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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?
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?
Mucous retention cyst
What am I? A variation of a mucocele which affects the sublingual gland, resulting in a floor of the mouth location?
What am I? A clinical white patch of the oral mucosa that cannot be characterized clinically or pathologically as any other disease?
Four etiologies of leukoplakia?
1. Smoking
3. Irritants
4. Dentures
Two most common locations of leukoplakia?
1. Buccal mucosa
2. Commissures
(uncommon on alveolar ridge, soft palate, gingiva)
Why are we worried about leukoplakia?
High rate of dysplasia and malignant transformation. (surgical removal is indicated whenever possible)
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?
Which sex is SCC of the oral cavity most commonly seen in?
Male > Female
Which race is SCC of the oral cavity most commonly seen in?
White > Black
Seven risk factors of SCC of the oral cavity?
2. Smoking
3. Sun exposure/radiation
4. Low socioecomic status
5. Work in textile industries
6. Chronic infections
7. Plummer Vinson
what is significant about people that combine smoking and ETOH in regards to risk of SCC of the oral cavity?
7x increase in risk
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?
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?
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
Which embryologic structure is the parotid gland derived from?
oral ectoderm
Which embryologic structure is the submandibular and sublingual glands derived from?
oral endoderm
Two functional types of salivary glands?
1. Mucous
2. Serous
Two functions of mucous salivary glands?
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?
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
At what fetal age does the parotid gland begin to develop?
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
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?
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?
Mixed (predominantly mucous)
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
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?
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.
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?
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
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?
perineural invasion, slow growing
four most common spots of metastasis of an adenoid cystic carcinoma?
1. bone
2. lungs
3. liver
4. brain
what is the 5 yr. survival rate of adenoid cystic carcinoma?
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?
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
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
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)
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
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
A shelflike circumferential ring that involves the GE junction is called a?
Schatzki ring
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
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
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
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)
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?
describe the histology of esophagitis
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. 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 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?
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?
(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?
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?
a sydrome characterized by GI symptoms including vomiting, nausea, diarrhea and abdominal discomfort is known as?
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?
(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?
(manifests as watery diarrhea)
which type of toxin, released by bacteria in the GI, would cause damage to the mucosa?
(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?"
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
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?
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?
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?
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?
describe the stools seen in cholera
rice water appearance, no blood
mortality rate of untreated cholera?
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?
(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)
(optional, shortens duration)
leading bacteria that causes food poisoning?
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
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?
(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?
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?
*rose spots
*dry cough
*neuro symptoms (50% mortality once these are seen)
antibiotics used to treat typhoid fever?
newer cephalosporins
it is possible to be a typhoid carrier - where does S.typhi "live?"
gall bladder
(can be shed for long periods of time)
what type of bacteria is Listeria monocytogenes?
gram status?
gram positive
there are 1700 cases of Listeria annually in the US. What is the mortality rate?
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?
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?
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?
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:
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?
which PPI is the least influenced by renal or liver dysfunction?
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?
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)
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?
(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?
(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?
(cut pyloric muscle longitudinally)
inflammation of the gastric mucosa is known as gastritis. acute gastritis usually occurs in which portion of the stomach?
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
*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?
(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?
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