GI Flashcards
causes of esophagitis
GERD (most common), infection, pill, caustic ingestion, radiation, autoimmune, eosinophilic esophagitis
causes of infectious esophagitis
usually in immunocomp (aids, transplant): candida, HSV, CMV,
typical and atypical GERD symptoms
typical:
GERD causes
lower eso sphincter incompetence, hiatal hernia, meds, increased intra-abdo pressure (obesity, pregnancy), incomplete emptying of stomach
alarm symptoms, that require f/u or endoscopy in GERD
weight loss, progressive dysphagia, blood in stools, anemia, age >50
caustic ingestion: why are alkalis worse than acids
acids produce coagulation necrosis which limits tissue injury (bc is causes an escahar), alkalis produce tissie liquefaction necrosis which allows for continued damage.
mgmt of caustic ingestion:
airway assessment, NPO, pain mgmt, PPI, abx if perf suspected.
DO NOT: place NGT, give anything by mouth, avoid charcoal
dispo: likely as per poison control
note: household bleach ingestion <100 mL unlikely to do any damage
mgmt of mallory weiss
supportive and symptomatic usually adequate
what to rule out with mallory weiss (2 things)
peritonitis and esophageal perf
pathophys of eso perf
rupture of all layers of eso and surrounding pleura –> non sterile contents into mediastinum or thorax
causes of eso perf
iatrogenic, Boerhave’s (rethching after etoh or large meal), trauma
s/s of eso perf
variable… most commonly epigastric pain that radiates to neck,
pleuritis pain made worse by neck flexion and swallowing
Mackler triad: vomiting, chest pain subcutaneous emphysema
+/- fever/hypotension/shock
dx of eso perf
cxr: can reveal pneumomediastinum, ptx, pleural effusion, widened mediastinum, but is not sensitive (esp early on)
esophgram using water siluable ocntrast (NOT BARIUM) or EGD can make diagnosis
can consider CT chest if above studies not available.
mgmt of eso perf
NPO, broad spectrum abx, surgical consult
why are button batteries bad, what is the timeline
alkali –> liquefaction necrosis
burns esophagus within 2 hours and perfs within 4-6 hrs
where do most eso fbs lodge in adults and childern
areas on anatomic narrowing
children: cricocopharyngeus muscle -> C6
adults: lower eso sphincter –> T10
imaging for eso fb
usually not necessary if food bolus
start with cxr, then CT if not identifiable
coins in trachea vs eso on xr
trachea they will appear sideways and then and in eso will appear head on
button battery vs coin on xray
BB with have double density or “stack of coins sign”
mgmt of eso fb
Look at highlights
distinguishing UGIB from LGIB
hemetemsis/coffee ground emesis = UGIB
BRBPR with CLOTS = LGIB
melena or hematochezia (w/o clots) can be either). up to 70% UGIB will have these
NG aspirte: specific but not sensitive for UGIB (only picks up 23% in pt w/o hemetemesis
BUN/Cr ratio > 30 ; 93% sp for UGIB
age < 50 more likely UGIB
if hemodynamic instability assume UGIB
cause of UGIB
gastritis/esophagitis
ulcers
mallory weiss
malignancy
varices
dieulafoy lesion
aorto-enteric fistula (think of this is aortic graft)
idopathic
cause of LGIB
CHAND
NG in GIB
specific, but no sensitive for UGIB (will miss over 75% if no hemetesmsis). not generally indicated.
can consider if going to intubate and needing to empty the stomach first.
mgmt of GIB
octreotide is moderate priority, 2008 cochrane review –> prevents re-bleeds in variceal and non varicel ugib, decrease splanchnic blood flow, although not lifesaving can be considered.
also need to reverse anticoagulation: if on DOAC or warfarin –> octaplex 2000 units and vitamin K IV if on warfarin
TXA –> nope
walk through balloon tamponade in UGIB
go
walk through SALAD intubation in UGIB
go
Score for outpt mgmt of UGIB
Glasgow-Blathchford score , score <3 can consider dc
diagnostic tests for LGIB
-colonscopy is best, but usually not possible if active/brisk bleeding
-angiopgraphy
-tagged RBC scan
endoscopic therapies for UGIB
epi injection, banding, cautery, sclerotherapy
upper vs lower GIB: location and icnidenc
proximal to ligament of Treitz = upper
2/3rds are UGIB, 1/3 are LGIB
what is shock index? how to use in GIB
HR/SBP, if > 1 consider MTP (?seems like low threshold), in practice should use this as trigger to have PRBCs down and transfuse, if needing > 4/hr or no response to 4 then trigger MTP
how to diagnose and when to consider aortoenteric fistula
known AAA (esp if grafted) and GIB is AEF until proven otherwise, get CT abdo or angiography in stable pts, if unstable resuscitate and STAT OR
note present like upper or lower GIB
causes and complications of gastritis
NSAIDS, EtOH, H pylori, autoimmune, corrosive agents, also shock/hypovolemia!
comp: ulcers, GIB, perf,
zollinger-ellison syndrome
gastrin secreting endocrine tumour, accounts for 1% of all PUD
Treatment regimen for h pylori
mgmt of gastritis
PPI, d/c nsaids, etoh and outpt tx for h pylori.
note gastrits/PUD w/o cause, should Ix for h pylori, or at leats send test for it first, if GERD trial PPI first
Ix options for H pylori
serology –> only tests for past exposure
urea breath, stool Ag and endoscopy can confirm active infection or eradiction
4 entities of stomach disease
gastritis, PUD (gastric and duodenal ulcers), gastrinoma, gastric adenoca
PUD pain symptoms
epigastric pain, worse at night (can wake from sleep), belching, early satiety, nausea, abdo distention
most common sign: epigastric pain to palp
invasive vs non-invasive gastroenteritis
non-invasive = mild systemic symptoms, n/v, diffuse abdo tenderness,
dehydration
invasive = more severe systemic symptoms, bloody diarrhea, FEVER, tender abdomen
mgmt of gastro
supportive, usually resolves by 14 days
get GPMP/O&P if longer than 14 days, severe, recent travel, recent abx, outbreaks, etc
Bugs that cause bloody diarrhea
most common cau of gastric/duodenal perf
eroded ulcer
causes of small bowel perf
infection (typhoid/TB), tumours, strangulated hernia, IBD, ischemic colitis, FB, meds, blunt or penetrating trauma, SBO
Large bowel perf causes
LBO, colon cancer, diverticulitis, iatrogenic
mgmt of bowel perf
surgical consult, NPO, IVF, broad spectrum abx
bloody diarrhea more common in chrons or UC
UC!
Chrome vs UC: distinguishing features
dx of toxic megalcolon
colon >6 cm on radiograph with signs of systemic toxicity = high risk for perf
complications of UC
GIB, colorectal CA, toxic megacolon
complications of chrons
SBO, fistula, abscess, stricture, toxic megacolon, colorectal CA
extraintestinal manifestations of IBD
simple SBO vs strangulation
simple = impairs lumen only
strnagulation, results in loss of blood flow and can lead to necrosis/perf etc, often results from “closed loop” obstruction
causes of SBO
adhesions, neoplasm, hernias, chrons, volvulus, intussusception (<2 y/o), gallstone ileus.
stool and flatus in SBO
can pass fro up to 24 hrs after complete SBO
AXR findings and sensitivity for SBO
sensitivity: 70-80%, findings= dialted loops of small bowel with air fluid levels and decompressed colon, can see string of pearls sign,
causes of ileus
post-op
acute abdo process eg peritonitis
hypokalemia
meds
severe medical illness (eg sepsis)
lactate and bowel ischemia, sensitivity and specificity
sensitive but not specific, although can still have necrotic bowel with normal lactate
mgmt of SBO
note gastrografin and NGT for pts with significant vomiting and distention
meckel diverticulum rule of 2’s
2% of population, 2% symptomatic, 2:1 male, 2 feet proximal to TI, most commonly present in pts <2yrs of age
how does meckel diverticulum present
can mimic appy or present with acute onset, massive “brick-red” painless rectal bleeding
radiation proctocolitis 2 types
acute: rectal bleeding, abdo pain and tenesumus during course of radiation
chronic: months to years after tx, slow onset of diarrhea, tenesums, fistulas and strictures.
** note chronic is a diagnosis of exclusion, need ot r/o other shit first
why can bowel obstruction, esp LBO lead to sepsis
bacterial translocation
NGT in LBO?
if distention or vomiting
3 top causes of LBO in order
colorectal ca
diverticulitis
sigmoid volvulus
cecal volvulus
why does LBO lead to dehydration
bowle edema and transudative fluid losses
pathophys and tx of LBO from:
colorectal ca
diverticulitis
sigmoid and cecal volvulus
most common age of appy
10-19
most common cause of atraumatic abdo pain in children >1 year old?
appy
appendix symptoms
quite vague:
-can cause nausea/vom
-diarrhea, constipation or normal.
-periumbilical pain that migrates to RLQ is most common
-retrocecal app will cause flank pain
-can cause dysuria or hematuria
-in pregnanayc can present with RUQ pain, but still RLQ is most common
most common non-obsterical surgical emergency in pregnancy
appy
what does rovsing’s sign indicate
right sided peritoneal irritation
Alvarado score, sensitivity in appy
72%, clinical judgment is better.
no one sign, use them all in combo
if question is appy, yes or no, what two normal tests make the diagnosis very unlikely
normal WBC AND CRP, make dx unlikely if pre test prob is low, cannot use them in isolation
Ddx of appendicitis
size of appendix on u/s and CT that confirms appy?
> 6mm
what is accepted standard of care in acute appy?
appendectomy
%age of 80 yr olds with diverticulosis
> 80%
when is rt sided diverticular disease more common
asian or african descent
uncomplicated vs complicated diverticulitis, pathophys
uncomp: obstruction of diverticula with stool, leading to inflammation into pericolonic fate
complicated: inflammation extending beyond peri-colonic fat with abcess formation +/- microperf
diverticular bleeds: %age of LGIB and mechanism
40%, result from erosion of diverticula into mucosal wall, painless and are not occurring when ppl diverticulitis
symptoms of diverticulitis
fever, anorexia, focla abdo pain, n/v.
if complicated will get more abdo pain, +/- peritonitis, can be systemically unwell if bigger perf
2 classification of anorectal abcess
and their pathophys
- peri anal (simple anorectal)
- peri-rectal (complex anorectal)
obstructed anal gland, with subsequent polymicrobial infection. either stays superficial or spreads higher up.
peri anal vs peri rectal abscess symptoms and dx
ANAL: easily palpable mass, close to anal verge, rectal pain often wirse with defaction or valsalva
dx= clinical, can get CT to exclude peri-rectal abcess
RECTAL: can be few outward signs, need DRE to feel for fluctuance.
CT if oftne first diagnositc test, but often need MRI or u/s for small fistulas etc.
peri anal vs peri rectal abscess mgmt
ANAL: drain in ED with cruciate incision, clavulin or cipro/flagyl, if systemically unwell surgical consult and CT to exclude peri-rectal. + sitz-baths!!! 50% recurrence rate, if recurring referral to gen sx
RECTAL:
should be managed by gen surg, likely taken t OR
causes of anal fistula
peri-rectal abcess
chrons
UC
radiation
HS
causes of proctitis
what is proctitis
inflmmation of rectum
causes = STIs (most commonly: HPV, G+C, syphillis, herpes, chancroid), UC, radiation, enteric pathogens
what is a pilonidal abcess
chornic, acquired infection of hair follicles in gluteal cleft, from being obese and sitting on them. NO anorectal involvement
these are a painful palpable fluctuant mass at top of gluteal cleft, posterior and midline!
what is Goodsall’s rule for fistulas?
most common location for fistulas
midline and posterior, less commonly midline anterior, if off midline suspect systemic disease (IBD, TB, Syphillis, HIV etc)
most common cause of rectal bleeding in infants and children
anal fistula
what test to consider after rectal fb removal?
sigmoidoscopy to check for bowel injury
which rectal fb should be removed by surgeon?
sharp, large, proximal, etc
degrees of hemmroids?
1st = not prolapse
2nd= temporary prolapse, but spont reduce
3rd+ require manual reduction
4th = irreducible
internal vs external hemmroids
internal = above dentate line, painless
external= below dentate line and may painful, but very painful when thrombosed
what is an uncomplicated hemorrhoid? what is the tx?
non thrombosed external and non-prolapsed internal –> conservative
ie sitz baths, high fibre diet,
incomplete bs complete rectal prolapse
incomplete = only mucosa (children)
complete = all bowel layers
causes of unconjugated (indirect) hyperbilirubinemia
hemolysis, crigler-nijjar, gilberts, hemtoma resorption
causes of conjugated (direct) hyperbilirubinemia
long list –> anything that can cause hepatitis, obstructive HOB dz, shock liver
viral Hepatitis
LOOK at presentation
Hep B serologies
HCV transimission
IVDU, blood products before 1992, rarely sexual
what is cirrhosis
final common pathway of many liver disease, defined by hepatocellular injury leading to fibrosis
confirmatory and screening test for HCV
confirm: HCV RNA = active dz
screen = anti HCV
stigmata of chronic liver disease?
3 most common organisms in SBP
e coli, strep, enterococcus
diagnostic criteria for SBP
PMN > 250 from diagnostic para
treatment for hepatic encephalopathy?
lactulose, titrated to stools
pathophys of hepatorenal syndrome, prognosis?
poorly understood. ?severe portal HTN leads to splanchin vasodilatin which leads to renal artery vasocontriction –> 10 days median survival, 90% 2 months mortality
most common causes of liver abcess in North america?
secondary to cholangitis or biliary obstruction
organism for amebic liver abcess?
entamoeba histolytica
empiric treatment for liver abcess?
cover both bacterial and amebic causes with ceftriaxone and flagyl
risk factors for gallstones
fat, female, fertile, first nations, >forty years old
lab and u/s findings of choledocolithiasis
elevated ALP/GGT/bili
dilated CBD of hepatic ducts on u/s
who gets alcalculous cholecystitis
chronically debilitated, on TPN or in ICU
cutoff of gallbladder wall thickening for cholecytitis
> = 3 mm
what test to order if u/s unequivocal for cholecytitis
HIDA scan (textbook), although CT would work too?
complications of cholecytitis
gangrene gallbladder, empyema, perforation, gallstone ileus, sepsis, abscess, fistula
charcot triad for cholangitis
RUQ pain, fever, jaundice (present 70% of time)
rayndauds pentad for cholangitis
charcot triad + AMS + hypotension = suggests sepsis
causes of cholangitis
gallstones, ampullary lesion, bile duct stricture, pancreatic cyst
what is porcelain gallbladder?
linear/punctate calcifications within GB, 3% of time related to malignancy so refer for elective chole
causes of pancreastitis
Gallstones and etoh are 80%
then: hyperlipidemia, scorpion bites, trauma, steroids, ERCP, drugs, mumps, autoimmune
diagnosis of pancreatitis, do you need imaging, if so when?
-lipase 3X ULN is diagnostic
- CT only if diagnostic uncertainty or concern for nectrotizing pancreatitis
-can consider u/s for gallstones
- imaging not usually required for dx
mgmt of pancreatitis
admit, pain control, anti-emetics, IVF (250 mL/hr), NPO, surgical consult if stones for ERCP +/- chole, abx only if septic or nectrotizing pancreatitis
pancreatitis mortality score
Ranson score
necrotizing pancreatitis?
elevated wbc, fever (although mild fever present in 50% of non-nec panc), SHOCK
Mesenteric ischemia vs ischemic colitis
MI: can be occlusive or non-occlusive dz, most commonly from embolism to SMA
IC: low flow state through IMA leading colonic ischemia
What is chronic mesenteric ischemia
Recurrent abdo pain, usually post prandial, think intestinal angina
Lactate in mesenteric ischemia
Sensitive but not specific
Symptoms of acute mesenteric ischemia
Pain out of proportion, colicky/poorly localized,
Elevated lactate
May have vomiting or diarrhea
Cause of occlusive and non occlusive mesenteric ischemia
Imaging of mesenteric ischemia
CTA is best test
CT can have indirect signs, ie bowel wall edema or intramural gas
Axr: pneumotosis intestinalis
Initial mgmt of mesenteric ischemia
Early surgical consult
Aggressive IVF rehydration
Broad spectrum abx
Consider heparin if embolic source, non-urgent OR etc
Rectal bleeding in mesenteric ischemia/ischemic colitis
Common in ischemic colitis
Can happen, but defs not always in mesenteric ischemia
reducible, vs incarcerated vs strangulated hernia?
you should just know this
when do hernias need emergency surgical consult?
strangulation, obstruction, systemic s/s
also need abx and IVF
which organisms are apslenic pts at risk of?
encapsulated: Haemophilus influenza, neisseria menigitidis, strep penumo)
also gram neg: eg e coli, psuedomonas,
