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247 Cards in this Set

  • Front
  • Back
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. UC
2. Crohn's
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
2. propantheline
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
2. 6-mercaptopurine
3. methotrexate
4. cyclosporine
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
2. antiinflammatory
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
2. hydralazine
3. procainamide
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
no envelope
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?
Latex agglutination
(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
no envelope
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
low-grade fever
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
no envelope
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
3. adhesions
*remember, could also be a thrombus but that is not a mechanical cause*
where are transmural infarctions common in the large intestine?
splenic flexure
(watershed area)
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
skip lesions
creeping fat
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
noncaseating granulomas
lymphoid aggregates with germinal centers
*see "cobblestoning"
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
3. pseudopolyps
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*
intermittent cramping
constipation, distention
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
mucous production
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
3. bronchospasm/wheezing
4. right heart failure
three causes of obstruction leading to appendicitis?
1. fecalith
2. pinworms
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
2. lipolysis
3. solubilization
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
2. Glycocholic
3. Taurochenodeoxycholic
4. Taurocholic
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
2. edema
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
genetic link
how does a typical case of gluten sensitive enteropathy present?
young age (6-24 months)
* failure to thrive
* chronic diarrhea
* abdominal distention
* irritability
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
*crypt hyperplasia
*inflammatory cells
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
3. nausea
4. flatulence
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
2. Pork
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
2. whipworm
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)?
rectal prolapse
inflammatory diarrhea
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
*muscle pain
*respiratory distress
*weakness, malaise
*CNS involvement
*myocardial involvement