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Anatomy and Phyisology > upper GI tract disorders > Flashcards

upper GI tract disorders Flashcards

1
Q

congenital defects of the upper tract

A

cleft lip and cleft palate

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2
Q

cleft lip and cleft palate causes

A

multifactorial; environmental and genetic and problems arise in the second or third month of gestation

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3
Q

cleft lip

A

may be unilateral or bilateral and results from failure of the maxillary processes to fuse with the nasal elevations, or failure of the upper lip to fuse

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4
Q

cleft palate

A

failure of the hard and soft palate to fuse, creating an opening between the oral cavity and the nasal cavity

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5
Q

problems associated with cleft palate

A

feeding problems, risk of aspirating fluid in respiratory passages, and speech developments

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6
Q

treatment for cleft palate

A

surgery and speech therapy

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7
Q

aphthous ulcers

A

canker sores/ aphthous stomatitis; cause is unclear there are contributing possible factors

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8
Q

factors contributing to aphthous ulcers

A

minor injury to the mouth, toothpastes, food sensitivities, lack of vitamins, allergic response, H pylori, hormonal shifts, emotional stress, celiac, IBDs, bechat disease, a faulty immune system, and HIV

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9
Q

what ingredient in toothpaste causes aphthous ulcers?

A

sodium lauryl sulfate

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10
Q

foods that may cause aphthous ulcers

A

chocolate, coffee, strawberries, eggs, nuts, cheese, or spicy and acidic foods

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11
Q

what lack of vitamins may cause aphthous ulcers

A

B12, zinc, folate, or ion

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12
Q

what do aphthous ulcers appear as?

A

small, shallow, painful lesions occurring on the moveable mucosa, the buccal mucosa, the floor or the mouth, the soft palate, or the lateral borders of the tongue

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13
Q

example of resident flora of the oral cavity

A

viridans streptococci and staphylococcus aureus

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14
Q

risk of infection in the oral cavity

A

resident flora are normally harmless but can cause opportunistic infections such as candidiasis or secondary infections when there are open lesions; may also enter the bloodstream and travel to the heart (bacterial endocarditis)

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15
Q

what medication may help with oral cavity infections?

A

amoxicillin

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16
Q

oral candidiasis

A

fungal infection caused by candida albicans which are part of the normal flora of the mouth; common in those who have received broad-spectrum antibiotics, chemo, or glucocorticoids, or those who have diabetes or are immunosuppressed

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17
Q

initial infection of AIDs

A

oral candidiasis

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18
Q

what does oral candidal infection appear as?

A

a red, swollen area or irregular patches or white curd like material on the mucosa of the tongue of the mouth

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19
Q

treatment for candidal infections

A

nystatin, a topical antifungal agent

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20
Q

what is herpes virus caused by and transmission?

A

the herpes simplex virus type 1 (HSV-1) and is transmitted by kissing or close contact

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21
Q

why does herpes not persist early on?

A

it remains dormant in a sensory ganglion, often in the trigeminal nerve

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22
Q

herpes simplex signs

A

burning or stinging at the site, following by vesicles/blisters as thee virus reproduces and causes necrosis of the host cell, leaving a shallow, painful ulcer

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23
Q

when is herpes simplex activated?

A

via stress, trauma, or another infection

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24
Q

treatment for herpes simplex

A

no cure but treated with antiviral medications such as acyclovir, valtrex, and famvir

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25
Q

where may herpes simplex travel to?

A

the eyes, causing conjunctivitis and keratitis

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26
Q

what is syphilis caused by?

A

the spirochete treponema pallidum

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27
Q

stages of syphilis

A

initial stage is a painless ulcer on the tongue, lips, or palate, followed by a red macules or papules on the palate, and a rash

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28
Q

another name for tooth decay and cavities

A

dental caries

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29
Q

dental caries

A

is an infection involving any number of bacteria found in the oral cavity

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30
Q

primary microorganisms causing dental caries

A

streptococcus mutans and lactobacillus

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31
Q

how do dental caries form

A

from the bacteria acting on sugars in ingested food to create large quantities of lactic acid that dissolves the minerals in the tooth enamel

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32
Q

pulpitis

A

infection of the internal structures of the teeth and can be caused when dental caries are untreated

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33
Q

risk for developing dental caries

A

sugars and acids such as carbonic acid in soda, dry mouth, plaque formation, and periodontal disease

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34
Q

dry mouth name

A

xerostomia

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35
Q

how does fluroide work?

A

is decreases the solubility of the minerals in the enamel (replaces hydroxyapatite) and enhances the remineralization process

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36
Q

hypocalcification

A

excessive fluoride ingestion and can result in a deficient calcification of tooth enamel

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37
Q

periodontitis

A

the infection and damage to the periodontal ligament and bone by microorganisms and the subsequent loosening and possible loss of teeth

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38
Q

how many categories of periodontal disease are there?

A

8; range from mild gingival disease to severe periodontitis

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39
Q

what is the periodontium

A

the gingivae and the anchoring structures (alveolar bone, cementum, and the periodontal ligament

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40
Q

what is periodontal disease caused by?

A

poor oral hygiene but can be aggravated by some systemic diseases and medications

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41
Q

gingivitis

A

the inflammation of the gingia which causes the gingival tissue to become red, soft, swollen, and bleed easy

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42
Q

causes of gingivtis

A

accumulated plaque, in which the microbes secrete substances that enable them to adhere to the tooth surface and its plaque

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43
Q

what is plaque?

A

a mass of bacteria and debris adhering to the teeth

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44
Q

what is tartar?

A

aka calculus; is calcified plaque, which is even more irritating to the tooth due to its hard, rough surface

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45
Q

how improper brushing cause gingivitis?

A

can create extensive grooving on the tooth surface, increasing plaque retention and tooth sensitivity

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46
Q

dark line of the gingival margin

A

indicative of lead poisioning

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47
Q

overgrowth of gums

A

may occur from hormonal changes associated with pregnancy and the use or oral contraceptives

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48
Q

gingival hyperplasia

A

occurs with the long-term use of drugs such as phenytoin or cyclosporine

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49
Q

necrotizing periodontal disease

A

aka trench mouth; an infection caused by anaerobic opportunistic bacteria in those who tissue resistance is decreased

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50
Q

causes of necrotizing perodontal disease

A

stress, smoking, disease, or nutritional deficets

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51
Q

appearance of necrotizing periodontal disease

A

lower jaw teeth are affected, showing white necrotic areas surrounded by red and swollen areas that are painful and bleed easy

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52
Q

periodontitis

A

a more serious more of periodontal disease that develops when there is an increase in activity of gram-negative anaerobic bacteria as they enter the plaque and secrete enzymes

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53
Q

common microbes in periodontal disease

A

porphyromonas gingivalis, actinobacillus actinomyectem comians and bacteroides forsythus

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54
Q

what is periodontitis caused by?

A

poor oral hygiene cancer, smoking, diabetes mellitus, and HIV infection

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55
Q

what does periodontal disease result in?

A

inflammation around the tooh and beneath the gingival margin, forming a pocket around the tooth; mucosa is also red, swollen, and bleeds easily

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56
Q

hyperkeratosis and example

A

thickening on the skin in certain areas; ex. leukoplakia

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57
Q

leukoplakia

A

a whitish plaque or epidermal thickening of the mucosa that occurs on the buccal mucosa, palate, lower lip, or tongue

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58
Q

common cancer of the oral cavity

A

squamous cell carcinoma

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59
Q

squamous cell carcinoma risk population

A

common in smokers, those over 40, those with alcohol abuse, and those with a preexisting leukoplakia

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60
Q

squamous cell carcinoma

A

malignant tumors inside the oral cavity; poor prognosis because they are hidden and painless; common around the floor of the mouth and the lateral borders of the tongue

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61
Q

what does squamous cell carcinoma appear as?

A

a whitish thickening and then develops into a nodular mass or an ulcerative lesion

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62
Q

kaposi carcoma

A

common in AIDS patients; lesion is a brownish or purple lesion, usually on the palate which eventually becomes a nodular mass

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63
Q

lip cancer

A

usually on the lower lip, it obvious, accessible, and has a good prognosis; common in pipe smokers

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64
Q

sialadenitis

A

inflammation of the salivary glands, most commonly affecting the parotid gland by infectious agents and tumors

65
Q

mumps

A

aka infectious parotitis; is a viral infection leading to marked, usually bilateral, swelling of the glands

66
Q

noninfectious parotitis

A

develops in debilitated or elderly patients who lack adequate fluid intake and mouth care

67
Q

most frequent malignant tumor of the salivary gland

A

mucoepidermoid carcinoma which occurs primarily in the parotid glands

68
Q

dysphagia and causes

A

is difficulty swallowing; many causes such as a neurological deficit, a muscular disorder, or a mechanical obstruction

69
Q

neurologic causes for dysphagia

A

infection, stroke, brain damage, and achalasia (failure of the lower esophageal sphincter to relax)

70
Q

results of achalasia

A

an accumulation of food in the lower esophagus, causing inflammation and reflux of the food; increased risk of esophageal carcinoma in chronic conditions

71
Q

mechanical obstructions causing dysphagia

A

congenital atresia, stenosis, esophageal diverticula, and tumors

72
Q

congenital atresia

A

a developmental defect in which the upper and lower esophageal segments are separated, causing reflux of feeding, leading to aspiration

73
Q

stenosis of the esophagus

A

the narrowing of the esophagus which can be developmental or acquired

74
Q

causes of esophagus stenosis

A

usually is secondary to fibrosis from chronic inflammation, ulcers, or radiation therapy, or from scar tissue from chemicals

75
Q

esophageal diverticula

A

outpouchings of the esophageal wall that either result from congenital defects or inflammation; food will accumulate here and obstruct the flow of food, causing irritation, inflammation, and scar tissue

76
Q

signs of esophageal diverticula

A

dysphagia, foul breath, chronic cough, and hoarseness, and sometimes bleeding

77
Q

esophageal cancer

A

primary cancer is squamous cell carcinoma which forms in the distal esophagus; can grow into the lumen and cause dysphagia; prognosis is quite poor

78
Q

what is esophageal cancer associated with?

A

chronic irritation like alcohol, smoking, or inflammation

79
Q

hiatal hernia

A

occurs when part of the stomach protrudes through the opening (hiatus) in the diaphragm into the thoracic cavity

80
Q

two types of hiatal hernia

A

sliding and rolling or paraesophageal

81
Q

sliding hernia

A

more common and occurs when a portion of the stomach and the gastroesophageal junction move above the diaphragm; standing in slides back down but occurs in a supine position

82
Q

rolling or paraesophageal hernia

A

occurs when part of the fundus of the stomach moves up through an enlarged or weak hiatus in the diaphragm; can cause vessels to be compressed, leading to ulceration

83
Q

risks associated with hernias

A

food can lodge in the pouch, causing inflammation of the mucosa, a reflux of food up the esophagus, and dysphagia; chronic conditions can cause fibrosis and stricture (narrowing of a passage)

84
Q

factors increasing risk for developing a hiatal hernia

A

shortening of the esophagus, weakness of the diaphragm, and pregnancy due to increased abdominal pregnancy

85
Q

signs of hiatal hernia

A

heartburn or pyrosis (burning sensation following by a sour taste in the mouth), belching, and discomfort eating, lying down, or coughing

86
Q

why is dysphagia common in hiatal hernia’s?

A

because of the inflammation caused in the esophagus or the mass of food collected in the pouch that compresses the esophagus

87
Q

how to reduce discomfort from hiatal hernia’s?

A

frequent, small meals and avoiding a recumbent position (horizontal) after meals

88
Q

GERD

A

gastroesophageal reflux disease; involves the periodic flow of gastric contents into the esophagus and is often in conjunction with hiatal hernia; severity depends on the position of the lower esophagus sphincter

89
Q

how does GERD occur?

A

a decrease in LES pressure or an increase in intra abdominal pressure which causes gastric contents to reflux back into the esophagus

90
Q

what is the result of frequency reflux og gasric acid?

A

inflammation and ulceration of the mucosa, and eventually fibrosis and stricture in the esophagus

91
Q

how to prevent GERD

A

reducing caffeine, fatty foods, alcohol, smoking, and certain drugs

92
Q

diagnosis of GERD

A

includes an upper endoscopy, ambulatory acid probe test, esophageal manometry, and X-ray of the upper digestive tract

93
Q

treatment for GERD

A

antacids that neutralize stomach acids such as Tums or mylanta, medications to reduce acid production like H2 receptor blockers (nizatidine or cimetidine), proton pump inhibitors (lansoprazole), medication to strengthen the LES

94
Q

gastritis

A

an inflammation of the stomach; can be acute or chronic

95
Q

acute gastritis

A

the gastric mucosa is inflamed and appears red, edematous, and sometimes ulcerating and bleeding, which can be a result of poor circulation

96
Q

what may cause acute gastritis

A

infection from microorganisms such as bacteria and/or viruses, allergies, ingestion of spicy foods, excessive alcohol, ingestion of aspirin, ingestion of toxic substances, or chemotherapy or radiation

97
Q

basic signs for gastrointestinal irriation

A

anorexia, nausea, or vomiting are most common; can also be pain, cramps, or fever and headache that occur with infection

98
Q

treatment for acute gastritis

A

heals on its own within a day or two; electrolyte and fluid replacement is good when diarrhea or vomiting occurs, and antimicrobial drugs may be used for infections

99
Q

food or water-borne illnesses

A

may involve a large number of cases, sometimes infecting communities

100
Q

rotavirus

A

cause serious infection including vomiting and diarrhea, sometime along with ulcers

101
Q

where are outbreaks of gastroenteritis common?

A

daycare centres and institutions

102
Q

clostridium difficile

A

common in those on broad-spectrum antibiotics when bacteria like E coli are killed off; it is a gram-positive bacteria and is common in hospitals

103
Q

Escherichia coli

A

a normally harmless microbe that can adhere to the mucosa and secrete enterotoxin, causing gastroenteritis or ‘travelers diarrhea’; has five forms

104
Q

5 forms of escherichia coli infection

A

enterotoxigenic E coli, enteroinvasive E coli, enteropathogenic E coli, enteroaggregative E coli, and enterohemorrhagic E coli

105
Q

enterotoxigenic E coli

A

causes diarrhea in infants and travelers; the organism produces enterotoxins

106
Q

enteroinvasive E coli

A

causes severe diarrhea and fever; the organism does not produce enterotoxins

107
Q

enteropathogenic E coli

A

similar to enteroinvasive, but enterotoxins are produced and it is similar to shigella

108
Q

enteroaggregative E coli

A

produces persistent diarrhea and a hemolysin that causes UTIs; produces an enteroaggregative heat-stable toxin

109
Q

enterohemorrhagic E coli

A

damage to the mucosa blood vessels can affect blood vessels in the kidneys; present in cows and infection is due to food and water contaminated with particular strains

110
Q

what strain causes enterohemorrhagic E coli

A

O157:H7

111
Q

what is enterohemorrhagic E coli commonly caught from?

A

ground beef, unpasteurized milk, or contamination from other oral fecal routes

112
Q

what do the strains of enterohemorrhagic E coli release?

A

O157:H7 release verocytotoxins that are similar like Shiga-like toxins

113
Q

general effects of E coli

A

diarrhea (can progress to bloody diarrhea), cramps, hemolysis of blood cells leading to anemia, acute renal failure, and neurologic effects such as seizures

114
Q

chronic gastritis

A

characterized by atrophy of the mucosa of the stomach, with loss of the secretory glands; loss of parietal cells cause achlorhydria and lack of secretion of intrinsic factor

115
Q

what infection is often associated with chronic gastritis?

A

H pylori

116
Q

what individuals often display chronic gastritis?

A

chronic peptic ulcers, alcohol abuse, the elderly, and some includes with autoimmune disorders such as pernicious anemia

117
Q

signs of chronic gastritis

A

mild epigastric discomfort, anorexia, or intolerance for spicy and fatty foods

118
Q

increased risk for those with chronic gastritis

A

peptic ulcers and gastric carcinoma

119
Q

treatment for chronic gastritis

A

antibiotics and proton pump inhibitors

120
Q

where are peptic ulcers found?

A

commonly occur in the proximal duodenal but are also found in the antrum of the stomach or lower esophagus

121
Q

peptic ulcers

A

usually appear as single, small, round cavities with smooth margins that penetrate the submucosa; surrounding tissues are damaged due to acid from the gastric wall

122
Q

effects of peptic ulcers

A

ulcers may erode into a blood vessel wall, causing bleeding and sometimes hemorrhages

123
Q

mucosal of the stomach

A

tightly packed epithelial cells that can regenerate quickly and are covered by a thick layer of HCO3- rich mucous

124
Q

causes of gastric ulcers

A

impaired mucosal defences and H pylori

125
Q

causes of duodenal ulcers

A

increased acid secretion and H pylori

126
Q

relationship of H pylori and peptic ulcers

A

major significance of developing ulcers due to the microorganism secreting cytotoxins and the enzymes protease, phospholipase, and urease which all damage the mucosa

127
Q

how might the mucosa lining of the GI tract be damaged?

A

H pylori, an inadequate blood supply due to vasoconstriction, excessive glucocorticoids, aspirin, NSAIDS, alcohol, chronic gastritis, increased gastric secretion, increased pepsin-acid, and rapid gastric emptying

128
Q

how does stress contribute to gastric ulcers?

A

by reducing mucosal blood flow and increasing glucocorticoid effects; as well by stimulating stressful coping mechanisms like smoking, caffeine, and alcohol

129
Q

healing of peptic ulcers

A

isolating the causes is difficult so healing takes a long time and ulcers may reoccur; granulation tissue breaks down and scar tissue may develop

130
Q

complications of peptic ulcers

A

may cause a hemorrhage, perforation, chemical peritonitis, and obstruction of the GI tract

131
Q

perforation

A

occurs when the ulcer erodes completely through the wall, allowing chyme to enter the peritoneal cavity; results in chemical peritonitis

132
Q

chemical peritonitis

A

inflammation of the peritoneal membrane and other structures in the abdominal caivty

133
Q

general causes of peptic ulcers

A

H pylori, genetic factors (O blood group), older individuals, and though taking NSAIDs

134
Q

signs and symptoms of gastric ulcers

A

epigastric burning after meals and at night, heartburn, nausea, vomiting, and weight loss

135
Q

diagnostic tests for peptic ulcers

A

fiberoptic endoscopy or barium x-ray

136
Q

treatment for peptic ulcers

A

combination of drugs including antimicrobial drugs to treat H pylori, reduce acid secretion, inhibit the proton pump, and a coating agent; also reducing exacerbating factors such as caffeine partial gastrectomy may also be required

137
Q

examples of drugs to treat peptic ulcers

A

helidac treats acid secretion, tetracycline treats H pylori, cimetidine treats H2 receptors, and omeprazole reduces gastric secretions

138
Q

stress ulcers causes

A

result from traumas such as burns or head injuries or those with serious systemic problems such as hemorrhage or sepsis

139
Q

curling ulcers

A

ulcers in the presence of burns

140
Q

cushing ulcers

A

ulcers in those with head injuries; increased vagal stimulation of acid secretion occurs

141
Q

first indicator of stress ulcers

A

hemorrhages

142
Q

where does gastric cancer occur?

A

occurs in the mucous membrane, often in the antrum and pyloric areas

143
Q

most common gastric cancer

A

adenocaricoma

144
Q

adenocarcinoma

A

cancer that starts in the glands lining organs

145
Q

early gastric carcinoma

A

effects the mucosa and submucosa

146
Q

advanced gastric carcinoma

A

involves the muscularis layer; eventually it spreads and involves the serosa, lymph nodes, liver, and ovaries

147
Q

prognosis for gastric cancer

A

is poor due to not being detected early on

148
Q

causes of gastric carcinoma

A

H pylori, diet, food preservatives such as nitrates and smoked foods, and genetic factors (A blood group)

149
Q

signs of gastric carcinoma

A

initial signs are anorexia, indigestion, epigastric discomfort, weight loss, fatigue, and fullness; iron-deficiency anemia also occurs

150
Q

treatment for gastric carcinoma

A

gastric resection, chemo, radiation therapy, and B12 injections after gastrectomy

151
Q

dumping syndrome

A

occurs when control of gastric emptying is lost and occurs often after gastric resection or a partial gastrectomy; the storage stage in the stomach is lost

152
Q

effects of dumping syndrome

A

hypoglycemia, cramps, nausea, diarrhea, along with dizziness, weakness, rapid pulse, and sweating

153
Q

dumping syndrome and osmosis

A

the hyperosmolar chyme draws fluid from the vascular system into the chyme; this can cause dizziness, weakness, rapid pulse, and sweating

154
Q

why does hypoglycemia occur with gastric dumping?

A

the rapid emptying leads to initial high blood glucose levels, but these drop very quickly; causes tremors, sweating, and wekaness

155
Q

treatment for dumping syndrome

A

small meals that are high in protein and low in simple carbs; fluids should be taken between meals rather than with meals

156
Q

pyloric stenosis

A

narrowing and obstruction of the pyloric sphincter usually due to scar tissue

157
Q

signs of pyloric stenosis

A

regurgitation of food, projectile vomiting lacking bile, small and infrequent stoll,s and failure to gain weight

158
Q

treatment for pyloric stenosis

A

surgery to remove the obstruction

Anatomy and Phyisology (71 decks)

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