Glossary of Block VII, Week II
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- in which parts of the GI tract is Ulcerative Colitis found?
- rectum and colon
- in which parts of the GI tract is Crohn's disease found?
- describe the extent of the inflammation seen in UC vs. Crohns
- Crohns - transmural
UC - surface mucosa
- compare the typical location and timing of abdominal pain in:
- 1. LLQ (prior to BM)
2. RLQ (exacerbated by eating)
- define tenesmus
*is it more suggestive of UC or CD?
*more suggestive of UC (b/c UC involves the rectum)
- an anticholinergic would be prescribed to relieve what symptom?
- cramping/abdominal pain
- 3 examples of anticholinergics?
- 1. dicyclomine
3. tincture of belladonna
- two antidiarrheals used to treat IBD?
- two antibiotics commonly prescribed for IBD?
- two classes of anti-inflammatory agents prescribed for IBD?
- 5-ASA formulations
- two 5-ASA formulations used to treat IBD?
- 5 immunomodulators used to treat IBD?
- 1. azathioprine
5. infliximab (remicade)
- typical maintenance therapy for both UC and CD?
- 1. 5-ASA to prevent flare-ups
2. if azothiaprine or mercaptopurine were used stay on those
- what is the active ingredient in aminosalicylates?
(most are prodrugs and form mesalamine in the GI tract)
- what are the actions of aminosalicylates on epithelial cells?
- 1. antioxidant activity - reduce tissue damage and inflammation
- how does the delivery method of aminosalicylates differ if treating UC vs. CD?
- UC - best to use a formulation that releases 5-ASA in the colon
CD - best to use a continuous delivery of 5-ASA throughout the small and large intestine
- sulfasalazine is broken down into what by what, where?
- sulfapyridine and 5-ASA by bacterial azoreductases in the large intestine
- which 5-ASA derivative has an ethylcellulose coated membrane, therefore facilitating delivery of mesalamine throughout the small bowel and colon?
- Mesalamine (Pentasa)
- which 2 5-ASA derivatives have delayed release primarily in the colon?
- Asacol and Colozal
- how is olsalazine "broken down?"
- olsalazine is two mesalamine molecules conjugated - they are cleaved in the colon by azoreductases.
- sulfasalazine is split into mesalamine and sulfapyridine. what is the role of each?
- mesalamine - anti-inflammatory
sulfapyridine - antibacterial
- what is the reason for most adverse effects seen with sulfasalazine?
(these patients do tolerate other aminosalicylates)
- what does it mean when sulfasalazine adverse effects are idiosyncratic?
- there is no correlation with the dose
- major adverse effect seen with sulfasalazine?
- SLE like syndrome
- three other drugs that are known for causing SLE-like syndrome?
- 1. asulfadine
- is 5-ASA more sucessful in maintaining remission in UC or CD?
- in the case of UC: which form of 5-ASA would be optimal?
- a combination of both topical and oral
- what is of great efficacy when attempting to acheive remission of CD or UC (but is not used for maintenance due to many systemic side effects)?
- what is the corticosteroid of choice to treat CD?
- budesonide (entocort)
(releases in distal ileum and right colon)
- Azathioprine (AZA) is a prodrug of?
- 6-mercaptopurine (6-MP)
- MOA of 6-MP?
- induces T-cell apoptosis
(use when corticosteroids don't work)
- with 6-MP: how long does it take for induction of remission?
- 3-6 months
- adverse effects of 6-MP?
- myalgia, headache, diarrhea
RARE - bone marrow suppression, infection, pancreatitis, liver abnormalities
- MOA of cyclosporine?
- prevents clonal expansion of T cell subsets
(used as salvage therapy in colitis when colectomy is only option)
- MOA of infliximab (Remicade)?
- anti-TNF monoclonal antibody with potent anti-inflammatory effects (IV)
- what is the black box warning on infliximab?
- serious infections may occur
- when is infliximab used in IBD?
- when it is refractory to conventional therapy
- which neoplasms does infliximab increase the risk of?
- lymphoma and other neoplasms
- effect of nicotine on UC?
- may have protective effect
(opposite is true for CD)
- top four viruses that cause gastroenteritis in infants in the US?
(in order of incidence)
- Rotavirus (56%)
- describe the structure of the rotavirus
- double-layered, icosahedral capsid
- describe the genome of the rotavirus
- segmented genome
can undergo reassortment
- where in the cell does rotavirus replicate?
- cell cytoplasm (matures in ER)
- which serogroup of rotavirus is the most common in the US?
- Group A
- function of VP4 and VP7 structural proteins on outer capsid of rotavirus?
- induce neutralizing antibodies
- what makes it difficult to create a vaccine for the rotavirus?
- antigenic variation
- what age group of children does the rotavirus tend to infect?
- 6-24 months of age
(most are immune by age 2)
- why do we only see rotavirus infections starting at 6 months?
- breast milk contains protease inhibitors and IgA (passive immunity)
- is there a seasonality to rotavirus infections?
- winter months in temperate zones
year round in tropical zones
- how is rotavirus transmitted?
- fecal-oral route
(as few as 10 particles can cause disease)
- is rotavirus stable?
- YES (very - can be transmitted on fomites)
- where in the GI tract does rotavirus infect cells?
- duodenum and proximal jejunum
- how does rotavirus cause gastroenteritis?
- blunts the villi - this leads to a decrease in absorptive surface in the small intestine -> results in a transient malabsorptive state. (also stimulates enteric nervous system causing increased intestinal secretion of fluid and electrolytes)
- besides infecting the GI tract, what else is rotavirus known to infect?
- CSF - can cause neurological complications (seizures, encephalitis, cerebellitis, encephalopathy)
- immunity after a rotavirus infection is correlated with which antibody?
- intestinal IgA (not serum IgG)
- Diagnostic tests available for rotavirus?
(self-limiting disease, usually don't need diagnosis)
- therapy for a rotavirus infection?
- goal - prevent dehydration
(use oral rehydration salts)
- what 4 things are oral rehydration salts made of?
- when would you have to treat a rotavirus infection patient with more than ORS?
- when there is severe vomiting (then treat with IV fluids)
- which family do Noroviruses belong to?
- describe the genome of noroviruses
only 3 reading frames
- is there a seasonality to norovirus infections?
- what are outbreaks of noroviruses associated with?
- contaminated water or food (shellfish, ice, salads)
- why could outbreaks of norovirus occur for months?
- reinfections can occur with the same agent, therefore the outbreak is hard to control
- pathogenesis of norovirus infection?
- blunting of villi, malabsorption of fats and sugars
- clinical s/s of a norovirus infection?
- abdominal cramps
- timeframe of norovirus symptoms?
- 12-48 hrs
(disease is self-limiting)
- diagnosis of norovirus?
- treatment for a norovirus infection?
(IV fluids rarely needed)
- describe the genome of astroviruses
- astroviruses primarily infect which age group?
- infants and young children
(also elderly and immunocompromised)
- transmission of astroviruses?
- fecal-oral route
(contaminated food and water, person to person)
- seasonality of astroviruses?
- is there any immunity associated with previous astrovirus infections?
- treatment for an astrovirus infection?
- which infection is more severe, rotovirus or astrovirus?
- molecular detection of astrovirus?
- compare adenovirus infections to rotovirus infections
- adenovirus symptoms are less severe, but infection lasts longer
- what is the progenitor cell for all the intestinal cell types and where is it found?
- undifferentiated crypt cell
(found in the crypts)
- other functions of the undifferentiated crypt cell?
- *release of IgA-receptor complex into crypt lumen
*synthesis of secretory component
* secretion of Cl- and H2O
- which intestinal epithelial cell produces acidic glycoproteins?
- goblet mucous cells
- which intestinal epithelial cell produces lysozyme?
- Paneth cells
- which intestinal epithelial cell has a role in the uptake of luminal substances for "sampling" by the intestinal immune response?
- M cells
- which intestinal epithelial cell produces a variety of hormones?
- endocrine cell
- what is the underlying cause behind Hirschsprungs disease?
- failure to develop Meissners and Auerbacks plexi - get a lack of peristalsis in the colon
- there is a connection between Hirschsprungs disease and what congenital disorder?
- downs syndrome
- gross manifestations of Hirschsprungs disease?
- dilated descending colon
- a transmural infarction tends to involve which segment of bowel?
- small intestine
(usually involves obstruction of a major mesenteric vessel)
- what are 3 MECHANICAL events causing ischemic bowel disease?
- 1. torsion
2. strangulated hernia
*remember, could also be a thrombus but that is not a mechanical cause*
- where are transmural infarctions common in the large intestine?
- splenic flexure
- how can you tell if the transmural infarction of the bowel is due to an arterial or venous occlusion?
- arterial - sharp demarcation
venous - no clear cut division
- how long will an ischemic bowel take to become gangrenous and perforate?
- 1-4 days
- where in the bowel will a mural and mucosal infarction most commonly occur?
- can occur anwhere in GI tract
- what happens when there is chronic ischemia to the bowel?
- *mucosal ulceration and inflammation
*segmental and patchy
*fibrosis and stricture
- hemorrhoids are dilations of?
- anal and perianal venous plexi
- internal hemorrhoids are a dilation of?
- the superior venous plexus
- external hemorrhoids are a dilation of?
- the inferior venous plexus
- what characterizes Chron's disease?
- transmural involvement
any segment of GI tract may be involved
- which areas of the GI tract does UC affect?
- rectum and left colon
sometimes entire large intestine
- in which race is there a higher incidence of IBD?
- in which SES is there a higher incidence of IBD?
- higher SES
- by age 60, which is more prevalent: UC or CD?
- what is the relation between smoking and UC and CD?
- UC - smoking decreases risk
CD - smoking increases risk
- what are some acute complications of IBD?
- in which form of IBD is there an especially high increased risk of CA?
- what type of CA is a patient with CD more prone to?
- Hodgkin's and non-hodgkin's lymphoma
- what is the string sign and which form of IBD is it seen with?
- string sign - due to thick fibrous walls narrowing lumen: seen in barium Xray
*seen in CD
- what other gross manifestations are seen in advanced CD?
- fat creeping over the bowel wall
thick fibrous mesentery
- what type of inflammation is seen in CD?
- transmural inflammation
lymphoid aggregates with germinal centers
- when there is extensive involvement of CD in the terminal ileum, what lab abnormalities would be seen?
- 1. decreased albumin
2. decreased B12
3. decreased bile salts (due to steatorrhea)
- are skip lesions seen in UC?
- microscopic abnormalities seen in UC?
- 1. crypt abscess (neutrophils in crypts)
2. no erosion to muscle layers
4. fibrosis with no obstruction
- which antibody is present in 50-75% of UC patients?
- which antibody is present in 55% of CD patients?
- ASCA (Ab to cell wall mannan of Saccharomyces cerevisiae)
- herniation of the mucosa through the muscular wall is known as?
- diverticular disease
- 95% of diverticular disease occurs in what location?
- sigmoid colon
- any connection between diet and diverticular disease?
- related to low fiber diet
- why does diverticular disease happen in the location it does?
- muscular weaknesses in the colon wall (due to points of arterial penetration or inbetween the taenia coli)
- what are some symptoms of diverticular disease?
- *only 20% of pts develop symptoms*
- what is intussusception?
- when a segment of bowel telescopes into a distal segment
- where is intussusception MC seen?
- in the terminal ileum/cecum
- what is the difference between a pedunculated polyp and a sessile polyp?
- pedunculated - has a stalk
sessile - no stalk
- GI manifestations of tuberous sclerosis?
- inflammatory polyps
- are hyperplastic polyps neoplastic?
(no clinical significance)
- peak age of hyperplastic polyps?
- 6th-7th decade
- histological characteristics of hyperplastic polyps?
- * well formed glands, crypts
* goblet or adsorptive cells separated by lamina propria
* serrated border
- clinical s/s of hyperplastic polyps?
- 80% of juvenile polyps are found in which segment of the GI tract?
- two types of hamartomatous colon polyps?
- 1. juvenile
2. Peutz-Jeghers polyps
- inheritance pattern of Peutz-Jeghers syndrome?
- autosomal dominant
- what are the components of Peutz-Jeghers syndrome?
- 1. hamartomatous colon polyps
2. melanotic pigmentation of mucosa
3. increased risk of other malignancies (pancreas, lung, ovary, uterus)
- do the polyps seen in Peutz-Jeghers have malignant potential?
- neoplastic polyps are also known as?
- adenomatous polyps
- what is the MC type of adenomatous polyp?
- tubular adenoma (75%)
- gross presentation of a tubular adenoma?
(stalk with raspberry like head)
- micro characteristics of a tubular adenoma?
- neoplastic epithelium, decreased goblet cells, atypia
(may have submucosal invasion)
- what is a good indicator of the risk of malignancy in a tubular adenoma?
(the larger the polyp, the greater the malignant potential)
- which type of adenoma has the highest potential for malignancy?
- villous adenoma
- where are most villous adenomas found?
- sigmoid colon and rectum
- gross characteristics of a villous adenoma?
lobular and velvety
(larger than tubular adenomas)
- histo characteristics of a villous adenoma?
- fingerlike branching papillae
often see submucosal invasion
- clinical s/s of a villous adenoma?
- rectal bleeding
- gross description of a tubulovillous adenoma?
- resemble tubular adenomas but surface is covered by villi
- malignant potential of tubulovillous adenomas?
- in between tubular and villous adenomas.
- hereditary pattern of familial polyposis?
- autosomal dominant
(risk of malignant transformation approaches 100%)
- at what average age is diagnosis of familial polyposis made?
- 2nd-3rd decade
- which type of polyps are seen in familial polyposis
- tubular adenoma
- three variations of familal polyposis?
- 1. Gardner syndrome
2. Turcot syndrome
3. attenuated FAP
- what is the treatment for familal polyposis coli (FAP)?
(almost 100% malignancy transformation rate)
- how does Gartners syndrome differ from FAP?
- * polyps along with osteomas and soft tissue tumors.
* same risk of malignancy as FAP
- how does Turcots syndrome differ from FAP?
- * polyps along with tumors of the CNS (gliomas, medulloblastomas)
- what is the peak age incidence in colon adenocarcinoma?
- 6th to 7th decade
- what are some dietary risk factors for colon adenocarcinoma?
- 1. low fiber content
2. high CHO diet
3. high fat
4. red meat
5. smoking, ETOH
6. decreased intake of calcium, vitamins A,C,E
- what is the rationale behind low fiber content increasing the risk of colon adenocarcinoma?
- low stool bulk -> causes increased fecal transit time -> alters bacterial flora (they break down bile salts into carcinogens)
- what is the rationale behind a high CHO diet increasing the risk of colon adenocarcinoma?
- a high CHO diet increases the synthesis of cholesterol and bile acids by the liver
- in which race is the risk of colon adenocarcinoma greatest?
- in which sex is rectal adenocarcinoma MC?
M:F = 2:1
- in which sex is adenocarcinoma of the rest of the colon most common?
- equal between M:F
- describe the differences in adenocarcinoma growth in the right colon versus the left colon.
- right colon: polypoid, fungating (presents late)
left colon: annular growth (obstructs, presents earlier)
- adenocarcinoma of which side of the colon would cause occult blood or anemia?
- right side
- what serum antigen can we look for to help us in the diagnosis of colon cancer?
- CEA - Carcinoembryonic antigen
(not specific for colon cancer)
- describe the spread of colon adenocarcinoma
- regional nodes
- where are carcinoid tumors MC found?
- small intestine (esp. appendix)
- what is the metastatic potential of carcinoid syndrome?
- low, but when it metastasizes causes carcinoid syndrome
(MC metastasizes to the liver)
- what exactly causes carcinoid syndrome?
- release of excessive vasoactive peptides, especially seratonin
- 4 clinical manifestations of seratonin release in carcinoid syndrome?
- 1. cutaneous flushing
2. water diarrhea, abdominal cramps
4. right heart failure
- three causes of obstruction leading to appendicitis?
- 1. fecalith
3. lymphatic hyperplasia
- how often is the epithelium of the intestine re-lined?
(cells originate in the crypts and migrate outward)
- where in the GI tract does most water absorption take place?
- small intestine (esp.jejunum)
- where are most water soluble micronutrients absorbed?
- small intestine
(most via passive absorption)
- sources of B12?
- milk, cheese, meats
- where do proteins and sugars "go" once they have been absorbed from the intestinal lumen?
- portal vein
- where does fat go once it has been absorbed from the intestinal lumen?
- what two forms are CHO digested as?
- which enzyme hydrolizes starch oligosaccharides?
- pancreatic amylase
- which enzyme is found on the brush border and assists in the digestion of starch?
- disaccharidasas break down
1. lactose into?
2. sucrose into?
- 1. glucose and galactose
2. glucose and fructose
- in what form are proteins
1. absorbed from the intestinal lumen
2. when they enter the portal blood
- 1. amino acids or dipeptides
2. amino acids
- which enzyme hydrolyzes fat in the intestinal lumen?
- pancreatic lipase
- what are the luminal events involved in triglyceride digestion? (4)
- 1. emulsification
4. diffusion across membrane
- what are the mucosal events involved in triglyceride digestion (5)?
- 1. uptake
2. transport to ER
3. triglyceride resynthesis
4. chylomicron formation
5. lymphatic transport
- describe the absorption of fat soluble vitamins
- bile acids make them soluble in micelles --> diffuse across membrane
- what are the four bile salts?
- 1. Glycochenodeoxycholic
- what percentage of bile is reabsorbed via the enterohepapic circulation?
- where in the GI tract are most bile acids reabsorbed?
- distal ileum
- how are medium chain fatty acids absorbed?
- hydrolyzed by lipase
becomes water soluble and diffuses across.
then absorbed into the portal vein (Bypasses lymphatics)
- give an example of a short chain fatty acid
- coconut oil
- three symptoms of malabsorption?
- 1. diarrhea
3. wasting and weight loss
- why would parasthesias or tetany be seen in some cases of malabsorption?
- 1. decreased serum [Ca+] and [Mg++]
2. due to decreased absorption of Ca, Mg, and/or vitamin D
- why would ecchymoses be seen in some cases of malabsorption?
- Vit. K deficiency
(increases prothrombin time)
- Glossitis is due to which vitamin malabsorption or deficiency?
- vitamin B
- what is borborygmi?
- loud intestinal sounds
- what is a very common malabsorptive cause of abdominal distention, borborygmi, flatulence and watery stools?
- carbohydrate malabsorption, fermentation, and decreased absorption of water and electrolytes
- what is the test usually done to see if steatosis is present?
- fat balance test
- why is the presence of steatorrhea so important?
- it is the hallmark of malabsorption (most causes)
- what is and isn't absorbed in lactase deficiency?
- impaired absorption of disaccharides
(monosaccharides are absorbed fine)
- where is vitamin B12 absorbed?
- what is the difference between malabsorption and maldigestion?
- malabsorption - mucosal defect
maldigestion - intraluminal problem
- when classifying malabsorption: besides attributing it to maldigestion and malabsorption, what other disorder can cause it to occur?
- lymphatic obstruction
- which 3 malabsorption syndromes make up 95% of the causes of chronic diarrhea and malnutrition?
- 1. CF
2. Gluten Sensitive Enteropathy (celiac disease)
3. Chronic Giardiasis
- pathogenesis of gluten sensitive enteropathy?
- immune mediated
- how does a typical case of gluten sensitive enteropathy present?
- young age (6-24 months)
* failure to thrive
* chronic diarrhea
* abdominal distention
- how is gluten sensitive enteropathy diagnosed?
- small bowel biopsy, screen with a tissue transglutaminase IgA
- treatment for gluten sensitive enteropathy?
- gluten free diet for life
- histo characteristics of gluten sensitive enteropathy?
- *no villi
- clinical s/s of lactose intolance?
- explanation for diarrhea in lactose intolerance?
- osmotic diarrhea secondary to non-absorbed sugars
- explanation for gas seen in lactose intolerance?
- lactose -> lactic acid, acetic acid and CO2
- regarding parasites: what defines the definitive host?
- the host where sexual reproduction occurs
- in which host(s) do protozoans undergo sexual and asexual reproduction?
- both in definitive host
- what is the most common intestinal protozoan parasite in humans?
- what are the two forms of Giardia?
- cyst (outside of body)
trophozoite (in body)
- why does the Giardia trophozoite look like a little bitty monster?
- because it has 2 pronuclei (from germ cells that never fuse)
- micro changes seen in intestinal lining in a giardia infection?
- shortening of villi
inflammed crypts and lamina propria
lesions of mucosal cells
- 5 clinical s/s of a giardia infection?
- 1. steatorrhea
2. abdominal distention
5. weight loss
- a giardia infection can cause a deficiency of which nutrients? (3)
- what is the cause of amoebic dysentery (amoebiasis)
- how is an entamoeba infection contracted?
- via ingestion of cysts in contaminated food, water or hands.
- are the cysts of entamoeba hardy?
- yes! they can survive for up to 12d and in temperatures under 50 degrees C
- what is unique about the trophozoites in an entamoeba infection?
- they spread
(invade submucosal tissue and spread to liver and lungs)
- how do trophozoites invade the intestinal mucosal epithelium?
- secrete histolysin
- what are the two forms of an entamoeba infection?
- 1. luminal - asymptomatic carrier (transmits disease in stool)
2. invasive - no transmission occurs because almost all are trophozoites
- invasive amoebiasis is also known as?
- amoebic dystentery
- s/s of amoebic dysentery?
- *severe diarrhea (w/blood and mucous)
(sx. appear after a 1-4 wk. incubation period)
- when is cryptosporidium a problem?
- in immunocompromised individuals
- how is cryptosporidium contracted?
- contaminated water
- intestinal trematodes are also known as?
- specific fluke that invades the GI tract?
- Fasciolopsis buski
- describe the lifecycle of Fasciolopsis buski
- 1. eggs passed from feces, enter water
2. infects snail
3. matures (becomes a cercariae)
4. abides on water or plant - human or pig ingests
5. becomes Excyst in duodenum
6. becomes adult in small intestine - sheds eggs in feces
- what does F.buski feed on?
- lumenal nutrients and on the intestinal mucosa
(this leads to inflammation, ulcerations, abcesses)
- where are the following tapeworms found?
1. Taenia saginata
2. Taenia solium
3. Diphyllobothriasis latrum
- 1. Beef
3. Broad fish
- why must adult tapeworms be removed?
- to prevent human cysticercosis
(formation of cysts in other tissues)
- what causes human cystercercosis?
- ingestion of tapeworm egg (rather than cyst)
- in human cysticercosis, where do cysts MC form?
- skeletal muscle
(also eyes, lungs, SQ tissue)
- from what is Diphyllobothriasis latrum contracted?
- consumption of undercooked or raw fish muscle
- severe D. latrum infections interfere with uptake of what nutrient?
- what are the common names for the following intestinal nematodes?
1. enterobius vermicularis
2. Trichuris trichiuria
3. Ascaris lumbricoides
4. Ancylostoma duodenale
5. Necator americanus
- 1. pinworm
3. giant roundworm of man
4. old world hookworm
5. New world hookworm
- in an enterobius vermicularis infection: where does the gravid female choose to lay her eggs?
- in the perianal folds
(then she dies)
- in an enterobius vermicularis infection: where do mature worms live?
- in the ileocecal region
- what part of the GI tract does Trichuris trichuria (whipworm) prefer to inhabit?
- MC colon
(also appendix and rectum)
- how does host infection of trichuris trichuria (whipworm) occur?
- by ingestion of contaminated food or water or from fingers
(eggs are shed in feces - infective larval form develops 3-6wks later)
- in the human host, where do the larva of Trichuris trichuria (whipworm) hatch?
- in the upper small intestine
*then they burrow into intestinal epithelium*
- once mature, where does trichuris trichuria (whipworm) live?
- cecal region
(embed anterior end deeply into colon submucosa)
- clinical s/s of heavy infections of Trichuris trichuria (whipworm)?
- s/s of Ascaris lumbicoides infection?
- 85% asymptomatic
*upper abdominal discomfort
*inflammation associated with IgE response
*loss of appetite, possible malnutrition
- how is hookworm contracted?
- from walking barefoot
- encystment of trichinella can lead to what s/s?
- *orbital edema
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