GI Flashcards
LLQ pain most likely DX
diverticulitis
PUD men vs women
3 to one in favor of men
PUD hpylori
90% of duodenal ulcers and >75% of gastric ulcers
PUD caused by meds
NSAIDS, ASA and glucocorticoids
Duodonal ulcer main age range
30-55
gastric ulcers main age range
55-65
PUD alcohol and diet
not really associated, role of stress is uncertain, more commin in greater than 1/2 ppd smokers
PUD S and S
GNAWING epigastric pain
releife when eating- duodenal
pain worse when eating - gastric
PUD physical findings
often unremarkable, maybe some mild epigastric tenderness
gi bleed in 20%
5-10%perf
PUD lab
maybe anemia, consider endoscopy after 8-12 weeks of treatment
consider H pylori testing
PUD H2 receptor antagonists
ines- cimetidine 800mg, rinatidine300mg, famatidine40mg, nizanidine300mg, before bed
QD
then BID
then PPI in am
PPI 30 minutes before meals
azoles- 30 min before meals
lansoprazole
reberprazole etc
Mucosal protective agents when to give
2 hours apart from other agents
sucralfate 1g qid (carafate) dosing pearl
requies an acidic environment, avoid antacids and H@ blockers they are associated with a DECREASE IN nosocomial pneumonia
bismuth sulfate (pepto)
has direct antibacterial action against HPylori
promotes prostaglandin productiona and natural bicarb
Misoprostol (Cytotec) four times daily with meals
profolaxyis against NSAID ulcers
stims mucus and bicarb produciton
MAY STIM UTERINE CONTRACTION AND INDUCE ABORTION
discontinue offending agent first if possible
this is the PPI in pts who cannot stop NSAIDS
NSAIDS and h2 blockers (zoles) caraate adn antacids
do not prevent nsaid induced ulcers,
antacids (mylanta, maalox, MOM etc)
do not reduce the amount of gastric acidity or secretions-
H. Pylori Eradication therapy pearls
resistant quickly to
Must be combo
quickly resistant to - Metonidaole (flagyl) and clarithromycin- (biaxin)
H.Pyori eradication therapy no quick resistance to
amoxicillin or tetracycline
Hpylori combo therapy
2 abx + a ppi (zole) or bismuth QID (has direct anti H pylori action)
H pylori combo therapy MOC
MOC
Metro-flagyl 500 bid
prilosec (zole) 20mg bid premeal
clarithromycin (Biaxin) 500mg BID with meals for 7 days
H Pylori combo therapy AOC
AOC
ammox- 1g bid with meals
prilosec (zole) 20mg BID beofre mieals
clarithromycin(biaxin) 500 bid before meals for 7 days
Hpylori combo therapy MOA
metrinodizole -flagyl, 500bid with mealls
prilosec 20mg and amoxicillin 1g bid with meals for 7 dyas
Hpylori has bismuth regimin but has more side effects
bsmuth sunsalicylate 2 tabs fur times a day
flagyl 250 four times a day
tetracyn 500mg foru times a day
all with meals and then at bedtime
can add prilosec to this as well am and qhs for 7 days
antiulcer regimine is reccomended post h pylori eradication for 3-7weeks to ensure ulcer healing
for duodonal- omeprazole priolsec PPI 40mg qday or lansoprazle prevacid 30mg per day for 7 weeks
antiulcer regimine post H pylori H2 (dines)
H2 like famantodine Pepcid of sucarafate for 6-8 weeks
PUD in hospital management
IV access and fluids cbc,ptt,BMP 02 endoscopy, gi angioagraphy (sx consult) urinary cath NPO with ng tube for lavage - bleeding stops sopontaneously in 80 percent of cases
PUD in hospital upright films
show free air in 70% of the cases monitor ab IV H2 blockers- the dines famtadine ffp for coagulopathy transfuse with plat if below 50K H2 or sucarlfate fro 6-8 weeks
perf bowl sounds
quiet
normal plt
150-400k
HEP ABC
viral
HEP A
fecal oral,
common from food or water (huricane busted pipes)
Hep A blood and stool
infectious during the 2-6 week incubation period
HEP A mortality
rate is low, fulmination hep A is rare
Hep B where is it
blood born DNA virus present in the serum, saliva, senem and vag secretions
Hep B transmission
via blood to blood, sex, mother fetus
Hep C what is it
blood born RNA virus where source is often uncertain
Hep C transmission
associated with blood, think drug needles (50%)
Hep C signs and symptoms pre icteric
per-icteric- fatigue, malaise, NV HA, aversion to smoking and ETOH
Hep C icteric
weight loss, jaundice, pruritius , RUQ pain, CLAY COLORED STOOL, dark urine
may have low grade fever or hepatosplenomegaly
Hep C labs
WBC low to normal
UA- protein and bili
Elevted AST and ALT (500-2000IU/L
LDH, Bili,Alk phos, and PT are normal to slightly elevated
Serology testing for Hep A-
look for antibody (anti-HAV) and IGM-which would imply recent infection
these peak during first 6 weeks then disappear in 3-6 months these are diagnostic of acute hep A
diagnostic of acute hep A
ANTI-HAV AND IGM ANTIBODY
IGG antibody to hep A implies previous exposure and on its own is not diagnostic of acute HAV infection -could be previous exposure, noninfectivity or immunity to recurring HAV infeciton
serology of active HEP A
anti-hav and IGM
serology of recovered hep A
anti HAV and IGG
Hep B serology first
first is HBSAG- will remain positive in asymptomatc carriers and chronic hep B patients
Hep B serology second
second is antibody to HBcAG or ANTI-HBC and IGM shortly after HBSAG goes away but before anti HB (antibody to HB appears)
Hep B serology third
HBeAG - protein derived from HBV core and indicates circulating HBV and HIGHLY INFECTIOUS SERA only in HBsAG+ sera presence indicates infectivity
anti hep B
often apears when HBeAG dissapers and signals diminished viral replication and infectivity
serology summary
active hep B
HBSAG, HBEGA, ANTI-HBC, IGM ie the hep B surface antigen, the protine derived from the core and the antibody plus IGM
serology
chronic Hep B
hep B surface antigen, anti Hep B, anti, HBE, IGM and IGG
serology
recovered Hep B
anti HBc, Anti HBsAG
hep B actute vs chronic
acute has HBeAG and anti HBC plus only IGM
chronic has anti HBE, and IGG
Hep c how to find
enzyme immunoassay detects presence of antibodies to Hep C
sens and specificity are low- when suspected RIBA assy detects antibodies to HCV antigens
PCR used to differentiate between prior exposure and current viremia
Hep C acute
Anti HCV-HCV, RNA
Hep management
supportive, rest during the acute phase increase fluids 3-4L per day avoid alcohol, detox the liver no or low protein diet serax if sedation is necessary vitamin K for prolonged PT (>15sec) Lactulose 30ml oray or rectally for elevated ammonia. or hepatic encephalopathy
BS with obstruction
high pitched tinkling
normal ast alt
less than 35-40
IgM vs IGG for hep A
IGM immediate
IGG gone
HBS AG is the tip off for B
HBE-AG is high virl load
anti HBE-ag is diminished load
IGM is immediate
IGM and IGG equals chronic
recoverd hep B
just anti anti
hep C needs PCR to tell
acute vs chronic
Diverticulitis
LLQ disease more common in women
low fiber diet
diverticulitis
infammation or localized perf of one or more diverticula with abcess formation
diverticulitis causes and incidence
more common in women, low fiber diet
diverticulitis s and s
mild to moderate aching LLQ pain
constipation vs loose stool vs both
nausea and emisis
physical findings diverticulitis
low grade fever
LLQ tenderness and pain on palpation
free perf features more dramatic presentaiton
Diverticulitis labs and diagnostics
mild to moderateleukocytosis, elevated esr stool and heme + in 25% of cases sigmoidoscopy shows inflamed mucosa may consider CT to evaluate for abcess plain ab films are OBTAINED ON ALL PATIENTS TO LOOK FOR EVIDENCE OF FREE AIR - pneumoperitenouwm
diverticulitis inpatient management
npo
IV fluids
IVABX (flagyl, cpro, ceftaidime clinda, ampicillin
if significan gi bleed present treat like PUD
20–30% of patients require sx
cholycystitis what
associated with gall stones in 90% of cases
cholycystitis when s and s
often after a large fatty meal
SUDDEN STEADY SEVER EPIGASTRIC PAIN, RO RIGHT HYPOCHNDRIUM
vomiting leads to relief
cholysystitis exam
murphys sign: deep pain on inspiration, while fingers are placed under the R rib cage
RUQ tender to palpation, canfeel gallblader in 15% of cases
musclegaurding
fever
cholecystitis exam
WBC's 12-15K serum Bili may be up serum ALT,AST,LDH,and alk phos levels are all up amylase ma be up plain films show radioopaque gallstones HIDA sccan
cholecystitis gold standard exam
ULTRASOUND
Cholysystitis management
pain managemnt ngt for decompression npo crystoloid syloutions Broad spectrum ABX like Piperacillin surgical consult for lap choley
Acute pancreatitis (autodigestion of pancreas by enzymes) causes
gallbladder disease, etoh, High calcium, High lipids, trauma, meds-sulfonamides, thiazides, lasix, estrogen, azathioprie (imuran)
acute pancreatitis S and S
abrupt onset of steady sever pain EPIGASTRIC, WORSE BY WALKING AND LYING SUPINE, IMPROVED BY SITTING AND LEANING FORWARD, RADIATES TO THE BACK MOST COMMONLY BUT CAN GO ELSEWHER
nausea and emisis usually present, weakness sweating and anxiety in severe attacks
E
acute pancreatitis exam
upper ab pain WITHOUT GAURGIND RIGIDITY OR REBOUND
distended ab
absentbowel sounds if associated with paralytic illius
fever
tacchycardia
pallor,cool skin
mild jaundice
aacute pancreatitis with hemmorage
grey turner- flank discoloration
cullens sign- umbilical
acute pancreatitis labs and diags
wbc elevation depends on degree
hyperglycemia
serum LDH and AST elevation
Serum Amylase 50-180 and ipase 14-289 elevated in 90% of cases BUN and coag my be up as well
acute pancreatitis and calcium
levels below 7mg/dl associated with tetany , chvoseks sign or treseaus
acute pancreatits elevated CRP
suggestive of pancreatic necrosis
acute pancreatitis imaging
CT is better than ultrasound
acute pancreatitis Ransons criteria- 5-6 risk factors +40% mortality, >7 risk factors +100% mortality
george washington go lazy after taken on admisisonn
Greatr than 55years of age or 70 with gall stones Wbc over 16K Glucose over 200 LDH over 350 AST over 250
ransons at 48 hours for acute pancreatitis
he broke CABE
Hct drop of >10 BUN increase >5 Calcium <8 Arterial 02 <60 Base deficit >4 Estimated fluid sequestration >6000ml
Acute pancreatitis tx.
bed rest npo aggressive iv volume repletion ng suction pain control pain free with bowel sounds can start clear liq diet
bowel obstruction causes
adhesion, hernia, tumor, fecal impaction, illeus, volvuls
bowel obstruction S and S
cramping and periumblical pain later pain is constant and diffuse vomiting within minutes of pain (proximal obstruction) within two hours of pain is distal minimal or no fever
bowel obstruction physical findings
minimal distention is proximal ornounced distention is distal mild tender but no peritoeal findings high pitched, tinkling bowel sounds cant pass stool or flatus
bowel obstruction labs
normal labs initially
later may see dehydration level rise in wbc’s
plain films show DIALATED LOOPS OF BOWEL AND AR FLUID LEVELS
air fluid level pattern in small bowel obstruction
HORIZONTAL IN SMALL BALL
FRAME PATTERN IN LARGE BOWEL
bowel obstruction management
fluid recuss ngt suction broad spectrum abx surgery in ALL CASES OF COMPLETE OBSTRUCTION partial obstruction may med manage
UC definition
an idopathic inflammatory condition characterized bu diffuse mucosal inflammation of the colon, unlike chrons disease, UC invariably involves the rectum and may extend upward involving the whole colon. The diseae is characterized by symptomatic episodes and remissions
UC signs and sx
BLOODY DIARRHEA IS THE HALLMARK SYMPTOM
UC labs and diagnosis
stool studies are negative
sigmoidoscopy establishes the diagnosis
UC management
mesalamie (canasa) suppositories or enemas for 3-12 weeks
hydrocortisone suppositories and enemas
Mesenteric infarct-
a syndrom as a result of inadequate blood flow inthe mesinteric cir leading to ischemia and gangreen of the bowel
UC appearance
cobblestone
UC is inflammatory and starts from
bottom up
Messinteric infarct causes
arterial or venous embolus or thrombus atherosclerosis smoking usually occurs in older adults coagulopathy such as that from recent surgery (cardiac, AAA, increases the risk
messinteric infarct S and S
sudden onset cramp and colickly ab pain potentially after eating pain out of proportion to exam findings NV, Fever, ab gaurding and tenderness hyperactive to absent BS, \+ perotoneal findings shock
messinteric infarct lab
elevated amylase, leukocytosis, ab films, CT
messinteric infarct tx
emergent surgery
appendicitis
inflamaiton of the appendix, precipitated by obstruction of the lumen, if untreated gangrene and perf can develop in 3 hours, most common presentationis men 18-30 years, affects 10% of the population.
appy causes
fecalith, foreign body, inflammation, neoplasm
appy signs and symptoms
vague colicky umbilical pain
pain shhifts to RLQ after several hours,
nausea with 1-2 episodes of vomiting LOTS OF EMISIS SUGGESTS ANOTHER DIAGNOSIS
pain is worse and is localized with coughing
appy labs and diagnosis
RLQ gaurding WITH REBOUND TENDERNESS
local ab tenderness
pain worse with cough
appy psoas sign (illiopsoas test
pain with R thigh extension
appy obturator sign
pain with internal rotation of the flexed right thigh
appy positive Rovsings sign
RLQ pain when pressure is applied to the LLQ
appy fever
is low high fever suggest perf and another diagnosis
appy and WBCs’
10k to 20k
appy diagnosis
CT or ultrasound
appy management
surgery
iv abx
iv fluids
pain managemnt
gero considerations for GI
decreased- jaw strength thirst and taste perception gastric motility and delayed emptying increased transit time impaired defication signal decreased liver size and liver blood flow
gi gero risk of
poor nutirition
altered metabolism of drugs
gerd
nsaid induced ulcers
gi gero constipation
not a normal finding, most common causes include lack of fiber, deceased exercise, poor dentition, history of lax abuse, and impaired mental status
gerd causes
dleayed emptying or incompetent lower esophegal sphincter
gerd s and s
retrosternal burning bitter taste in mouth delching hicciups excessive salivation frequently at night or recumbant may be releived by sitting up water or food
exam is worthless
gerd diagnostics
conside refferral for EGD, rule out cancer, barretts or PUD
gernd non pharma
elevated HOB, avoid ETOH and caffine spices peppermint etc, stop smoking weight reduction
gerd pharma
antacids prn
H2 blockers the tdines in high dose at night or bid
ppi zoles if h2 blockers are inneffective
gi surgical consult prn
