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Patho > Topic 3 - GI Disorders > Flashcards

Topic 3 - GI Disorders Flashcards

1
Q

What are the roles of saliva?

A
  1. Cleanse mouth (antibacterial properties)
  2. Moistens and compacts food
  3. Enzymes that begin digestion of starches (amylase and lipase)
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2
Q

What are the three salivary glands?

A

Parotid, submandibular, subglossal

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3
Q

What kinds of things trigger salivation?

A

PSNS –> food, irritations in lower GI tract

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4
Q

What kinds of things inhibit salivation?

A

SNS, dehydration, antihistamines, antidepressants, radiation

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5
Q

What is the medical term for dry mouth?

A

Xerostomia

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6
Q

What is the name for inflammation of the oral mucosa?

A

Stomatitis

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7
Q

What can cause stomatitis?

A

–> Microorganisms
–> Trauma
–> Chemotherapy
–> Nutritional deficiencies
–> AIDS
–> HSV (Cold sores)

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8
Q

What is the name for erosive inflammation with cracking or ulceration of the corners of the mouth?

A

Angular stomatitis / Angulae cheilitis

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9
Q

What might cause angular stomatitis/cheilitis?

A

B12 deficiency, IDA - might be accompanied by opportunistic fungal or bacterial infection.

Mask wearing exacerbates problem.

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10
Q

What might cause strawberry tongue?

A

Scarlet Fever (Group A strep)

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11
Q

What is Candida albicans?

A

Oral thrush, an oral fungal infection.

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12
Q

How is a salivary gland infection treated?

A

Antibiotics

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13
Q

How is a salivary gland stone treated?

A

Removed of stone (with needle or surgically)

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14
Q

How are salivary gland tumors treated?

A

By removing the affected gland

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15
Q

How does myxovirus affect the body?

A

Mumps causes inflammation of the parotid glands and has a 25% risk of affecting the testes in adult males.

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16
Q

How does mumps cause sterility in males?

A

Mumps has a 25% chance of spreading to the tested. The increased temperature due to the infection can harm the germ stem cells and cause fertility issues or sterility.

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17
Q

What is the name for the disorder characterized by decreased peristalsis of the esophagus, loss of tone of the GE sphincter between meals, and decreased relaxation of the GE sphincter in response to swallowing

A

Achalasia

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18
Q

What causes achalasia?

A

Degeneration of esophageal ganglion cells and atrophy of smooth muscle

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19
Q

What of the symptoms of achalasia?

A

Dysphagia (increased by stress), vomiting, nausea, weight loss.

Risk of pneumonia due to aspiration.

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20
Q

How is achalasia diagnosed?

A

With a barium swallow

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21
Q

How is achalasia treated?

A

Treatment targets the GE sphincter. Issues with lack of relaxation can be managed by eating small meals with lots of fluids or sleeping with the head elevated.

More invasive treatment options include pneumatic dilation of the GE sphincter, myotomy, or botox.

Side effect of these treatments include GERD

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22
Q

What is GERD?

A

Gastroesophageal Reflux

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23
Q

What can frequent or long term reflux cause?

A

Esophagitis

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24
Q

What are the symptoms of GERD?

A

Substernal pain that is exacerbated by supine position, pulmonary aspiration is a risk. Over time, damage to the muscularis is possible.

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25
Q

How is GERD diagnosed?

A

Endoscopy + biopsy, pH measurements, barium swallow to reveal associated conditions - such as a hiatal hernia, pr a shortened or ulcerated esophagus.

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26
Q

How can GERD be treated?

A

–> Antacids
–> Elevation of head
–> Weight reduction
–> H2-blockers
–> PPIs

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27
Q

What do H2-blockers do?

A

Make histamine unable to exert its normal effect on acid production in stomach

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28
Q

Which three hormones are responsible for causing acid production in the stomach?

A

Gastrin, Ach, and histamine

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29
Q

What is a PPI

A

A proton pump inhibitor inhibits the mechanism that produces acid in the stomach.

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30
Q

Why are PPIs not recommended for long-term use?

A

Because their use over an extended period might lead to malabsorption of vitamin B12, Iron, magnesium, and calcium

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31
Q

What is Barrett’s esophagus?

A

When epithelial cells in the esophagus change from stratified squamous cells to simple columnar cells due to repeated exposure to stomach acid - this has a high probability of leading to cancer.

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32
Q

What are the phases of long term complications due to GERD?

A
  1. Inflammation
  2. Erosive esophagitis
  3. Barrett’s esophagus
  4. Adenocarcinoma
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33
Q

Why are esophageal cancers so serious?

A

They are hard to treat due to their location and because they spread very easily.

They are usually asymptomatic until unresectable, and 16% of cases survive five years past diagnosis.

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34
Q

What is a sliding hiatal hernia?

A

When the stomach slides through the esophageal hiatus when supine or when intra-abdominal pressure increases. It slides back when standing.

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35
Q

Which kind of hiatal hernia presents the risk of developing GERD?

A

A sliding hernia

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36
Q

What are some potential causes of a sliding hiatal hernia?

A

Defect in diaphragm or weakening of the diaphragm muscles (might be caused by progesterone during pregnancy)

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37
Q

What percentage of hiatal hernias are sliding, as compared to rolling?

A

Sliding - 90%
Rolling - 10%

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38
Q

What is a rolling (paraoesophageal) hiatal hernia?

A

When part of the greater curvature of the stomach protrudes through a 2nd or enlarges opening in the diaphragm.

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39
Q

If GERD common in someone with a rolling hiatal hernia?

A

Not usually, because the GE sphincter remains the the same place.

Gastritis and ulcers in herniated area are common.

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40
Q

How is a paraoesophageal hernia treated?

A

A rolling hernia is treated promptly by surgery to avoid necrosis of herniated tissue.

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41
Q

What is an esophageal varices?

A

A varicose veins within the esophagus

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42
Q

What causes esophageal varices?

A

Portal hypertension - common in someone with advanced cirrhosis

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43
Q

What are the dangers or esophageal varices?

A

Thin walled veins in the area are subject to rupture. This leads to a tremendous amount of bleeding into the GI system, even first time bleeds have a 40% mortality rate.

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44
Q

Why should lipid soluble drugs like alcohol and NSAIDS (and bile salts) not be taken in large quantities?

A

These substances easily cross the mucosa into the bloodstream and can create pathways as they do this - this leads to gastric bleeding

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45
Q

how do caffeine and nicotine affect gastric secretions?

A

They increase the amount and the acidity of gastric secretions.

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46
Q

Which drug decreases output of mucous by gastric secretions?

A

Aspirin

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47
Q

How does prolonged stress or corticosteroids affect the lining of the stomach?

A

Increase acid and pepsinogen secretion and decreases blood flow to stomach wall

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48
Q

How does insulin affect gastric secretion?

A

It increases them.

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49
Q

What are the motor responses to the emetic centre?

A
  1. Skeletal muscle of abdominal wall + diaphragm
  2. GE sphincter relaxes
  3. Soft palate rises to close off nasal passages
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50
Q

What are the concerns of prolonged vomiting?

A

–> Dehydration
–> Acid-base balance issues

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51
Q

Where is the emetic center of the brain?

A

In the medulla

52
Q

How does Gravol reduce nausea?

A

By antagonizing H1 receptors - reduces activation of vestibular and emetic canters via histaminergic neural pathways.

53
Q

What is the term for inflammation of gastric mucosa?

A

Gastritis

54
Q

What causes acute gastritis?

A

–> Superficial erosion of gastric mucosa
–> H pylori, NSAIDS

55
Q

Why do NSAIDS cause gastritis?

A

They inhibit prostaglandin release.
PGs stimulate mucus secretion –> lack of PGs means stomach mucosa has less protection from acidic environment

56
Q

What symptoms are characteristic of acute gastritis?

A

Vague abdominal discomfort, epigastric tenderness, bleeding

57
Q

What are the symptoms of an H Pylori infection?

A

–> Inflammation
–> Pain
–> Nausea
–> Vomiting

Can lead to ulcers or cancer

58
Q

How is acute gastritis treated?

A

Usually it spontaneously heals within a few days, but this healing can be aided by:
–> antacids, PPIs, H2 Blockers
–> stopping a problem drug
–> taking antibiotics if the issue is H pylori

59
Q

How do we test for H pylori?

A

A urease breath test is most often used
–> H pylori embeds in the stomach and produces urease to neutralize the acidity

60
Q

What are the two kinds of chronic gastritis?

A
  1. Fundal (A)
    –> Autoimmune in origin
    –> Causes impairment in pepsin, intrinsic factor, and HCl production
  2. Antral (B)
    –> Not associated with function loss
    –> Often due to H pylori
61
Q

Which kind of chronic gastritis is most common?

A

Type B, antral, is 4xmore common

Type A, fundal, is most rare, but also the most severe

62
Q

What are some symptoms of chronic gastritis?

A

In addition to the symptoms of acute gastritis, chronic gastritis also presents with
–> Anorexia
–> Persistent fullness
–> Nausea
–> Vomiting
–> Pain
–> Gastric bleeding

63
Q

How is chronic gastritic treated?

A

Small meals and a bland diet, avoiding triggers such as NSAIDS or alcohol.
Antibiotics for antral type.

64
Q

Where are peptic ulcers most common?

A

In the top portion of the duodenum (80%)

Stomach and esophagus follow

65
Q

What are the risk factors for developing a peptic ulcer? Why?

A

–> Smoking (Nicotine is a vasoconstrictor)
–> H pylori (Infection)
–> NSAIDs (PG inhibitors)

66
Q

Which demographic is most commonly affected the duodenal ulcers?

A

–> Young people
–> Those with type O blood
(Reason not known, might be due to hypersecretion of acid and pepsin, easier binding of H pylori, or enhanced inflammatory response to H pylori.

67
Q

Although H pylori is the major cause of duodenal ulcers, it alone is not enough. What are are risk factors that create an environment for ulcers?

A

–> Excess parietal cells in gastric mucosa
–> Stress
–> Prolonged high serum gastrin
–> Too rapid gastric emptying
—> Use of NSAIDS
–> Cigarette smoke stimulated secretion of acid

68
Q

What are the symptoms are duodenal ulcers?

A

–> Chronic, intermittent epigastric pain with onset 30mins-2hrs after eating.
–> Pain that is relieved by food or antacids
–> With some older adults the first sign is hemorrhage or perforation

69
Q

How are duodenal and gastric ulcers diagnosed?

A

Take a detailed history. Then, we need to differentiate between gastric ulcers and a carcinoma.

Barium x-ray, a flexible endoscopy, or gastric biopsy are all used

70
Q

How are duodenal and gastric ulcers treated?

A

–>Antacids, PPIs, or H2 blockers
–> Antibiotics
–> Ulcer coating agents, such as sucralfate or colloidal bismuth

71
Q

Which age range is usually affected by gastric ulcers?

A

Ages 55-65

72
Q

Gastric atrophy, mostly watery secretions and a lack of intrinsic factor are often linked to what?

A

Gastric ulcers

73
Q

What are some symptoms of gastric ulcers?

A

Pain right after eating.

Because the patient is more likely to associate the pain with food, they may present with anorexia, vomiting, and weight loss.

74
Q

Which age group is usually impacted by gastric carcinomas? What is the prognosis?

A

Usually ages 60-65. Less than 30% live past five years of diagnosis

75
Q

What are some risk factors for gastric carcinomas?

A

–> Smoking
–> Processed meats
–> H pylori
–> Positive family history

76
Q

Why are processed meats a risk factor for developing a gastric carcinoma?

A

Processed meat contains nitrites, which are broken down into nitrosamine.
Nitrosamine is a carcinogen.

77
Q

Why are gastric carcinomas so dangerous?

A

They have a poor prognosis and easily metastasize

78
Q

What are some symptoms of a gastric carcinoma?

A

Symptoms are very vague:
–> Early satiety
–> Loss of appetite
–> Weight loss
–> Abdominal pain
–> Vomiting
–> Bleeding

79
Q

What is the only definitive diagnosis for a gastric carcinoma?

A

A gastric biopsy

80
Q

How is H pylori treated?

A

With long course antibiotics - often 2-3 of them.

81
Q

what causes gallstones?

A

A supersaturation of bile salts with cholesterol
–> Especially if combined with stasis of bile fluid

Causes crystalizing, and formation of biliary calculi (gallstones)

82
Q

What is obstructive jaundice?

A

A blockage in the outflow pathway of bile leads bilirubin to be moved back into the bloodstream.

83
Q

How are gallstones treated?

A

By sugically removing the gallbladder

84
Q

What causes Cirrhosis?

A

Chronic liver injury which leads to extensive fibrosis and regnerative nodules.

Conditions finished with liver failure.

85
Q

how does cirrhosis lead to ascites?

A

Fibrosis leads to bands of scar tissue which lead to portal hypertension

Portal hypertension leads to fluid build up in peritoneal cavity (ascites)

86
Q

Describe the process of how alcohol leads to cirrhosis.

A
  1. Alcohol becomes 1° metabolic fuel
    This has a direct affect of cellular and organelle membranes, as well as mitochondrial function
  2. Leads to the generation of reactive oxygen species (Free radicals)
  3. To exacerbate the problem, alcoholism is usually also associated with malnutrition
87
Q

What is CF?

A

Cystic Fibrosis is a defective gene on the CFTR on chromosome seven.

This gene codes for a chloride channel that is necessary for mucus to have the right consistency.
For those with CF, mucus is not watery enough and has too much mucin. This means it is too viscous.

88
Q

Ho does CF affect the exocrine pancreas?

A

Thick mucus prevent pancreatic exocrine function by blocking ducts –> Fibrosis and degeneration of secretory tissue –> absence of pancreatic enzymes in duodenum –> incomplete digestion and malabsorption

89
Q

What is lactose intolerance?

A

A deficiency in the brush border enzyme lactase.

This is normal for most populations, as the gene that codes for is it “turned off” around age four.

90
Q

What are the symptoms and causes of lactose intolerance?

A

Diarrhea –> Lactose creates osmotic gradient

Gas + bloat –> Microbiome bacteria process lactose and produce gas in large intestine.

91
Q

What is the cause of small volume diarrhea?

A

Inflammatory disorders, such as ulcerative colitis or Chron’s disease

92
Q

What are the three kinds of large volume diarrhea?

A
  1. Osmotic (lactose intolerance)
  2. Secretory (bacterial endotoxins, like cholera)
  3. Motility (often unknown reason)
93
Q

How is diarrhea evaluated?

A

Ask about history of travel, drug therapy,.

Take stool culture, an abdominal x-ray, or intestinal biopsy.

94
Q

How is diarrhea treated?

A

Restoration of fluids + electrolytes

Management of symptoms, and treatment of causal factor

95
Q

Which two things can cause malabsorption?

A
  1. Digestive issues
    –> Pancreatic secretion
    –> Biliary secretions
  2. Absorption issues
    –> Can be a single substance or many nutrient groups
96
Q

Describe celiac disease.

A

Gliadin, a protein in gluten is toxic to the intestinal epithelium of genetically susceptible individuals - when gluten is consumed villi become flattened or absent and epithelium becomes disorganized and cuboidal rather than columnar. Brush border thickens and this causes the malabsorption of almost everything.

97
Q

Is Gluten-Sensitive Enteropathy more common in men or women?

A

Women, onset often occurs in young adulthood

98
Q

What are the clinical signs of Celiac disease?

A

–> Frequent, foul-smelling, fatty stool
–> Weight loss
–> Malabsorption of fat-soluble vitamins
–> Muscle wasting
–> Hypo-proteinemia
–> Failure to thrive

99
Q

How is Celiac disease diagnosed?

A

Screen for antibodies for gliadin and for markers of inflammation.

Definitive diagnosis is done by endoscopy combined with intestinal biopsy

100
Q

How is Celiac treated?

A

–> Remove barley, wheat, and rye from diet
–> Assume lactose intolerance until epithelium is repaired

101
Q

Chron Disease and Ulcerative Colitis are both grouped as ____

A

Inflammatory bowel diseases

102
Q

What are some clinical signs of Chron Disease (IBD1)

A

–>Having an irritable bowel for several years
–> Malabsorption of vitamin b12 + tenderness in lower right abdomen (if ileum is involved)
–> Weight loss
–> Blood in feces
–> Nausea and vomiting
–> Intestinal obstruction or fistula

Correlated with several autoimmune diseases and an increased risk of intestinal adenocarcinoma

103
Q

What are skip lesions?

A

Damage to the mucosa and deeper that causes a cobblestone appearance to the bowel.

104
Q

how are fistulas and stenoses diagnosed?

A

Through medical history and clinical signs - radiographer shows narrowing

105
Q

How is Chron Disease treated?

A

By suppressing the immune response (corticosteroids or methotrexate)

Surgery as needed to relieve abscesses, strictures, or obstructions.

106
Q

What vitamins do the large intestine’s flora synthesize?

A

B complex vitamins and vitamin K.

107
Q

What kinds of things might cause constipation?

A

Constipation is caused by too much water being absorbed
Might be caused by:
–> lack of fiber
–> Lack of exercise
–> Emotional upset
–> laxative abuse

108
Q

What is diverticulitis?

A

Puckering of haustra muscle with stuck material - associated with long-term constipation

109
Q

What kind of intestinal obstruction is characterized by the structure slipping through a muscle opening?

A

A hernia

110
Q

What kind of intestinal obstruction is characterized by an intestine coiling around itself in a knot like way?

A

A vovulvus

111
Q

What kind of intestinal obstruction is characterized by an intestine curling in on itself like a telescope?

A

Intussusception

112
Q

What kind of intestinal obstruction is characterized by scar tissue wrapping around an blocking part of the structure?

A

An adhesion

113
Q

What are the clinical signs of an intestinal obstruction?

A

–> Severe, acute cramping
–> Vomiting
–> Diarrhea
–> Risk of hypovolemic shock + septic shock

114
Q

What are precipitating factors for hemorrhoids?

A

Constipation + pregnancy (which causes constipation due to progesterone’s smooth muscle relaxing effect)

115
Q

What are the clinical signs of Ulcerative Colitis? (IBD2)

A

There are periods of flare up and remission, so symptoms vary
–> Increased frequency of BMs
–> Bleeding
–> Pain

116
Q

What occurs during ulcerative colitis?

A

The bowel (starting at the rectum and moving proximally) fills with a bloody mucoid secretion.

117
Q

How is ulcerative colitis diagnosed?

A

–> Medical history
–> Sigmoidoscopy, barium x-ray to check for a loss of haustra, ulceration or irregular mucosa
–> Rule out infectious agents with stool culture

118
Q

What are some important distinctions between colitis and irritable bowel?

A

–> IBS does not damage the intestinal wall
–> IBS is not linked to an increased risk of colorectal cancer

119
Q

What are some possible triggers for IBS flare ups?

A

IBS flare up triggers are personal to the individual, but can include:
–> Intestinal infection or bacterial overgrowth
–> Food allergies or intolerances
–> Stress
–> Hormones (Especially towards end of luteal phase?)

120
Q

What can help alleviate symptoms in someone with IBS?

A

Avoiding personal triggers and increasing fiber in diet

121
Q

Which demographic in most affected by IBS?

A

Women - often linked to depression and anxiety as well

122
Q

What are the clinical signs of Appendicitis?

A

Pain in the lower right quadrant, nausea + vomiting, low-grade fever, rebound tenderness, might have elevated WBC count.

123
Q

What are polyps?

A

Benign growths in the colon and rectum that have the potential to metastasize and cause problems elsewhere.

124
Q

What are adenocarcinomas?

A

Cancers of the epithelium with long pre-invasive phases and slow growth

125
Q

How would colon cancer be diagnosed?

A

By taking a family history and asking about diet, colonoscopy, and testing for liver enlargement, ascites, lymph node enlargement. Barium enema also helps.

126
Q

What are some risk factors for developing cancer of the colon?

A

–> Genetic link
–> high fat, low fiber and calcium diet

127
Q

How is colon cancer treated?

A

Surgery, radiation, AND chemotherapy.

Patho (14 decks)

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