uworld GI Flashcards
describe how the hormonal and mechanical changes of pregnancy affect the GI tract
- esophagus
- GB
- intestines
- rectum
- ↑ progesteron –> GERD
- ↑ estrogen + progesteron –> cholestasis + cholelithiasis, cholecystitis
- ↑ progesterone (+gravid mechanics) –> constipation, farting, bloating
- ↑ mechanical P –> hemorrhoids
how does cirrhosis –> pulm HTN affect
- plasma oncotic P
- splanchinc vascular resistance
- effective blood volume
- RAAS
- capillary permeability
- plasma oncotic P –> ↓
- splanchinc vascular resistance –> ↓ (N.O. release)
- effective blood volume –> ↓ (blood pooling in the splanchnic beds secondary to dec SVR)
- RAAS: ↑
- ADH: ↑
- capillary permeability –> unchanged
young child w an incidental finding of an abd cyst connected to the umbilicus and ileum by a fibrous band is most likely what?
what is the embryologic cause? what other pathology can result from the same embryologic mistake?
vitelline duct cyst
- x vitelline duct obliteration = persistant connection between midgut and yolk sac
persistant vitelline duct –>
- if small, connect small intesting to outside via umbilicus –> meconium discharge from umbilicus at birth
- Meckels = most common= partial closure, opened on ileum side : ONLY 2% are sx!!
- vitelline sinus = partial closure, opened at the umbilicus
- vitelline duct cyst= partial closure, middle part stays open
differentiae the clin presentations of the dif hepatitis viruss??
- transmission
- clin presentation
- clin course/prognosis
- liver biopsy
- carrier state?
HAV
- fecal-oral = shellfish, travelers, day care
- usually asx: can present as low grade fever, anorexia/nausea, and dark colored urine in YA returning from endemic regions
- is an acute illness only, good progosis (A-okay)
- hepatocyte swelling, monocyte infiltration, = ballooning degeneration (via ATP depletion) Councilman bodies (Adjourn)
- no carrier state = “alone”
HBV
- Blood (parenteral), Banging (sex), Birthing (perinatal)
- long incubation time before present (months) :initial present as serum sickness (fever, arthralgias, rash)
- may progress to carcinoma : adults = mostly full resolution, neonates = worse prognosis (Bad Baby)
- “ground glass” eosinophilic granular appearance, w cytotoxic T cells mediated damage (Break-in scene)
- carrier state common
HCV
- primarily blood (IVDU, post transfusion)
- long incubation time (months) before present
- most develop stable, chronic Hep C: may progress to cirrhosis or carcinoma
- lymphoid aggregrates w focial areas of macrovesicular steatosis (chunky=fat)
- carrier state v common
HDV
- parenteral, sexual, perinatal (Same as B) : superinfection OR co-infection
- same as HBV w serum sickness (fever, arthralgias, rash)
- superinection –> worse prognosis
- same liver biopsy as HBV (break in scene w ground glass and CD8 toxic infiltrate)
- needs HBV prior infection: the HBsAg (surface Ag) needs to coat the HDV viral particles for them to be able to enter the hepatocyte (Defective Doorway) = “replication defective” virus bc it can’t get into the hepatocyte = no able to replicate its RNA
HEV
- fecal oral, especially waterborne : mostly endemic
- mostly pregnant women (expecting), Enteric ds
- present w fulminant hepatitis, high w mortality in pregnant women (End)
- patchy necrosis
- no
what histologic changes are seen in the small bowel in the setting of
- lactase deficiency
- celiac ds
- crohn ds
- ulcerative colitis
- lactase deficiency
- NONE
- celiac ds
- atrophy of intestinal villi due to gluten exposure
- crohn ds
- skip lesions sparing the rectum
- transmural inflammation leading to fistulas
- NONcaseating granulomas + lymphoid aggregrates (old crone granny, creeping down the cobblestone)
- cobblestoning mucosa, creeping fat, and bowel wall thickening (string sign)
- ulcerative colitis
- continuous colonic lesions ALWAYS involving the rectum (colitis= colon inflammation= “colonizers” who have ‘manifest destiny’ all the way to the rectum)
- mucosal + submucosal inflammation only, w friable mucosa ± deep ulcerations
- loss of haustra = (lead pipe sign- comparing colonization to ‘karen’ is like comparing a lead pipe to a string’)
- crypt abscesses + ulcers
compare & contrast the
- transmission
- clin presentation (type of diarrhea, epidemiology if relevant)
- histology / dx findings
for
- cryptosporidium
- C. dif
- E. histolytic
- enteropathogenic E. Coli
- giardia
- mycobacterium avum
- salmonella
- cryptosporidium
- fecal oral
- watery diarrhea : self limited in immunocomp, life-threatening loss of fluid in immunosupp (esp advanced AIDS)
- parasite: _cystic organism_s on modified acid fast stain of stool :biopsy of oocysts lining the brush border
- C. dif
- recent abx use
- toxic mediated inflammatory coliits: blood in stool
- G+, spore forming bacteria, usually w fecal leukocytes or blood
- Entameba histolytica
- fecal oral
- cause dysentry (bloody diarrhea)
- ameoba, show anchovie past abscesses in right lobe of liver /// flask shaped ulcers in colon w foamy tropozoites
- enteropathogenic E. Coli
- eat from meat
- watery diarrhea
- attach to and efface small bowel epithelium: G- rod
- giardia
- fecal-oral (contaminated water)
- foul smelling, greasy diarrhea and excessive flatulence
- protozoa: oval cysts or trophozoites seen on stool
- mycobacterium avum
- oppurtunistic infection associated w AIDS
- diarrhea and weight loss
- acid fast bacteria are found within macrophages
- salmonella
- common, food borne infection
- acute, self-limited diarrhea, vomiting, fever, abdominal cramping
- G- bacillus (rod)
presentatino of cryptococcus vs cryptosporidium
cryptococcus = meningitis or pulm infection
- AIDS defining
- fungus
cryptosporidium = watery diarrhea
- self-limited in immunocompetent, life-threatening in immunosupp
- parasite
newborn presenting w large, reducible midline abd protrusion covered by skin
dx?
etiology?
assocatiated w? prognosis/trx?
congental umbilical hernia
- incomplete closure of the umbilical ring (abd Ms) at linea alba, allowing bowel to protrude through the abd musculature
- associated w down syndrome, but can occur isolated
- observe for spontanous closure, elective surgery by 5
what is the clin significance of the lac operon
what are the components, the function of each
-the lac operon is a classical example of genetic response to an environmental change:
- E. Coli- lac operon: when glucose is low (main food) AND lactose levels are high, E. Coli will make genetic changes at the lac operon to change expression of lactose
- effectively switch from mainly glucose metabolism to mainly lactose metabolism
3 regulatory points, 3 genes
- CAP site= activator protein site
- if bound by cAMP, will go on to activate the promoter sequence downstream
- presence of glucose = ↓↓ cAMP
- low glucose levels –> ↑↑ cAMP –> promoter activation
- promoter site
- operator locus
- lac I gene (upstream to the lac operon) constituitively express the repressor protein
- exists downstream of promoter site, is constituitively bound by the repressor protein = block transcription of the downstream genes for lactase
- lactose will unbind the repressor protein from the site –> allow promoter sequence to bind RNA polymerase and begin downstream transcription
IN ORDER TO EXPRESS LAC OPERON:
need low glucose AND high lactose
(double locked gate)
- lac Z
- encode β-galactidase
- enzyme that does lactose –> galactose + glucose
- lac Y
- encode permease
- allow lactose to enter the bacteria
- lac A
- encodes a transacetylase
- what is a total gastrectomy
- patients will have to take lifelong supplements of what post-op and why?
- what AE of the surgery might developy bc of the physical removal?
- =total removal of the entire stomach
- B12:
- parietal cells in the stomach produce intrinsic factor, which binds B12
- without intrinsic factor, intestinal absorption of B12 is severely dec
- dumping syndrome
- bc esophagus and small intestine are directly connected, there is no storage of food in the stomach anymore
- accelerated emptying of hyperosmolar food boluses = colicky abd pain, nausea, diarrhea
compare and contrast the characteristics of colorectal CA in pts w hx of IBD vs sporadic cases
- age
- origin and #
- location
- genetic mutations
- histology
pts w IBD (esp UC pts w pancolitis) are at increased risk of colorectal CA
IBD:
- younger
- from flat lesions, multifocal
- proximal colon > distal (esp in crohn)
- early= p53, late= APC
- poorly differentiated: mucinous / signet ring cells
sporadic
- older
- polypoid lesion, usually singular
- distal colon > proximal
- early = APC, late=p53
- well differentiated, rarely mucinous
by what mechanism does Shigella cause clinical sx
hemorrhagic diarrhea
- shigella invades M cells within the Peyer’s patches of the ileum
- there they induce host cell apoptosis, manipualte actin filaments to achieve immobility (shigella itself is IMmobile)
what are paneth cells and where are they
in the small intestine, at the base of the crypts of Leiberkun
=immune cells that are phagocytic, and can also secrete lysosomes (bacterial cell wall destruction) and defensins
outline the branching off the aorta that will make the blood supply to the
liver
duodenum
celiac trunk –> common hepatic A –> proper hepatic A + gastroduodenal A
outline the mechanism by which IBD can affect coagulation
how will it present
Crohn ds= often involve the terminal ileum
- terminal ileum is where bile acids are reabsorbed
- with inflammation of the terminal ileum –> less bile acid reabosroption –> less absorption of fats and Vit ADEK from the terminal ileum
- = ↓↓ Vit K ==> ↓↓ activation of coag factors 2, 7, 9 10
- presents as easy bruising, large hemarthroses after minor traumas, and prolonged bleeding after surgery
galactosemia is a ds resulting from the disruption of what metabolic processes (directly and indirectly)
compare the two tyes of galactosemia by..
- mutation
- presentation
x galactose metabolism
- galactose is a byproduce of lactose metabolism
- galactose metabolism feeds into glycolysis via produce G6P
screened at birth in the US
Type 1:
- x glucokinase (GALK) ==> excess galactose, gets shunted into galacticol
- not severe: presents in older children
- cataracts (galacticol build up) and urine (+) for reducing substance
- often no systemic sx
Type 2:
- xGALT = galactose 1-phosphate uridyl transferase ==> build up of toxic galactose-1-phosphate
- more serious, present in infancy
- neonatal vomiting, lethargy, failure to thrive
what two causes account for 80% of acute pancreattis cases?
what are the less common causes that account for the rest
MC =
- gallstones (old white ladies- US shows stones)
- alcoholism
less common:
- recent ERCP
- drugs = azithioprine, sulfasalazine, furosemida, valproic acid
- infections (mumps, coxsackie, M. pneumnoiae)
- hypertriglyceridemia (>1000 will overwhelm the album-binding system to FFA–> direct injury to pancreatic acinar cells)
- structural abnormality of pancreated duct or ampullary region
- surgery
- hypercalcemia
outline the step by step etiology that leads to hepatic encephalopathy
trx and MOA?
(in the setting of chronic liver failure/cirrhosis)
stressful preciptating event –> inability of liver to metabolize waste products –> intoxication of brain
- (sedative/narcotic use, hypovolemia, hypokalemia, GI bleed, infection, TIPS shunt)
i. e. GI bleed
↓
inc hgb deliver to gut = inc nitrogen deliver
↓
nitrogen converted to ammonia and delivered to bloodstream
↓
ammonia enter liver via portal V
↓
impaired liver detox ability = accumulation of ammonia and other toxins in the blood stream
↓
cross BBB
↓
impaired neurotransmitted metabolism + ↓ cerebral glucose metabolism
↓
inc inhibitory NTs (GABA) and dec excitatory NTs (glutamate, catecholamines)
↓
ataxia, asterixis, AMS
trx: dec toxin levels
lactulose–> induce diarrhea
rifaximin –> nonabsorbable abx against GI flora –> dec intestinal production and absoprtion of ammonia
what is the effect of alcoholic liver ds on the spleen
be specific
alc liver ds
↓
portal HTN
↓
**any cause of Portal HTN leads to splenomegaly bc the spleen is part of the portal system**
↓
congestive hypersplenism
- red pulp expansion = inc blood filled sinuses and cords
what pharm trx will rapidly decrease portal HTN
how?
octeotride = somatostatin analog
- work by direcly inhibiting splanchic vasodilation
- i.e. celiac trunk, IMA, SMA, and all their branches
–> splanchnic vasoconstriction–> dec feed into portal system –> dec portal venous P
odynophagia suggests what?
what are the causes in immunosuppressed individuals?
what are the dif endoscopic findings, microscopic findings, and trx?
odynophagia = painful swalloing = esophagitis
candida, HSV, CMV
flucanozole, acyclovir, gancyclovir
what are the Vs associated w hemorrhoids 2° to portal HTN
internal
super rectal V –> inferior mesenteric V
external
inferior rectal V –> internal pudendal V –> internal iliac V
what pathologic structure are the areas point at
if the specimen is taken from the esophagus, what is teh prognosis
keratin pearls
SCC of the esophagus has poor prognosis
intussusception
- most common location
- mc population
- mc clinical presentation
- dx and trx
=ileocolic junction
=younger than two (can be older, usually linked to another abn, such as meckel’s)
=intermittant colicky abd pain, N/V, current jelly stools
=barium enema can be dx and therapeutic: if no fix, surgical removal
what is the mechanism of ds in hereditar hemochromatosis
abn HFE gene = abn protein that binds transferring receptor on hepatocytes and leads to abn detection of body iron levels
↓
inc iron absorption via
- inc intestinal iron absorption
- dec hepcidin synthesis –> inc iron release into bloodstream
↓
inc iron deposition in organ tissues
what pathologic change is seen in this picture
if its from the colon, what is the likely ds
noncaseating granuloma
crohn
present w syncope, skin dark/tanned, and diastolic heart abnormalities
all normal labs except for hyperglycemia..
non tender hepatomegaly..
ds?
what other sx may be associated? associated w inc risk of what infections?
hereditary hemachromatosis
BRONZE DIABETES
fibrates used for dyslipidemia can have what AE effect on the bile tract, and how does it do this
fibrates = x ‘cholesterol 7 alpha hydroxylase’ –> = dec bile salt formation and inc chol excretion –> inc risk cholesterol gall stones
(existing bile becomes supersaturated with cholesterol)
focal nodular hyperplasia of the liver
pathology
clin
imaging/histo
FNH = highly vascular abn caused by local hyperperfusion causing secondary hyperplastic response
- benign and asx, usually found incidentally on autopsy/imaging for something else
- associated with young women
- characterisic solitary mass (can be big) w characteristic hypervascularity (i.e. enhanced contrast, the tissue is ligher than surrounding tissue)
- histo = small, solitary, pale nodules made of normal cells
- local increase in normal appearing hepatocytes, with a central depressed, grey-white stellate scar that has fibrous septae raditating from the center
- abnormally larger arteries surround the area
pt w chronic abd pain and diarrhea, with hx of regular alc use, and epigastric calcifications likely has what?
what is the pathogenesis
what other sx is it associated w
chronic alcoholic pancreatitis
- alcohol induced secretions of protien can block pancreatic ducts –> duct plugs –> calcification
- malabsorption, weight loss, frothy/fatty stools
new born baby w jaundice, inc birect bili, dark urine and light stool
likely dx?
biliary atresia
pt presents w weight loss, epigastric pain after meals, hx of PUD
what is seen on stomach histo below?
dx? other findings associated w the dx?
=gastric adenocarcinoma
- (vs ZES- which would feel better after meals, worse at night/fasting)
- see signet ring cells
- stomach will also show linits plastica (diffuse involvement of the stomach wall and loss of e-cadherin)
- virchow node, sister mary joseph nodule
what is seen on this CT
multiple mets to the liver
(likely from breast, lung, colon)
what is the class + MOA of each of these drugs in the GI tract
- fiber supplements
- polyethelene glycole, Mg-hydroxide, lactulose
- ducosate
- bisacodyl, senna
- lubiprostone
- methlynaltrexone
- fiber supplements
- buld forming laxatives
- binds luminal water –> dec stool consistency
- polyethelene glycol, Mg-hydroxide, lactulose
- ostomic laxatives
- draw water into colon lumen
- ducosate
- surfactant
- dec stool surface tension so that water can enter the stool
- bisacodyl, senna
- stimulant laxatives
- activate entereic Ns in myenteric plexus –> stimulate peristalsis
- lubiprostone
- chloride channel agonist
- Cl- efflux into intestinal lumen –> Na and water into lumen
- methlynaltrexone
- peripheral mu-receptor antagonist
- counteract inhibitory effect of opioids on peristalsis
anal squamous cell carcinoma
- risk factors
- manifestations
- histology
HPV= double stranded, non-enveloped DNA virus
- associated w immunocomp–> inc risk anal SCC
describe the gross appearance and composition of the pseudomembrane seen in C. dif
“white yellow plaques on the colonic mucosa, composed of fibrin and inflammatory cells”
which form of IBD is classically associated with fistulas and how could that present
why NOT the other type of IBD
crohn’s
- enteroenteric fistulas = between 2 adjacent bowel loops
- fistulas between the bowel and another organ (bladder or vagina) = feces coming out the wrong hole
- enterocutaneous fistula = bowel contents and feces draining to the out the skin of the abdomen
not associated with UC bc inflammation is confined to the mucosa and submucosa
vitamin A deficiency can result from what problems in the GI tract
how will it present
pt presents with hx of a sudden urge to defecate and then bright blood in the stool (no pain), with the following finding on colonoscopy.
dx? how does this differ in etiology and sx from the two other very similar and related diseases?
risk factors?
diverticulosis = painless hematochezia + multiple outpouchings seen on colonoscopy
hepatitis
- how are the different strands transmitted, and what class virus is each
- which strands have a short vs long incubation period
- which strands have an acute presentation,
- which have a chronic presentation - explain each
- long term conditions associated with any strain
- for chronic strains- what is the mechanism of chronic
- which have good prognosis and which have bad
- diff liver biopsy findings
- who has a carrier state
- class & transmission
- HepA = picornovirus, fecal oral shellfish, travelers, daycare
- HepB = DNA hepadnavirus: sex, birth, blood
- HepC= flavivirus : needles (blood)
- HepD= RNA deltavirus: sex, birth, blood
- HepE = hepevirus, fecal-oral
- incubation
- short= hepA, hepE, superinfection of hepD
- long= hepB, hepC, coinfection hepD
- acute
- hepA, hepB+D, hepE
- chronic
- hepB+D, :
- associated w HCC, MGN (thick BM), MPGN (tram track BM)
- hepB has reverse transcriptase, replicate both in and out of nucleus
- hepC
- cirrhosis, HCC, cryoglobulinemia
- antigenic variation
- hepB+D, :
- prognosis
- good= hepA, hepB in adults, hepD coinfection, hepC
- bad= hepD superinfection, hepE –> fulminant hep in pregos
- biopsy
- hepA= hepatocyte swelling, monocyte infiltration, councilman bodies
- hepB+D= ground glass infiltrate into liver and CD8 T cell damage
- hepC = chronic fibrosis and cirrosis OR lymphoid aggregates w focal areas of macrovesicular steatosis
- hepE= patchy necrosis
- carrier state
- hep B+C (carry on back(
what is the difference between a mechanical obstruction of the small bowel and a psuedoobstruction of the small bowel
