LES relaxation
  • increased gastric volume/pressure
    - increased acid production
    - gastric obstruction
  • alkaline injury
  • hiatal hernia: part of stomach above diaphragm; LES falls to the side, putting additional pressure on it
    - increases risk that LES will not maintain normal contraction
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28
Q

Describe the mucosal inflammation of the esophagus.

A
  • acid damages epithelium and underlying tissue (esophagus is not meant to resist acid damage)
  • infiltration of granulocytes
    - intraepithelial eosinophils
    - neutrophils are sign of more advanced disease
  • development of bleeding ulcers and exudate upon erosion of mucosa
    - edema
    - hemorrhage
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29
Q

Describe the progression of GERD/ reflux esophagitis.

A

Initial lesion produces scarring that increases likelihood of additional reflux b/c of damage to LES
Can produce:
- stricture as you get more scarring
- pain
- obstruction
- perforation can develop as acid eats away at the wall of the esophagus
- Barrett’s Esophagus–> pre-cancerous lesion

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30
Q

What is Barrett’s Esophagus?

A

Example of metaplasia
- esophageal epithelium changes from stratified squamous to columnar with substantial numbers of goblet cells
- goblet cells produce mucus that neutralizes the acid causing the damage

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31
Q

What is the treatment for GERD?

A

Mostly trying to prevent further damage to esophagus
- limit intake of foods that cause issues
- drugs to inhibit acid production
- surgery or other treatments to relieve gastric obstruction
- collapsed balloon to relieve pressure on LES and reduce esophageal reflux due to stricture and hiatal hernia

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32
Q

What is gastritis?

A

Inflammation of the stomach
- results from mucosal injury

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33
Q

List the types of gastritis.

A

Acute
- neutrophils in lesion
Chronic
- many different immune cells present
Gastropathy
- limited immune response
- visible injury and repair

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34
Q

Describe some of the mucosal defenses in the stomach.

A
  • mucus forms protective layer and bicarbonate helps neutralize acid
  • blood flow generally supports function of mucosa
  • any damage that does occur to epithelium can be repaired b/c of epithelium being highly regenerative
  • prostaglandins will help with blood flow
35
Q

Describe compromised mucosal defenses.

A

Cells
- damaged 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

36
Q

Compromised mucosa continued…

A
  • necrotic damage to mucosa
  • leaves gap (ulcer) in protective barrier
  • inflammation occurs in mucosal CT and submucosa
  • damage may perforate muscularis mucosae
  • shallow ulcer will typically just be mucosal
    - image in slide shows a deeper ulcer
    - granulation tissue is response to the damage
37
Q

Etiology of Ulcers

A

Chemical
- gastric acid (excessive)
- duodenal reflux: pancreatic secretions of duodenum get up into stomach
Drugs
- NSAIDs
- aspirin
Infection
- H. pylori
Lifestyle
- alcohol
cigarette smoke

38
Q

Mobility defects and ulcers

A

Duodenal Reflux
- Duodenal contents re-enter through pyloric sphincter
- contain bile acids
- Delayed emptying of gastric contents
- increased acid exposure
- Food retention increases gastric acid production

39
Q

NSAIDs and Ulcers

A

Prostaglandins
- increase mucosal blood flow
- promote bicarbonate and mucus secretion
- stimulate mucosal repair and renewal
NSAIDs inhibit prostaglandin production (Ibuprofen, Neproxin)
- non-steroidal anti-inflammatory drugs
Deficiency predisposes to gastritis and ulcers by reducing mucosal defenses in multiple ways
- if you inhibit prostaglandin production–> decrease mucosal blood flow–> reduce bicarbonate and mucus secretion–> inhibit mucosal repair/renewal

40
Q

What is Helicobacter pylori?

A

-Curved gram-negative bacterium that has adapted to the environment of the human stomach
-The bacterium infects the lower part of the stomach and causes inflammation of gastric mucosa
- in a paper published in the 1980s, stated that the bacterium was present in almost all patients with active chronic gastritis, duodenal ulcer, or gastric ulcer and thus may be an important factor in the etiology of these diseases

41
Q

Mucosal infection by H. pylori

A
  • It infects and lives in the mucosa
  • presence induces invasion of neutrophils and production of lymphatic nodules
  • b/c bacteria is in mucus, the immune cells try to eradicate it and end up causing a lot of damage to epithelium
42
Q

H. Pylori Effects

A

Not known to directly invade mucosa
Increased acid production (increased gastric acidity
- through gastrin, somatostatin release
Compromised defenses
- mucosal damage secondary to immune response
- reduced bicarbonate secretion due to urease–> high ammonium levels inhibit transporters
Increased acidity + decreased bicarbonate secretion = ulcers

43
Q

What is the treatment for H. pylori infection?

A

Abx that kill H. pylori
- then inflammation stops and stomach can recover and ulcers will heal

44
Q

What is stress-related gastritis?

A

Ulcers secondary to stress
- shallow ulcers (alcohol, drugs, stress)
- including trauma, surgery, or serious medical disease
Damage most likely due to ischemic damage
- systemic hypotension due to trauma
- reduced gastric perfusion due to stress response (fight or flight response)
- also role for systemic acidosis secondary to disease
- lowers intracellular pH of mucosal cells–> making it more difficult for cells to produce acids an bicarbonate

45
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 parietal cells, intrinsic factor, gastrin
46
Q

Chronic gastritis and other diseases

A

Results from:
- H. pylori infection (most common)
- autoimmune
Implicated in:
- pernicious anemia
- gastric adenocarcinoma–> can get goblet cell metaplasia (pre-cancerous metaplasia lesion)
- GI endocrine hyperplasia–> caused by increased production of gastrin

47
Q

Gastritis Pathology

A

H. Pylori infection
- superficial plasma cells responding to presence of bacteria
Autoimmune
- response is to parietal cells
- deeper lesions near base of gland
- gland atrophy

48
Q

Pernicious Anemia

A
  • vit. B12 is required for thymidine synthesis
  • failure of DNA synthesis affects hematopoiesis
  • megaloblastic (abnormally large blood cells and precursors)
  • hypersegmented neutrophil in peripheral blood smear is characteristic of megaloblastic anemia
49
Q

What is a duodenal ulcer?

A
  • more common than gastric ulcers
  • result of H. pylori infection
    - altered mucosal immune response
    - excess acid
50
Q

What are the risk factors of duodenal ulcer?

A
  • diet (no specific associations)
  • smoking
  • excessive alcohol consumption
51
Q

What is a volvulus?

A

Intestinal obstruction caused by twisting of the bowel (can be in large or small intestine)
- rotates around mesenteric contact point
Also causes vascular blockage b/c of twisting of mesentery
- therefore obstruction and infarction

52
Q

Symptoms of volvulus

A
  • obstruction: abdominal pain and distension, vomiting, constipation
  • infarction: abdominal pain and tenderness, nausea, vomiting, bloody diarrhea (when hemorrhage present), melanotic stool (dark bloody stool)
53
Q

Treatment for volvulus

A

surgery to untwist bowel or remove that section and reattach the bowel depending on damage level

54
Q

What is intussuception?

A
  • most common cause of intestinal obstruction in children under 2 years
  • segment of intestines slides into next segment
    - usually happens during constriction due to peristalsis
    - segment becomes trapped: will drag mesentery in with it, which then blocks this section of the intestines
  • may develop into obstruction, mesenteric vessel constriction, possible infarction
55
Q

What is the treatment for intussuception?

A

contrast/air enemas may reverse it
- if not, surgery is required

56
Q

What is malabsorption and what causes it?

A

Most common clinical symptom is chronic diarrhea
Defective absorption of food contents
- fats
- vitamins (lipid or water soluble)
- proteins, carbohydrates
- electrolytes, minerals, water
Common causes:
- celiac disease (not autoimmune)
- pancreatitis
- cystic fibrosis
- inflammatory bowel disease

57
Q

What is celiac disease?

A

Immune-mediated enteropathy
- triggered by gluten-containing grains–> gluten is broken down into something the body is responding to (NOT autoimmune)
- NOT producing autoantibodies; producing antibodies to one of the breakdown products of gluten
- damage from immune response
- loss of brush border on enterocytes
- loss of villi (intestines)
- reduced surface for absorption = malabsorption
- immune cells recruited
- natural killer cells (CD8+ T lymphocytes)
- APCs will recruit CD4+ lymphocytes
- additional cells recruited

58
Q

Celiac Pathogenesis

A

gluten–> gliadin–> deamidated gliadin–> APC–> immune response
- Not gluten sensitivity; immune disease

59
Q

Treatment for celiac

A
  • avoid gluten intake
  • anti-inflammatories
60
Q

Celiac pathology

A

Inflammatory infiltrate
- still have intestinal glands, but no villi
T lymphocytes in epithelium
- reduced amount of brush border
- T cells w/in epithelium

61
Q

Describe the 2 types of inflammatory bowel disease (IBD)

A
  1. Infectious (Acute)
    - excluded by:
    - examining stool for infectious organisms
    - lack of responsiveness to abx
  2. Chronic (non-infectious)
    - characterized by flare-ups and remissions
    - NOT autoimmune
    - spontaneous remissions–> makes treatment difficult b/c you do not know if treatment fixed the problem or if the patient underwent spontaneous remission
62
Q

What is Acute IBD?

A

Infectious Enterocolitis
- Infection may be viral, bacterial, or parasitic
- Common infectious agents
*Vibrio Cholera (Cholera)- bacteria
* Campylobacter jejuni (Traveler’s Diarrhea)- bacteria
* Salmonella enteritidis (non-typhoid)- bacilli
* Salmonella enterica (Typhoid fever)- bacilli
* Clostridium difficile (Pseudomembranous colitis)- bacteria
* Escherichia coli (multiple)- bacilli

63
Q

What is Cholera?

A

Vibrio cholera produce a toxin
- actual bacteria are non-invasive, but do colonize epithelium
- limited histological changes to tissue
- not a really strong immune response

64
Q

Describe the pathogenesis of Cholera.

A

toxin taken into cells–> unfolded–> transported–> can impact intracellular signaling–> affecting cystic fibrosis transport membrane regulator (CFTR)–> causes excessive outflow of chloride–> sodium follows chloride–> affects water uptake in colon–> leads to watery stool/ severe diarrhea, which is associated with cholera

65
Q

Treatment for Cholera

A
  • remove vibrio cholera
  • supportive care with fluids until they can clear toxins/bacteria from the system
66
Q

What is Traveler’s Diarrhea?

A
  • Residents are generally resistant
  • Caused by:
    * campylobacter spp.
    * salmonella enterica (typhi and paratyphi)
    * ETEC (enterotoxigenic E. coli)
    * and others
67
Q

What is campylobacter jejuni and how is it associated with traveler’s diarrhea?

A
  • associated with ingestion of undercooked chicken, unpasteurized milk, and contaminated water
  • colonize mucosa
68
Q

Pathology of acute IBD (campylobacter jejuni)

A

-Camp. jejuni: mucosal and intraepithelial neutrophil invasion, including in the crypts
- crypt abscesses: neutrophil accumulation in crypt
- maintenance of crypt architecture (similar to EIEC)

69
Q

Escherichia Coli: ETEC, EHEC, EIEC

A

Most E. coli are not pathogenic (normal microbiota)
3 listed pathogenic E. Coli:
1. ETEC (Enterotoxigenic E. Coli)
- principal cause of traveler’s diarrhea
- produce 2 toxins (heat labile and heat stable)
* labile similar to cholera
* stable similar but through cGMP instead of cAMP
2. EHEC (Enterohemorrhagic E. coli)
- cows are reservoir (assoc. with contaminated beef)
- toxins cause dysentery-like disease–> bloody diarrhea
3. EIEC (Enteroinvasive E. coli)
- similar to shigella; resistant to acid
- proliferate intracellularly in the M cells overlying Peyer patches

70
Q

Pathology of acute IBD (EHEC and EIEC)

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 jejuni)

71
Q

What is Typhoid Fever?

A

Caused by Salmonella enterica
- 2 subtypes: typhi and paratyphi (both assoc. with typhoid fever)
- also nontyphoid Salmonella bacteria (do NOT cause typhoid)
Affects Peyer patches in ilium
- increases their size dramatically
- enlarged mesenteric lymph nodes in response to infection
- neutrophil accumulations in superficial mucosa
- also debris-filled macrophages, lymphocytes, and plasma cells in lamina propria
- will cause ulceration and possible perforation of the ilium
Damage to spleen and liver as well

72
Q

Treatment for Typhoid Fever

A

ABX

73
Q

What is Pseudomembranous colitis?

A

Antibiotic-associated colitis
- Clostridium difficile (C. difficile) overgrowth
* normal component of intestinal microbiota
* C. diff can overgrow w/ abx use b/c other components of intestinal microbiota are killed off
- Also caused by immunosuppression b/c immune system helps keep C. diff under control
- C. diff releases a toxin
* binds to small GTPases like Rho
* disrupts epithelial cytoskeleton (tight junctions)
* also induces cytokine release and apoptosis
- Can usually be diagnosed b/c stool is particularly foul smelling

74
Q

What are the 2 diseases that are both chronic IBD?

A
  1. Crohn’s Disease
    - occurs anywhere along GI tract
    - transmural–> go through entire thickness of wall
    - granulomatous
  2. Ulcerative Colitis
    - continuous–> starts in rectum and moves up
    - superficial
    - limited to colon mucosa
75
Q

What is involved in chronic IBD pathogenesis?

A
  1. Genetics
  2. Mucosal immune response
    - immunosuppressive therapy
  3. Epithelial abnormalities
    - cell-cell junctions
    - transepithelial transport
  4. Microbiota
    - likely difference b/t UC and Crohn’s
76
Q

Describe Crohn’s Disease.

A

Ulceration and inflammation are:
- discontinuous
- involve entire thickness of the wall
- can involve adjacent mesentery and lymph nodes
Results in nutrient deficiency b/c of damage to the colon
Initial clinical presentation includes:
- mild diarrhea
- fever
- abdominal pain
Attacks tend to be intermittent, but will cause damage to the wall of the intestines

77
Q

Crohn’s Disease Pathology

A
  • disordered crypts
  • granulomas –> mucosal, submucosal, and serosal
    * macrophage clusters
    * wall of threat
78
Q

Describe Ulcerative Colitis

A
  • Inflammation is limited to mucosa
  • Begins at anorectal junction and extends proximally
  • Characteristic necrotic lesions in the Crypts of Lieberkuhn
  • NO granulomas
79
Q

Similarities b/t UC and Crohn’s

A
  • 10% of patients have lesions characteristic of both
  • presentation is similar:
    * bloody diarrhea
    * malabsorption
80
Q

Difference b/t UC and Crohn’s

A
  • in UC, there is NO obstruction, perforation, or fistula formation
81
Q

What are Hemorrhoids?

A

Anal varices

82
Q

What causes hemorrhoids?

A
  • straining at defecation due to constipation
  • venous stasis due to pregnancy
  • portal hypertension (similar to esophageal varices)
83
Q

How do you treat hemorrhoids?

A
  • anti-inflammatory to reduce swelling
  • stool softener to prevent constipation
  • surgical removal
84
Q

Pathology of hemorrhoids

A
  • thin-walled, dilated, submucosal vessels that protrude beneath mucosa
  • tend to become inflamed and develop thromboses
  • may lead to superficial ulceration

Mechanisms of Disease (10 decks)

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