Glossary of Block VII, Week I
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- 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
- Two most common locations of leukoplakia?
- 1. Buccal mucosa
(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
- 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?
- 1. ETOH
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
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
- 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
3. High grade
- Regarding the mucoepidermoid tumors: four most common locations of metastastases?
- 1. regional nodes
- 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
- 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
- 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)
- ANY CAUSE OF PORTAL HYPERTENSION, namely
1. cirrhosis (ETOH)
2. portal vein thrombosis
3. hepatic vein thrombosis (Budd-Chiari)
- 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
- three consequences/complications of esophagitis?
- 1. bleeding
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
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)
- dietary risk factors for SCC of the esophagus? (4)
- 1. viatamin deficiencies (A, C, riboflavin, thiamine, pyridoxine)
2. trace metal deficiencies (esp. zinc)
- 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
- 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
- what virulence factor does H.pylori have that renders it resistant to stomach acid?
- urease production
- 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
- what are three tests that can be done on an endoscopic biopsy to look for H.pylori?
- 1. urease
- 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
- 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
- in encterobacteriaceae, the following antigens produce what virulence factor?
1. O antigen
2. K antigen
3. H antigen
- 1. LPS
- 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
- 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?
- WATERY DIARRHEA
non-inflammatory, large stool volume, N/V, cramping
- 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
- 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?
*neuro symptoms (50% mortality once these are seen)
- antibiotics used to treat typhoid fever?
- it is possible to be a typhoid carrier - where does S.typhi "live?"
(can be shed for long periods of time)
- what type of bacteria is Listeria monocytogenes?
- 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
- 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
- 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)
- MOA of H2RA?
- block histamine at cholinergic and H2 receptors -> reduces both acid secretion and volume
- MOA of PPIs?
- inhibit H+/K+ ATPase in parietal cells
(noncompetitive and irreversible inhibition)
- 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)
- 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:
3. duodenal and gastric ulcers
4. NSAID induced ulcers
- 1. PPIs more effective
3. PPIs more effective
4. PPIs similar in efficacy but better tolerated
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