Enteropathies Flashcards

1
Q

what are risk factors for cleft palate?

A

diabetes, smoking, topiramate; valproic acid

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2
Q

thyroglossal duct cysts are remnants of what embryological process?

A

descention of thyroid gland from from bas of the tongue at the foramen cecum into the neck

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3
Q

where on the anterior neck are thyroglossal duct cysts found?

A

below hyoid bone which is why the mass tends to move w/ swallowing

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4
Q

Tonsillitis is most common in what pt. population?

A

children 1-15 yrs.

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5
Q

70% of viral pharyngitis cases are caused by what viruses

A

Rhinovirus; Adenovirus; EBV; influenza virus

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6
Q

what is the most common bacterial pharyngitis in children

A

strep a

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7
Q

What is the most common cause of viral tonsillitis in neonates

A

Rsv

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8
Q

What are the most common causes of bacterial tonsillitis

A

Srep A; s. pneumoniae; S. aureus; H. influenzae

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9
Q

Compare and contrast the differences between bacterial streptococcal pharyngitis and viral pharyngitis

A

Streptococcal pharyngitis Has white patches viruses: the throat is abnormally red

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10
Q

Describe the characteristics of diphtheria pharyngitis

A

Necrosis of pharyngeal mucosa; Dirty Gray Pseudo Memberness White patches

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11
Q

What are the systemic complications of diphtheria

A

Heart blocks; myocarditis; peripheral neuropathies and paralysis

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12
Q

Oropharyngeal squamous pailloma Is associated with what viruses

A

HPV6 and 11

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13
Q

Oropharyngeal squamous pailliloma Is derived from what cells

A

Stratified squamous epithelium in the pharyngeal mucosa

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14
Q

What is the clinical criteria for leukoplakia

A

White patch that cannot be scraped off; cannot be explained by any other disease

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15
Q

Grossly what do Leukoplakia plaques look like

A

Demarcated borders That are usually raised

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16
Q

What does leukoplakia resemble

A

Dysplasia and carcinoma in situ

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17
Q

Erythrooplakia Is a precursor of what Malignancy

A

Carcinoma in situ

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18
Q

What are histological distinctions that can be made between leukoplakia and Erythropoplakia

A

Leukoplakia has an extensive keratin surface that is absent in erythroplakia

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19
Q

oropharyngeal carcinomas are commonly found in what structure of the mouth

A

Palatine tonsils

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20
Q

Squamous Cell carcinoma of the oropharynx is associated with what virus

A

HPV16

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21
Q

what are the epidemicillogical factors of squamous cell carcinoma of the oropharynx

A

Middle aged individuals who have a chronic history of smoke, tobacco and, alcohol use

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22
Q

Compare & contrast the differences in clinical presentation of SCC associated with HPV and not HPV

A

HPV Association:
younger patients
oropharynx
non keratinizing
no plakia precursor
metastasis rare
Good prognosis

Non HPV Association:
older patients
Oral cavity
keratinizing
plakia precursor
metastasis common
poor prognosis

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23
Q

SCC metastasizes to what local regions

A

Cervical lymph nodes

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24
Q

Scc of the orophaynx metastasizes to what distal regions

A

Metasteinal lymph nodes, lungs, liver, bones

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25
Q

What is a distinctive histologic characteristic of SCC

A

collagen forms in whorls

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26
Q

What is the mean age of Adenocarcinoma

A

55 years

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27
Q

Adenocarcinomas of the oropharynx commonly arise from what structure

A

Minor salivary glands

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28
Q

What oropharyngeal disease Also involves the lips

A

Oropharyngeal squamous papilloma

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29
Q

Unlike other oropharyngeal pathologies, leukoplakia can also be found in these regions

A

gingiva & buccal mucosa

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30
Q

Muco epidermoid carcinoma Has what distinctive histologic characteristics

A

Large cyst-forming mucus cells

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31
Q

What is the most common type of salivary gland cancer

A

mucoepidermoid carcinoma

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32
Q

What are the epidemiological factors of adenoid cystic carcinoma

A

In the minor salivary glands of people between the ages of 40 and 60

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33
Q

Describe the histologic characteristics of adenoid cystic carcinoma

A

Tubular and cribiform patterns That connect together to form micro cysts

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34
Q

where does adenoid cystic carcinoma metastasize to

A

perineural spaces

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35
Q

Adenoid cystic carcinoma cells are derived from what cells

A

ductal & myoepithelial cells

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36
Q

Non hot skin lymphoma can metastasize to these regions of the oropharynx

A

tonsils and base of the tongue

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37
Q

Not hot shins lymphoma metastasized to the oropharynx is usually what subtype

A

DLBCL

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38
Q

List the classifications of esophagitis

A

Grade A: 1 mucosal break less than five millimeters
Grade B: One mucosal break More than five millimeters
Grade C: One mucosal break that touches adjacent folds
Grade D: mucosal breaks that involve at least three fourths of the luminal circumference

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39
Q

What is the clinical criteria for gastroesophageal reflex disease

A

There has to be gross evidence of esophageal mucosal lining injuries; If not then the reflex disease gets categorized as non-errosive reflux disease

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40
Q

What are common clinical presentations of GERD?

A

heartburn; regurgitation; Sensitivity to body positions

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41
Q

What are the alarm signs Of GERD?

A

Hematemesis, melana, cachexia (weight loss); dysphagia, early satiety
Mnemonic: BCDEs

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42
Q

What is the definition of functional GERD

A

Frequent transient LES relaxation

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43
Q

What is the definition of mechanical GERD

A

Hypertensive LES

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44
Q

What are risk factors for GERD

A

Obesity, smoking, alcohol, pregnancy, dietary habits Of excessive intake of chocolate, peppermint, and caffeine

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45
Q

What are secondary complications that can arise from GERD

A

Barrett’s esophagus, stricture, and aspiration

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46
Q

What does barium esophagram allow you to assess

A

Evaluation of swallowing

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47
Q

What is endoscopy used for When assessing for GERD

A

Biopsies and direct visualization of the esophageal mucosa In its entirety

48
Q

What does a mandometry assess

A

Measures pressure gradients for evaluation of peristalsis

49
Q

What test given is confirmation of a reflux disease

A

Esophageal ph testing

50
Q

In the context of GERD, Imaging is most useful for what

A

evaluating the extent of a malignancy and extent of GI canal injuries

51
Q

What kinds of foods trigor GERD

A

Caffeinated and carbonated beverages; spicy and fried foods; citrus fruits; tomatoes; garlic; onions; peppermint and chocolate

52
Q

Besides dietary modifications what other lifestyle changes can be implemented to treat GERD

A

Losing weight; abstaining from reclining within three hours of a meal; smoking cessation; consumption abstenince; wearing loose fit clothing; raising the head of the bed

53
Q

what are typical clinical presentations of achalasia?

A

dilated upper esophagus w/ tapered narrowing of distal esophagus; Dilated Spinach

54
Q

What sign can be seen on an X ray for indication of achalasia?

A

Birds Beak deformity

55
Q

What are primary causes of achalasia?

A

Diffuse esophageal spasm; nutcracker esophagus; hypertensive LES

56
Q

what are secondary causes of achalasia?

A

scleroderma, dm, alcohol

57
Q

What i s Happening at the neurological level for Achalasia?

A

overstimulation of excitatory neurons: specifically Ach & substance P
OR
understimulation of inhibitor neurons: NO & VIP

In either case, the LES fails to relax and remains contracted

58
Q

What is the gold standard for diagnosing achalasia?

59
Q

What causes diffuse esophageal spasms

A

Uncoordinated contractions Of esophageal segments; In most cases all of the segments contract simultaneously and this prevents the propagation of bolus

60
Q

what is a common finding of DES with a barium swallow

A

cork screw esophagus

61
Q

What happens with a nutcracker esophagus

A

Contractions proceed in a coordinated manner but the amplitude of these contractions is significantly increased

62
Q

DES and nutcracker esophagus Have Many overlaps and the same clinical symptoms. How can they be distinguished

63
Q

What is the pathogenesis of esophageal dismotality i For scleroderma

A

Smooth muscle of the esophagus gets replaced by scar tissue Due to excessive production of collagen; This leads to progressive loss of peristalsis and weakening of the LES

64
Q

How does diabetes mellitus cause esophageal dismotality

A

glycosylation of small blood vessels causes sclerosis; This can damage nearby nerve fibers sending signals to and from the esophagus

65
Q

where is Zenker diverticulum commonly found?

A

Between the inferior constrictor muscle and the cricopharyngeus: Killian’s Triangle

66
Q

What is the most common life threatening complication Associated with zinc or diverticulum

A

Aspiration

67
Q

Compared to Other esophageal motility disorders, what are distinct clinical symptoms of Zenker Diverticulum

A

sensation of food sticking in throat; regurgitation of undigested food hours after eating; coughing after eating

68
Q

What is a esophageal stricture?

A

a narrowing of the esophageal canal

69
Q

What is a peptic esophageal structure

A

It is a esophageal structure caused by acid reflux

70
Q

What is the definition of dysphagia

A

Sensation of disordered swallowing

71
Q

what is the definition of odynophagia

A

pain with swallowing

72
Q

what is the definition of globus

A

Sensation of an object in the throat

73
Q

What is the definition of an esophageal ring

A

Concentric extension of normal esophageal tissue that consists of mucosa, submucosa, and muscle

74
Q

what is the definition of an esophageal web

A

Eccentric extension of normal esophageal tissue that consists of only mucosa and submucosa

75
Q

what is the most common location within the esophagus where webs are found

A

Anterior postcrycoid area of proximal esophagus

76
Q

where are Schatzki Rings commonly found?

A

squamocolumnar junction

77
Q

What is a common complication of zchatzki rings

A

Meet Impaction

78
Q

What are the epidemiological factors of primary eosinophilic esophagitis

A

20 to 30 year old males; More prevalent and developed countries

79
Q

What is the proposed etiology of PEE

A

Abarant immune response to antigenic stimulation

80
Q

Finding eosinophils in the esophagus is unusual. Why?

A

because unlike the rest of the gi tract, normal esophagus histology does not consist of eosinophils

81
Q

Compare and contrast the different symptoms associated with PEE in adult and pediatric patients

A

adults: dysphagia of solid foods, food impaction, retrosternal pain
pediatric patients: nausea and vomiting, weight loss & anemia
neonates: Refusal of food

82
Q

What preexisting conditions are associated with PEE

A

Asthma, food allergens, chronic rhinitis, and eczema

83
Q

What is Boerhaave syndrome

A

spontaneous rupture of the esophagus that is usually associated with increases in intraluminal pressures

84
Q

What would you expect to find upon physical examination for a patient suspected of having Boerhaave syndrome?

A

subcutaneous emphysema (crepitation)

85
Q

What is Mallory-Weiss Syndrome?

A

It’s more of a triad of symptoms:
forceful retching, hematemesis & mucosal lacerations of the distal esophagus

86
Q

What are the two most common associations for peptic ulcer disease

A

H pylori and NSAID use

87
Q

What region of the stomach involves a Type 1 gastric ulcer?

A

the stomach body

88
Q

what region of the stomach involves Type 2 gastric ulcers?

89
Q

Type 3 GUs involve what region of the stomach?

A

within 3 cm of pylorus

90
Q

Type IV Gus involve what stomach region?

91
Q

3/4 types of GU involve low gastric acid production. What type of GU is assoc. w/ high gastric production

92
Q

what metabolic substance would you expect to by decreased for duodenal ulcers?

A

bicarbonate

93
Q

what metabolic substance would by increased for DUs

A

gastric acid

94
Q

What secondary complications can arise from PUDs along the posterior wall of the stomach?

A

exudate from the ulcers can perfuse into the pancreas causing pancreatitis

95
Q

what secondary complications can arise from PUDs along the anterior wall of the stomach?

A

exudate from the ulcers can leak into the abdominal cavity causing peritonitis

96
Q

what are important clinical distinctions b/t GUs & DUs?

A

GU symptoms are more non-specific: N/V, weight loss, & pain caused by food

DU symptoms are more specific: pain 90-3 hrs. after last meal that is relieved by antacids or food & sleep disruption due to pain

97
Q

how do PUD symptoms differ for elderly pts. compared to adults

A

elderly are less likely going to report pain and are more likely to present with bleeding or perforation

98
Q

what type of food intolerance would you expect a PUD pt. to have?

A

fatty food intolerance

99
Q

For a pt. with a h/o PUD, what would be the presenting symptoms for a posterior penetrating gastric ulcer?

A

intermittent dyspepsia that radiates to the back

100
Q

For a pt. with a h/o PUD, what would be the presenting symptoms for a gastric outlet obstruction?

A

new onset of pain that worsens in intensity after a meal followed by subsequent vomiting of undigested food

101
Q

A pt. with a h/o PUD presents to your clinic complaining about a new onset of hematochezia & hematemesis. W/o knowing anything else, what secondary complication of PUD has likely transpired in this pt.?

A

hemorrhage

102
Q

A pt. is rushed to a nearby hospital by paramedics for an abrupt onset of severe abdominal pain. She has a h/o PUD. what secondary complication of PUD has likely occurred in this pt.?

A

perforation of an ulcer through the stomach wall

103
Q

what are the most common clinical presentations of ulcer bleeding?

A

tarry stools and/or coffee ground emesis

104
Q

what is the gold standard for diagnosis of PUD?

105
Q

what temporary measures can be taken to stop the cessation of bleeding for PUD emergencies?

A

injection of epinephrine & thermal therapy

106
Q

Is H. pylori gram -/+?

107
Q

how is H. pylori transmitted from one host to another?

A

fecal oral route of transmission; the bacteria colonizes the gastric mucosa

108
Q

Most cases of GUs & DUs present w/ evidence of active H. pylori colonization. Which type is always assoc. w/ H. pylori?

109
Q

How is Helicobacter pylori diagnosed?

A

fecal antigen testing and identification via light microscopy

110
Q

follow-up EGD is recommended for all patients with what type of PUD?

A

gastric ulcers

111
Q

What is the pathogenesis of Type A chronic atrophic gastritis?

A

autoimmune, predominantly affects the body

112
Q

What is the pathogenesis of Type B chronic atrophic gastritis?

A

H pylori related; predominantly affects the antral region of the stomach

113
Q

What are the symptoms of dyspepsia

A

Epigastric pain, heartburn, bloating, early satiation

114
Q

What are the main causes of organic dyspepsia

A

PUD, medications, gastric cancer

115
Q

what medications commonly cause dyspepsia

A

NSAIDS & selective inhibitors COX2

116
Q

List the alarming symptoms for dyspepsia

A

unintentional weight loss, progressive dysphagia; odynophagia, iron deficiency anemia, persistent vomiting, lymphadenopathy; Age > 60; FH of upper gastrointestinal cancer