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308 Cards in this Set
- Front
- Back
What am I? A space lined by granulation tissue and histiocytes, with a lumen filled with mucous and macrophages, most often found on lower lip?
|
Mucocele
|
|
what is the most common cause of a mucocele?
|
trauma to the ducts of the minor salivary glands
|
|
What am I? A variation of a mucocele in which there is a partial duct obstruction?
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Mucous retention cyst
|
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What am I? A variation of a mucocele which affects the sublingual gland, resulting in a floor of the mouth location?
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Ranula
|
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What am I? A clinical white patch of the oral mucosa that cannot be characterized clinically or pathologically as any other disease?
|
Leukoplakia
|
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Four etiologies of leukoplakia?
|
1. Smoking
2. ETOH 3. Irritants 4. Dentures |
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Two most common locations of leukoplakia?
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1. Buccal mucosa
2. Commissures (uncommon on alveolar ridge, soft palate, gingiva) |
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Why are we worried about leukoplakia?
|
High rate of dysplasia and malignant transformation. (surgical removal is indicated whenever possible)
|
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Leukoplakia can undergo malignant transformation to a squamous cell carcinoma. What are the two forms of malignancies seen?
|
1. Leukoplakia simplex
2. Erythroplakia |
|
Between leukoplakia simplex and erythroplakia, which is more common?
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Erythroplakia
|
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Which sex is SCC of the oral cavity most commonly seen in?
|
Male > Female
|
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Which race is SCC of the oral cavity most commonly seen in?
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White > Black
|
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Seven risk factors of SCC of the oral cavity?
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1. ETOH
2. Smoking 3. Sun exposure/radiation 4. Low socioecomic status 5. Work in textile industries 6. Chronic infections 7. Plummer Vinson |
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what is significant about people that combine smoking and ETOH in regards to risk of SCC of the oral cavity?
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7x increase in risk
|
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SCC of the oral cavity is most commonly found in what three locations?
|
1. Lower lip
2. Tongue 3. Floor of mouth |
|
What is the prognostic difference in SCC appearing on the upper lip vs. the lower lip?
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Upper lip: more aggressive, worse prognosis
Lower lip: less aggressive, 90% cure rate |
|
Which location of SCC of the tongue has the worst prognosis?
|
posterior 1/3 of tongue
(better prognosis: lateral border of middle 1/3, appearing on mobile portion of tongue) |
|
In blacks, what is the most common location of SCC of the oral cavity?
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Floor of mouth
(often advanced when diagnosed) |
|
Describe the metastatic pattern of SCC from the floor of the mouth
|
Metastasizes to the tongue, then to the cervical nodes
|
|
Three functions of salivary glands?
|
1. moistens mucous membranes
2. prepares food for digestion 3. controls bacterial flora of the mouth |
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Which embryologic structure is the parotid gland derived from?
|
oral ectoderm
|
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Which embryologic structure is the submandibular and sublingual glands derived from?
|
oral endoderm
|
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Two functional types of salivary glands?
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1. Mucous
2. Serous |
|
Two functions of mucous salivary glands?
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1. surface lubricant
2. block epithelial binding sites for bacteria |
|
What do serous salivary glands release?
|
Zymogen granules (amylase/pytaline, lactoferrin, lysozyme)
|
|
Function of amylase/pytaline (zymogen granules)
|
split starch into water soluble CHO
|
|
Function of lactoferrin/lysozyme?
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antibacterial
|
|
Function of myoepithelial cells in salivary glands? (3)
|
1. lie between epithelium and basement lamina
2. contract to speed the flow of saliva 3. participate in elaboration of basal lamina |
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At what fetal age does the parotid gland begin to develop?
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week 5
|
|
At what fetal age does the submandibular gland begin to develop?
|
week 6
|
|
what fetal age does the sublingual gland begin to develop?
|
week 7-8
|
|
what are the two lobes of the parotid duct?
|
1. Superficial lobe (overlies masseter)
2. Deep lobe (in parapharyngeal space) |
|
what is the other name of the parotid duct and where does it empty?
|
Stensens duct, empties opposite the maxillary second molar
|
|
what is the blood supply to the parotid duct?
|
external carotid/external jugular
|
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What are the lymphatics draining the parotid gland?
|
superficial and deep cervical nodes
|
|
What are the two encapsulated salivary glands?
|
Parotid and Submandibular
|
|
Which salivary gland has no capsule?
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Sublingual
|
|
Type of acini seen in the parotid gland
|
Serous acini
|
|
Type of acini seen in submandibular gland?
|
Mixed (predominantly serous, but some mucous with the crescentic cap of serous cells)
|
|
Type of acini seen in sublingual gland?
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Mixed (predominantly mucous)
|
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What is the other name of the submandibular duct and where does it open through?
|
Wharton’s duct: opens through the sublingual caruncle
|
|
What is the blood supply of the submandibular gland?
|
facial and sublingual arteries
|
|
Where are the lymphatics found that drain the submandibular gland?
|
located in the spaces between the mandible and the submandibular gland
|
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What are the two types of ducts coming from the sublingual gland and where do they go?
|
1. Rivinus ducts – open directly into oral cavity
2. Common sublingual duct (Bartholin’s) – unites with submandibular (Wharton’s) duct |
|
Blood supply of sublingual gland?
|
Sublingual and subventral arteries/external jugular
|
|
type of acini seen in the 500-1000 minor salivary glands?
|
mucous predominant
|
|
Most salivary gland neoplasms are found in which gland?
|
Parotid
|
|
Are most parotid tumors benign or malignant?
|
benign (65-80%)
|
|
In general, are tumors found in salivary glands other than the parotid benign or malignant?
|
Malignant (35-50%)
|
|
Which tumor type makes up 65-80% of all salivary tumors and where is it found?
|
Pleomorphic adenoma (mixed tumor), most commonly found in the parotid gland.
|
|
Pleomorphic adenomas are most commonly derived from?
|
ductal and myoepithelial elements
|
|
Pleomorphic adenomas are most commonly seen in which sex?
|
Female (2:1 F:M)
|
|
Peak age of incidence of pleomorphic adenomas?
|
30-50 yrs
|
|
Are pleomorphic adenomas benign or malignant?
|
benign, but tend to recur.
|
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What is the second most common benign neoplasm of salivary glands?
|
Warthins tumor (Papillary Cystadenoma Lymphomatosum)
|
|
Which salivary gland does the Warthins tumor almost always involve?
|
Parotid gland
|
|
Warthins tumors are most often seen in which age group?
|
>40 yrs
|
|
origin of a Warthins tumor?
|
salivary gland duct in parotid lymph nodes
|
|
Mucoepidermoid tumors are most commoly found in which gland?
|
parotid
|
|
Cell of origin of mucoepidermoid tumors?
|
epithelial cells of interlobular and intralobular salivary ducts
|
|
Are mucoepidermoid tumors benign or malignant?
|
can be benign or malignant
|
|
Three grades of mucoepidermoid tumors?
|
1. Low grade
2. Intermediate 3. High grade |
|
Regarding the mucoepidermoid tumors: four most common locations of metastastases?
|
1. regional nodes
2. bone 3. lung 4. brain |
|
regarding mucoepidermoid tumors: prognosis of a low grade vs. a high grade tumor?
|
*low grade tumor (well differentiated) -> 90% 5 yr. survival
*high grade tumor (poorly differentiated) -> 20-30% 5 yr. survival |
|
a salivary tumor that is composed of cells resembling the serous component?
|
Acinic cell carcinoma
|
|
Cell of origin of an acinic cell carcinoma?
|
reserve cells of terminal or intercalated ducts
|
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acinic cell carcinoma is most commonly found in which salivary gland?
|
parotid (99%)
|
|
are acinic cell carcinomas benign or malignant?
|
benign (seldom metastasize)
|
|
what is the most common malignant tumor in submandibular, sublingual and minor salivary glands?
|
Adenoid Cystic Carcinoma
|
|
cell of origin of adenoid cystic carcinoma?
|
reserve cells of intercalated ducts
|
|
what is characteristic of the growth of adenoid cystic carcinomas?
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perineural invasion, slow growing
|
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four most common spots of metastasis of an adenoid cystic carcinoma?
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1. bone
2. lungs 3. liver 4. brain |
|
what is the 5 yr. survival rate of adenoid cystic carcinoma?
|
30%
|
|
What is sialolithiasis?
|
calcified masses that develop in the ductal system of the salivary glands – cause obstructions
|
|
pathogenesis of sialolithiasis?
|
results from the calcification of debris accumulated in the ducts (bacteria, mucous plugs, cellular debris, foreign bodies)
|
|
which gland is the most frequent location of sialolithiasis?
|
submandibular
|
|
S/S of sialolithiasis?
|
swelling and pain that is most pronounced at meals
|
|
what happens to the salivary gland distal to the obstruction?
|
first it becomes inflammed, then it atrophies
|
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describe the development of the esophagus that occurs during the 4th and 5th week of embryogenesis
|
4th week: laryngotracheal groove develops in the floor of the foregut
5th week: groove is converted to a tube by the growth of a laryngotracheal septum |
|
what composes the upper sphincter of the esophagus?
|
cricopharyngeal muscle
|
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What type of epithelium normally lines the esophagus?
|
stratified squamous epithelium
|
|
What is esophageal atresia?
|
developmental defect in which the esophagus remains as a thin, non-canalized cord
|
|
pathogenesis of esophageal atresia?
|
two possibilities:
1. failure of complete separation of the esophagus from the trachea 2. faulty development of an already separated tracheobronchial tube and esophagus |
|
in a patient with esophageal atresia, what else should we look for?
|
another anomaly (present 50% of the time)
|
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what is the morphology of esophageal atresia 80-90% of the time?
|
tracheoesophageal fistula: the lower esophagus ends in a pouch which connects to the trachea
|
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What are esophageal webs?
|
mucosal hyperplasia protruding into the lumen of the esophagus (usually the upper esophagus)
|
|
what is the Plummer-Vinson triad?
|
1. esophageal web
2. iron deficiency anemia 3. atrophic glossitis *all due to iron deficiency, strongly linked to SCC of the esophagus* |
|
where are esophageal webs found vs. esophageal rings?
|
Webs – found above the aortic arch
Rings – found below the aortic arch |
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A shelflike circumferential ring that involves the GE junction is called a?
|
Schatzki ring
|
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what is a Schatzki ring composed of?
|
mucosa and submucosa
|
|
what is achalasia characterized by?
|
*persistent contraction of the LES
*absent esophageal peristalsis leading to dilation of the esophagus |
|
pathophysiology of achalasia?
|
decreased or absent ganglion cells in the myenteric plexus
|
|
S/S of achalasia?
|
dysphagia (difficulty swallowing)
regurgitation/aspiration of food at night |
|
possible consequences of achalasia?
|
sometimes leads to SCC of the esophagus
|
|
a condition where the upper portion of the stomach evacuates through the diaphragmatic hiatus is known as?
|
hiatal hernia
|
|
how does the incidence of hiatal hernias change with age?
|
incidence increases with age
|
|
types of hiatal hernias (2)?
|
1. sliding (axial)
2. rolling (paraesophageal, nonaxial) |
|
which type of hiatal hernia is most common?
|
sliding (axial) (95%)
|
|
causative agent of a sliding (axial) hiatal hernia
|
a short esophagus (congenital or aquired)
|
|
what is a rolling (paraesophageal) hernia?
|
when a separate portion of the stomach enters the thoracic cavity through the diaphragmatic hiatus
|
|
which type of hernia is associated with gastroesophageal reflux?
|
sliding (axial) hernia
|
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what are four possible complications of a rolling (paraesophageal) hernia?
|
1. ulcer
2. obstruction 3. volvulus 4. incarceration/strangulation |
|
what are the two kinds of esophageal diverticula and which is the most common?
|
1. false (pulsion) diverticula (MOST COMMON)
2. true (traction) diverticula |
|
pathophysiology of a pulsion (false) diverticula?
|
herniation of mucosa through defects in the muscular layer, possibly due to increased luminal pressure
|
|
pathophysiology of a traction (true) diverticula?
|
traction caused by inflamed, scarred lymph nodes causes formation of a diverticula consisting of mucosal, muscular and serosal layers
|
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what is a Zenkers diverticulum and where is it found?
|
a pulsion diverticula, located immediately above the UES
|
|
where are traction diverticula most commonly found?
|
immediately above the LES
|
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what is Mallory-Weiss Syndrome and what most commonly causes it?
|
a longitudinal tear of the mucosa at the GE junction, most commonly caused by severe retching.
|
|
Mallory-Weiss Syndrome is associated with what two things?
|
1. alcoholics after prolonged vomiting
2. bleeding (mostly mild but may be massive) |
|
What are esophageal varices?
|
dilations of subepithelial and submucosal veins due to portal hypertension
|
|
esophageal varices are associated with? (4)
|
ANY CAUSE OF PORTAL HYPERTENSION, namely
1. cirrhosis (ETOH) 2. portal vein thrombosis 3. hepatic vein thrombosis (Budd-Chiari) 4. tumors |
|
most common complication of esophageal varices?
|
bleeding (30%), may be massive/fatal
|
|
four risks for bleeding in esophageal varices?
|
1. variceal size
2. portal pressure 3. variceal wall tension 4. severity of associated liver dysfunction |
|
what is the most common and important cause of esophagitis?
|
REFLUX
|
|
describe the histology of esophagitis
|
inflammation
basal zone hyperplasia enlarged papillae |
|
three consequences/complications of esophagitis?
|
1. bleeding
2. stricture 3. Barrett’s esophagus |
|
in Barrett’s esophagus, squamous epithelium is replaced by?
|
intestinal epithelium (occasionally cardiac or fundic type epithelium)
|
|
three possible complications of Barrett’s esophagus?
|
1. ulcer
2. stricture 3. adenocarcinoma (10%) |
|
in relation to SCC of the esophagus: which sex, race and age is it most commonly seen in?
|
sex: males (much more than females)
race: black (B:W = 4:1) age: >50 |
|
dietary risk factors for SCC of the esophagus? (4)
|
1. viatamin deficiencies (A, C, riboflavin, thiamine, pyridoxine)
2. trace metal deficiencies (esp. zinc) 3. fungi 4. nitrites/nitrosamines |
|
lifestyle risk factors for SCC of the esophagus? (2)
|
ETOH, tobacco
|
|
is Barrett’s esophagus related to SCC of the esophagus?
|
NO! Barrett’s esophagus is related to adenocarcinoma of the esophagus, not SCC
|
|
what is the 5 yr. survival rate of SCC of the esophagus vs. adenocarcinoma of the esophagus?
|
*SCC -> 5-10%
*Adenocarcinoma -> <5% (unless early detection and resection: then 80%) |
|
where are most cases of adenocarcinoma of the esophagus found?
|
in the middle and lower 1/3 of the esophagus
|
|
what is the connection between adenocarcinoma and H. pylori?
|
H. pylori infection is inversely related to adenocarcinoma
|
|
what is the connection between esophageal adenocarcinoma and ETOH?
|
no connection
|
|
what is the connection between increased BMI and esophageal adenocarcinoma?
|
increased BMI = risk factor for esophageal adenocarcinoma
|
|
demographics of esophageal adenocarcinoma?
|
sex: F > M
Race: whites > blacks |
|
in relation to the immune system: what do the following stand for?
1. MALT 2. NALT 3. GALT 4. BALT |
1. Muscosal Associated Lymphoid Tissue
2. Nasopharynx Associated Lymphoid Tissue 3. Gut Associated Lymphoid Tissue 4. Bronchus Associated Lymphoid Tissue |
|
between monomeric and dimeric IgA - which is the most common soluble form of serum IgA?
|
monomeric
(monomeric form is the B cell surface receptor) |
|
where does dimeric IgA hang out?
|
mucosal tissues
(transported from serum into environment by specialized epithelial cells) |
|
three functions of IgA?
|
1. neutralization (blocks binding of microbes to epithelial surface)
2. agglutination (causes microbes to aggregate) 3. compliment activation (when aggregated) |
|
distribution of IgA compared to other antibodies?
|
LARGE!
75% of all B cells make IgA 60-70% of all Abs made are IgA |
|
(during pregnancy in the breast tissue) - Where do most of the IgAs migrate from and what is the significance?
|
migrate from the gut
significance - sIgA contained in the breast milk and colostrum is directed against intestinal antigens and microorganisms |
|
Peyers patches are primarily made up of what and are located under what GI tract cell?
|
*made up of lymphoid follicles
*located under M cells in the small intestine |
|
intestinal epithelial cells make IL-7. what is its function?
|
growth factor for B and T cells
|
|
function of M cells in small intestine?
|
endocytose and transport Ag from the lumen to be "sampled" by APCs below
|
|
do dendritic cells use M cells to sample antigens?
|
NO
(they directly sample the contents of the intestinal lumen) |
|
what type of lymphocyte is most commonly found in the intra-epithelial area?
|
CD8+ T cells
(recognize MHCI molecules) |
|
compare the intra-epithelial T cells with T-cells of the peripheral immune system
|
T cells of the peripheral immune system have more variability in their specificity.
|
|
which 4 pathogens use M cells to facilitate entry into the lamina propria of the gut?
|
1. Salmonella
2. Vibrio cholerae 3. Yersinia pestis 4. poliovirus |
|
IgE is present in which mucosal secretions?
|
nose
eye bronchi gut |
|
theory behind oral tolerance?
|
mucosal Ag exposure generates a strong Th2 response. This Th2 response inhibits the Th1 (peripheral) response therefore tolerance is seen.
|
|
which bacteria causes plaque and is associated with caries?
|
Streptococcus mutans
|
|
which bacteria is associated with chronic gingivitis?
|
Porphyromonas gingivalis
(gram neg. rod) |
|
what is characteristic about the bacterial infections of the mouth that cause abscesses?
|
always polymicrobial
|
|
what is the pathogenesis behind a bacterial infection of the mouth?
|
1. subgingival plaque leads to inflammation
2. inflammation leads to tissue destruction (necrosis) 3. bacteria can then invade to infect deeper tissues |
|
four appropriate antibiotics that can be used to treat infections of the mouth?
|
1. metronidazole
2. phenoxymethyl-penicillin 3. benzylpenicillin 4. clindamycin |
|
what virulence factor does H.pylori have that renders it resistant to stomach acid?
|
urease production
(raises pH) |
|
what type of immune response does H.pylori elicit?
|
Th1 response with IgG production and inflammation
|
|
what are two nonendoscopic tests used for diagnosis of H.pylori?
|
1. urea breath test
2. serology |
|
what are three tests that can be done on an endoscopic biopsy to look for H.pylori?
|
1. urease
2. culture 3. histology |
|
which race has a high prevalence of H.pylori infection?
|
african-americans
|
|
a sydrome characterized by GI symptoms including vomiting, nausea, diarrhea and abdominal discomfort is known as?
|
Gastroenteritis
|
|
difference between diarrhea and dysentery?
|
diarrhea - usually a disease of small intestine, fluid and frequent stool
dysentery - usually results from disease of large intestine, inflammatory disorder of GI tract, blood and pus in feces |
|
what is enterocolitis?
|
inflammation involving the mucosa of both small and large intestine
|
|
which type of toxin, released by bacteria in the GI, would act on the autonomic nervous sytem?
|
neurotoxin
(released by Staph enterotoxin b, Clostridium boltulinum, Bacillus cereus) |
|
which type of toxin, released by bacteria in the GI, would cause fluid secretion without damage to the mucosa?
|
enterotoxin
(manifests as watery diarrhea) |
|
which type of toxin, released by bacteria in the GI, would cause damage to the mucosa?
|
cytotoxin
(manifests as inflammatory colitis, dysentery) |
|
how can a Campylobacter infection be acquired?
|
ingestion of undercooked, contaminated poultry or contaminated milk.
|
|
which age group has the highest incidence of Campylobacter infections?
|
children <1 yr
|
|
2 species of Campylobacter that are MC associated with human disease?
|
C. jejuni
C. coli |
|
which causes a more severe infection: C. jejuni or C. coli?
|
C. jejuni
|
|
timeframe of a Campylobacter infection?
(when do sx. appear and clear) |
* symptoms appear 1-3 days post-ingestion
* clears w/i 1wk |
|
Campylobacter spp. expressing the O-19 LPS antigen have been associated with?
|
Guillian-Barre syndrome
(O:19 antigen mimics human ganglioside) |
|
what would Campylobacter look like on gram stain or darkfield microscopy?
|
curved motile rods
|
|
treatment for a Campylobacter infection?
|
*symptomatic management
* Erythromycin or Cipro |
|
what type of bacteria are the Enterobacteriaceae family?
|
gram negative rods
|
|
6 important GI pathogens that belong to the Enterobacteriaceae family?
|
1. Escherichia
2. Shigella 3. Salmonella 4. Klebsiella 5. Proteus 6. Yersinia |
|
in encterobacteriaceae, the following antigens produce what virulence factor?
1. O antigen 2. K antigen 3. H antigen |
1. LPS
2. Capsule 3. Flagella |
|
Enterobacteriaceae typically cause one of what three syndromes?
|
1. Dysenteric syndrome
2. Watery diarrhea 3. Enteric Fever |
|
of the enterobacteriaceae, which ones ferment lactose?
|
Escherichia ferments lactose
(Salmonella, Shigella, Yersinia do not) |
|
which bacteria is known to cause "bacterial dysentery?"
|
Shigella
|
|
what is unique about the infectious dose of Shigella?
|
very low (<200 bacteria)
|
|
what 2 things characterize bacterial dysentery caused by Shigella as inflammatory?
|
macrophage apoptosis
IL-1 activation |
|
what 2 parts of the GI tract are affected in dysenteric syndrome?
|
1. colon
2. small intestine |
|
describe the stools that accompany dysenteric syndrome
|
*low volume
*blood *mucous *leukocytes |
|
two toxins produced by Shigella?
|
1. Shiga-like toxin
2. Vero toxin |
|
which toxin is important in the pathogenesis of enterohemorrhagic E.coli dysenteric syndrome (EHEC)?
|
shiga-like toxin
|
|
in gingivitis normal flora is initially replaced by what bacteria?
|
Prevotella intermedia
(then later by Porphyromonas gingivalis) |
|
what is the MCC of bacteria acquired food poisoning in the US?
|
Campylobacter
|
|
is campylobacter easy to culture?
|
NO - very hard!
(therefore typically don't diagnose by culture) |
|
what is considered a virulence factor that is required for camplyobacter to colonize?
|
flagella
|
|
biochemical properties of coliforms?
|
ferment lactose to acid and gas
(indicates fecal contamination in drinking water) |
|
what happens when Shigella uses the type III secretion system?
|
allows it to invade epithelial cells and macrophages, then causes apoptosis
|
|
which bacteria is known to cause hemolytic uremic syndrome?
|
Enterohemorrhagic E.coli (EHEC)/ E.coli 0157:H7
|
|
enterotoxigenic E.coli (ETEC) typically causes?
|
travellers diarrhea
|
|
enterotoxigenic E.coli (ETEC) makes two endotoxins - how are they distinguished?
|
heat stabile enterotoxin (activates guanylate cyclase)
heat labile enterotoxin (activates adenylate cyclase) |
|
enteropathogenic E.coli (EPEC) causes what characteristic pathogenic change?
|
denuded microvilli on epithelial surface
|
|
which type of E.coli causes infant diarrhea?
|
enteropathogenic E.coli (EPEC)
|
|
clinical presentation of E.coli gastroenteritis?
|
WATERY DIARRHEA
non-inflammatory, large stool volume, N/V, cramping (rarely fever) |
|
general pathogenesis of Salmonella?
|
invade through intestinal epithelium via M cells, then they travel to mesenteric lymph nodes
|
|
salmonella is found in what foods?
|
poultry, meat, eggs, dairy
|
|
what type of GI symptoms does a Yersinia enterocolitica or Yersinia pseudotuberculosis infection cause?
|
Self-limited gastroenteritis
(can spread systemically causing enteric fever like disease) |
|
what method does Yersinia use to deliver toxins?
|
type III secretion
|
|
how does C. difficile mediate pseudomembranous colitis?
|
via toxins
(cytotoxin and enterotoxin) |
|
treatment of choice for C. dificile induced pseudomembranous colitis?
|
metronidazole
|
|
describe the stools seen in cholera
|
rice water appearance, no blood
|
|
mortality rate of untreated cholera?
|
50%
|
|
the cholera toxin belongs to which family of toxins?
|
AB family
|
|
pathogenesis of cholera?
|
*cholera toxin enters cell
* increases adenylate cyclase activity * causes increased cAMP * causes overactive ion "pumps" - loss of electrolytes into stool (water follows osmotically) |
|
management/treatment of cholera?
|
rehydration!
(cholera is a self-limiting disease if fluid loss can be kept up with: can lose up to 5gallons/day) |
|
antimicrobial therapy for cholera? (2)
|
tetracycline
amoxicillin (optional, shortens duration) |
|
leading bacteria that causes food poisoning?
|
Staphylococcus
|
|
s/s of Staph food poisoning?
|
N/V 1-6 hrs after ingestion
|
|
food poisoning from Staph is really due to?
|
ingested enterotoxins
(these enterotoxins directly stimulate vomiting) |
|
How does C. botulinum cause botulism?
|
ingestion of neurotoxins that block neurotransmitter release
|
|
what type of bacteria is C. botulinum?
|
Gram positive
spore forming anaerobe |
|
what causes food associated botulism?
|
improper preservation (canning) technique of meats, fish and vegetables
(pressure cooking required to kill spores) |
|
what is the cause of death in botulism?
|
respiratory paralysis
|
|
intestinal colonization of botulism in infants is associated with?
|
honey
(NO honey for infants under 1yr) |
|
which bacterial infection is associated with precooked, then reheated meats?
|
Clostridium perfringens
|
|
clinical s/s of a Clostridium perfringens infection?
|
* severe abdominal cramping
* water diarrhea w/o vomiting * illness lasts 24 hr. |
|
where in the GI tract does C.perfringens MC colonize?
|
ilieum
|
|
pathogenesis of C.perfringens infection?
|
* heat labile enterotoxin released
* inhibits glucose transport, damages intestinal epithelium * causes protein release into lumen |
|
which bacteria causes illnesses that are associated with fried rice and cream sauces?
|
Bacillus cereus
|
|
two toxins that Bacillus cereus forms?
|
*heat stable toxin (vomiting w/abdominal cramps)
*heat labile toxin (diarrhea, abdominal cramps, no fever) |
|
once GI symptoms are present, Typhoid fever progresses to?
|
*Fever
*headache *rose spots *dry cough *neuro symptoms (50% mortality once these are seen) |
|
antibiotics used to treat typhoid fever?
|
FQ
newer cephalosporins |
|
it is possible to be a typhoid carrier - where does S.typhi "live?"
|
Yes
gall bladder (can be shed for long periods of time) |
|
what type of bacteria is Listeria monocytogenes?
gram status? hemolysis? |
gram positive
motile B-hemolytic |
|
there are 1700 cases of Listeria annually in the US. What is the mortality rate?
|
40%
|
|
manifestations of Listeriosis in an adult?
|
meningitis or menigoencephalitis
(usally see infection in immunocompromised) |
|
listeria can survive within phagocytes. How does it escape from the vacuole?
|
Listeriolysin O
(a hemolysin) |
|
what allows Listeria to be motile once it has escaped the cell?
|
actin based motility via ActA
(*ActA is required for disease progression) |
|
management of Listeriosis?
|
ampicillin
-or- erythromycin |
|
does V.cholerae prefer to invade the small or large intestine?
|
small intestine
|
|
in general - regarding location of ulcers:
1. NSAIDs cause this type? 2. H.pylori causes this type? |
1. gastric ulcers
2. duodenal ulcers |
|
MOA of sucralfate?
|
binds to ulcer surface, protects ulcer and allows it to heal
(not used so often anymore) |
|
where in the GI tract does H.pylori colonize?
|
gastric epithelial cells (moves freely in & beneath mucous layer)
|
|
complications of a chronic H.pylori infection?
|
Gastric cancer, MALT lymphoma
|
|
three complications of an ulcer?
|
1. perforation
2. obstruction 3. bleeding |
|
recommended regimen to treat H.pylori infection?
|
2 antibiotics + PPI or H2RA
(abx - clarythromycin, amoxicillin or metronidazole) |
|
function of parietal cell?
|
secretes HCl (gastric acid)
|
|
three factors that influence HCl secretion by the parietal cell?
|
H2 receptor
Cholinergic receptor (vagus n) Gastrin receptor |
|
MOA of H2RA?
|
block histamine at cholinergic and H2 receptors -> reduces both acid secretion and volume
|
|
MOA of PPIs?
|
inhibit H+/K+ ATPase pumps in parietal cell -> reduces acid secretion and volume
|
|
name three H2RAs
|
1. Cimetidine (Tagamet)
2. Ranitidine (Zantac) 3. Famotidine (Pepcid) |
|
why is it recommended that H2RAs be administered at supper or bedtime?
|
reduces nocturnal acid secretion
|
|
problem associated with H2RA use?
|
tolerance acheived rapidly
|
|
when must the dose of H2RAs be adjusted?
|
decreased renal function
(if CrCl<30, then decrease dose by 50%) |
|
how are H2RAs metabolized?
|
CYP450 system (esp. cimetidine)
(watch for interactions with theophylline, TCA, antiarrythmics, warfarin, CCBs) |
|
which has a faster onset: H2RAs or PPIs?
|
H2RAs
|
|
name the only OTC PPI
|
Omeprazole (Prilosec)
|
|
PPIs are released as a prodrug. how are they activated?
|
acid catalyzed conversion
(must be under a certain pH for activation) |
|
MOA of PPIs?
|
inhibit H+/K+ ATPase in parietal cells
(noncompetitive and irreversible inhibition) |
|
which are more potent: PPIs or H2RAs?
|
PPIs
|
|
after discontinuing PPIs how long does it take for normal acid secretion to resume?
|
3-5 days
|
|
what is the preferred administration time for PPIs?
|
30 minutes before breakfast
|
|
compare PPIs and H2RAs in the treatment of:
1. GERD 2. esophagitis 3. duodenal and gastric ulcers 4. NSAID induced ulcers |
1. PPIs more effective
2. similiar 3. PPIs more effective 4. PPIs similar in efficacy but better tolerated |
|
which PPI has the most drug interactions?
|
omeprazole
|
|
which PPI is the least influenced by renal or liver dysfunction?
|
Pantoprazole
|
|
difference between GERD and esophagitis?
|
GERD - reflux of GI contents into esophagus
esophagitis - endoscopic demonstration of inflammation of esophageal mucosa |
|
7 non-drug treatments of GERD?
|
1. elevated head of bed
2. avoid tight fitting clothes 3. lose weight 4. dietary 5. remain upright 3-4 hrs after meals 6. stop smoking 7. avoid alcohol |
|
in GERD: treatment of choice if esophageal erosion is present?
|
PPIs
|
|
why is long term use of antacids advised against in the treatment of heartburn?
|
antacids do not:
1. heal the damaged esophagus 2. prevent complications of chronic reflux |
|
when should OTC H2RAs be taken?
|
30 minutes before a meal
|
|
MOA of Reglan (Metoclopramide) in the treatment of GERD?
|
*increase LES pressure
*speed stomach emptying (prokinetic agent) |
|
what is the only indication of Prilosec OTC?
|
frequent heartburn
|
|
when should Prilosec be prescribed, not OTC? (3)
|
GERD
esophagitis PUD |
|
What can be prescribed for the prevention of NSAID-induced gastroduodenal ulcers in high risk patients? (3)
|
1. standard dose H2RAs
2. Double doses of H2RAs and PPIs 3. Misoprostol |
|
MOA of misoprostol (Cytotec)?
|
prostaglandin E1 analog - inhibits acid secretion and has mucosal protective properties.
*replaces prostaglandins inhibited by NSAID use* |
|
is misoprostol well tolerated?
|
no
(that's why PPIs and H2RAs are more commonly used) |
|
when would Prevacid be prescribed to prevent an NSAID induced GU?
|
when there is a history of a documented GU
|
|
when would Nexium be prescribed to prevent an NSAID induced GU?
|
high risk individuals
- age>60 and/or documented history of GU. |
|
which gastric epithelial cell am I?
produces glycoprotein and bicarbonate to form a gel on the gastric, lumenal surface. (this neutralizes HCl) |
Surface foveolar-mucous cells
|
|
which gastric epithelial cell is the progenitor cell for all gastric epithelial cells?
|
mucous neck cell
|
|
other functions of the mucous neck cell?
|
1. glycoprotein production
2. production of pepsinogens I and II |
|
3 functions of oxyntic (parietal) cells?
|
1. production of HCl
2. production of intrinsic factor 3. production of bicarbonate |
|
2 functions of chief (zymogen) cells?
|
1. production of pepsinogens I and II
2. production of lipase |
|
which gastric epithelial cells produce gastrin?
|
endocrine cells
|
|
which sex is congenital pyloric stenosis more common in?
|
males
(M:F = 4:1) |
|
what is congenital pyloric stenosis?
|
hypertrophy of pyloric circular muscle
|
|
clinical s/s of congenital pyloric stenosis?
|
regurgitation/vomiting in first 2-3 wks of life
|
|
treatment for congenital pyloric stenosis?
|
pylorotomy
(cut pyloric muscle longitudinally) |
|
inflammation of the gastric mucosa is known as gastritis. acute gastritis usually occurs in which portion of the stomach?
|
antrum
|
|
what is the difference between erosive gastritis and an ulcer?
|
erosive gastritis does not penetrate the muscularis mucosa, whereas an ulcer does
|
|
clinical s/s of acute gastritis?
|
*may be asymptomatic*
*epigastric pain *N/V *if severe see hemorrhage, hematemesis, melena |
|
a defect in the gastric mucosa where the muscularis mucosa is penetrated is known as?
|
acute gastric ulcer
|
|
what is the pathogenesis behind cushings syndrome induced ulcers?
|
increased intracranial pressure causes vagal stimulation -> result is increased acid release
|
|
pathogenesis behind an ulcer induced by mucosal hypoxia?
|
ischemia causes damage to the mucosal barrier, direct injury to the mucosal cells allows acid entry
|
|
Is there any connection between gastric ulcers and peptic ulcers?
|
NO - gastric ulcers do not predispose to chronic peptic ulcers.
|
|
(top two) pathogenesis of chronic gastritis?
|
1. autoimmune
2. H.pylori |
|
autoimmune chronic gastritis affects which part of the stomach, whereas H.pylori mediated chronic gastritis affects which part?
|
autoimmune - mainly fundus
H.pylori - fundus and antrum |
|
most autoimmune cases of chronic gastritis are autoantibodies towards?
|
1. the parietal cell H+/K+/ATPase
this results in hypochlorhydria 2. intrinsic factor |
|
inheritance pattern of autoimmune chronic gastritis?
|
autosomal dominant
|
|
describe the H.pylori infection rate as age increases.
|
rate of H.pylori infection increases with age
|
|
in regards to peptic ulcers: what is the difference between penetration and perforation?
|
1. penetration - erosion into adjacent structure (ie. ulcer penetrating & eroding adjacent pancreas)
2. perforation - erosion into body cavity |
|
peptic ulcers are more common in what blood group?
|
O
(nonsecretors of blood group substances) |
|
common pathogenesis (explanation) for peptic ulcers?
|
imbalance between acid-pepsin secretion and normal defenses
(more acid made) |
|
what is the explanation behind increased incidence of peptic ulcers in chronic renal failure and hyperparathyroidism?
|
hypercalcemia causes increased gastrin production
|
|
are peptic ulcers usually solitary or multiple?
|
solitary (80%)
|
|
where are gastric ulcers most commonly found?
|
lesser curvature of the antrum
|
|
what is the gross presentation of a peptic ulcer?
|
*round punched out lesions
*margins slightly elevated |
|
compare a GU and a DU in the following regards:
1. onset after a meal 2. relieved by food? |
1. DU - onset 1.5-3h after meal, GU - onset 1/2h after meal
2. DU - relieved by milk, food, antacids, vomiting, GU- not relieved by food |
|
what is Menetriers?
|
idiopathic hyperplasia of gastric surface mucosa cells
(result is increased mucous, decreased acid, protein loss) |
|
other name for menetriers?
|
Hypertrophic gastropathy (or diffuse mucosal hypertrophy)
|
|
in hypertrophic gastropathy (Menetrier's): age of onset and sex characteristics?
|
age of onset: 30-60 yrs
sex: Males (75%) |
|
why do we see hypertrophic gastropathy in Z-E syndrome?
|
gastrin levels are elevated, cause parietal cell hyperplasia
|
|
what is the cause of 90% of Z-E cases?
|
islet cell hyperplasia/tumors of the pancreas
|
|
chronic gastritis often is associated with the formation of?
|
gastric polyps
(can be non-neoplastic (90%), or adenomas (10%)) |
|
5 dietary factors that increase risk of gastric adenocarcinoma?
|
1. nitrites derived from nitrates (preserved food)
2. smoked and salted foods 3. pickled vegetables 4. chili peppers 5. lack of fresh fruit and veggies |
|
why is chronic gastritis associated with gastric adenocarcinoma?
|
chronic gastritis causes hypochlorhydria. this favors H.pylori colonization (H.pylori is a known risk factor for gastric adenocarcinoma)
|
|
Gastric carcinoma is seen a little more commonly in patients with which blood group?
|
A
|
|
4 precursor lesions for gastric carcinoma?
|
1. epithelial polyps
2. chronic atrophic gastritis 3. intestinal metaplasia 4. gastric remnants of partial gastrectomy |
|
what is the difference between early gastric cancer (EGC) and advanced gastric carcinoma?
|
EGC - only invades mucosa and submucosa (not muscularis mucosa)
advanced - invades muscularis mucosa (dismal prognosis) |
|
top 2 locations of gastric carcinoma?
|
1. pylorus and antrum (50-60%)
2. lesser curvature (40%) |
|
gastric carcinoma matastasizes to what locations? (7)
|
1. regional nodes
2. peritoneal seeding 3. liver 4. lungs 5. ovary (Kruckenberg) 6. supraclavicular nodes 7. scalene nodes |