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Barium Swallow study: what is it
fluoroscopic xray with contrast medium
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Barium Swallow study: what is it used for
for structural abnormalities w/ esophogeus, stomach, duodueum
UPPER GI
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Barium Enema study: what is it
fluoroscopic xray of colon via contrast medium
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Barium Enema study: what is it used for
to detetct the presense of a tumor, diverticula and polyps in LOWER GI
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MRI: what is it
- magnetic resonance imagingin using radio frequencies
- - non invasive
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MRI: what is it used for
detect hepatobilliary disease, hepatic lesions, source of GI bleed, colorectal cancer
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EGD: what is it
visualize mucosal lining of esophogeus, stomach, duodoneum or stomach motility
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EGD: what is it used for
detects inflammation, ulceration, tumor, varices, Mallory Weiss tears
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prolonged vomiting is a risk for
metabolic alkalosis from loss of gastric HCL
-
melena
dark feces containing blood
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vomitting center is located in the
brainstem(medulla)
-
how to signals reach the brainstem, for N/V
- -afferent pathway from ANS
- -receptors in GI, kidney, heart and uterus
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describe the act ofvomitting
- -closure of glottis
- -deep inspiration
- -contraction of diaphragm
- -closure of pylorus
- -relax stomach and LES
- -contract abdominal muscle w/ increasing intraabdominal pressure
-
visceral and chemoreceptor chemicals released for N/V
dopamine and seratonin
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vestibular input for N/V
histamine and acetylcholine
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the antiemetics
- Compazine
- Phenergan
- Zofran
- reglan
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how do antiemetics work
act in the CNS via the CTZ to block neurochemicals that trigger N/V
-
compazine
block dopamine receptors
-
phenergan
- -decrease dopamine/histamine
- - decrease vertigo/CTZ stim
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Phenergan uses
motion sickness, post op, chemo
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phenergan side effects
drymouth, hypo, const, rash
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zofran
- -block serotonin
- -decrease CTZ
- - increase gastric emptying
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Zofran uses
chemo, post op, migrane
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zofran SE
const, diareha, HA, fatigue
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reglan
- -Prokenetic(promotility)
- - enhances ACH which increases gastric motility and emptying
-
reglan uses
- dysfunctional motility of upper gut
- -N/V
- -GERD
- -HIATIAL HERN
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reglan SE
anxiety, involuntary movements(tremors/twitches)
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bright blood indicates
a Mallory Weiss tear in the upper GI
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when N/V, what type of diet do you advanced to
high carb/low fat
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what is GERD
reflux of the acidic gastric contents into the esophogaus overwhelms the esophageal defense
-
GERD important facts
- -no one single cause
- -mild reflux 2x/week
- -most common upper GI prob in adults
- -can cause ulcers
-
GERD predisposing factors
- -incompetent LES
- -Impaired esophageal motility- defective mucosal defense
- -delayed gastric emptying
- -small intestine reflux of bile
- -reflux of gastric content
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what happens with GERD
HCL acid and pepsin reflux into the lower esophagus and cause inflamation
-
GERD symptoms
- heartburn
- dyspepsia
- regurgitation
- burping often
-
pyrosis
heart burn felt beneath lower sternum
-
dyspesia
pain in upper abdomen-midline
-
GERD S/S that might also be reported
- cough, wheeze, dypena
- -hoarse, sore throat
- -lump in throat
- -chest pain that can be relived by antacid
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GERD main diagnostic
usually based on S/S and response to therapy
-
-
manometric studies
-measure pressure in LES, esophgeus and esophageal motility
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why do a biopsy for GERD
to differenciate barrets from CA
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GERD complications
- -esophagitis and ulcers
- esophageal structures narrow
- dysphagia
- barrets
- respiratory
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GERD respiratory complications
- asthma
- chronic bronchitis
- pneumonia
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GERD interventions
- -weight
- -drugs/smoke/etoh
- -HOB at 30!!!
- -don't lie down for 2-3 hrs after eating
- -avoid foods that irritate or lower LES pressure
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GERD drug therapy goals
- -improve LES function
- -Decrease volume and acidity of reflux
- -increase esophageal clearance
- -protect esophageal mucosa
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drugs given for GERD and hiatial hernia
- antacid
- antisecretary
- cholinerginic
- prokinetic
- cytoprotective
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drug names for GERD and hiatial hernia
- -Pepcid
- protonix
- bethanechol
- reglan
- Carafate
- pepto
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antacids
- NEUTRALIZE HCL ACID
- take after food
- empty stomach 20-30 min
- full stomach 2-3 hrs
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antisecretary: what they do and the two types
- -decrease secretion of HCL
- -decrease irritation of esophageal and gastric mucosa
- -H2 receptor blocker
- -PPI
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antisecretary: H2 receptor blockers
- - famotidine(Pepcid)
- -decrease conversion of pepsinogen to pepsin
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antisecretary: PPI
- -pantaprazole(Protonix)
- -more effective than H2 blockers for healing and decreased HCL secretion
- -short term
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cholenergenic: what they do and the drug
- -bethanechol(urechoine)
- -increase LES pressure
- -increase esophageal/gastric emptying
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Prokenetic: what they do and the drug
- -metoclopramide(Reglan)
- -increase gastric motility
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Cytoprotective: what they do and the drug
- -Sulcrafate(Carafate), Pepto Bismol
- -protect stomach and esophageal lining
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Goal for GERD
reduce reflux by inhancing integrity of LES function
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GERD surgeries
- Neissen fundoplication(sutures)
- LINX(magnetic)
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wht is hiatial hernia
herniation of a portion of the stomach into the esophogeus through an opening or hiatus into diaphragm
-
hiatial hernia is more common in
women and older adults
-
two types of hiatial hernia
- -sliding(more common)
- -rolling(can be emergent)
-
sliding hernia
- more common
- -occurs when pt is supine and can go back when pt stands up
- -part of stomach goes above diaphragm
-
hiatial hernia contributing factors
- -weaking of muscle around LES
- -increased intraabdominal pressure
- -congenital
-
hiatial hernia S/S
- -asymptomatic
- -similar to GERD
- -when bent over pt has sharp pain but relived when standing
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GERD and Hiatial Hernia complications
- regurgitation
- ulcer
- bleeding
- stenosis
- esophagitis
- strangulation of hernia
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diagnostic studies for Hernia
-
chronic esophageal concerns
changes at the cellular level that may indicate cancer
-
hiatial hernia surgeries
- herniotomy
- herniorraphy
- gastroplexy
- nissen
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herniotomy
excision of hernia sack
-
herniorrhaphy
closure of hiatal defect
-
gastroplexy
attatchment of stomach subdiaphragmatically
-
gastritis: what is it
- inflammation of gastric mucosa as a result of breakdown in gastric mucosal barrier
- -stomach is at risk for breakdown from HCL and pepsin
-
gastritis causes-
- -drugs(nsaids, asprin, steroids)
- -Diet( spicy food, ETOH)
- - H. Pylori
- -Stress
- -autoimmune gastritis
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autoimmune gastritis
loss of parietal cells which leads to low chloride, inadequate production of intrinsic factor, b12, malabsorption and pernicious anemia
-
acute gastritis S/S
- -N/V
- -epigastric tenderness
- full feeling
- bleeding
-
acute gastritis duration
- self limiting
- few hours to a few days
- complete healing of mucosa is expected
-
chronic gastritis S/S
- -same as acute
- -could be asymptomatic
- -may cause perinicous anemia when paritel cells are lost
-
acute gastritis diagnostics
based on S/S and hx of drug or ETOH
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chronic gastritis diagnostics
- -may be delayed due to non specific symptoms
- -endoscopy w biopsy
- -cbc for anemia
- -test for h pylori
-
the h. pylori test
- -breath test for urea
- - gold standard: biopsy to test for urease(bi product of pylori)
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acute gastritis drug therapy
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chronic gastritis drug therapy
- -PPI and H2 receptor blocker
- -AB if H. pylori
- -cobalmin(B12) if pernicious anemia(lifelong)
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PUD: what is it
erosion of GI mucosa resulting from digestive action of HCL and pepsin
-
PUD types
- -esophageal, gastric or duodenal
- -80% are duodoneal
- -acute or chronic
-
things that destroy our mucosal barrier
- -chronic gastritis
- -h pylori
- -asprin and nsaids
- -corticosteroids
- -etoh
- -coffee
all in crease HCL except corticosteroid, which decreases mucosal renewal ad productive effects
-
stress related mucosal disease
- acute ulcers
- after major surgery, severe burns and trauma
-
gastric PUD S/S
- may be asymptomatic
- -upper epigastric pain 1-2 hours after meal
- -pain aggravated by food
-
duodoneal PUD S/S
- -may be asymptomatic
- -midepigastric pain 2-5 hours after meal
- -pain relived by food
-
three major PUD complications
- hemmorage
- perforation
- gastric outlet obstruction
-
hemmorage
- most common
- erosion of gran tissue
- ulcerate through major blood vessels
-
perforation
- -most lethalĀ
- -ulcer penetrates serosal surface and spills gastric or duodoneal contents into peritoneum= hypovolima and peritonis
-
perforation: small vs large
small: can seal themselves when fibrin is produced
Large: immediate surgery
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perforation S/S
- -sudden and dramatic
- -severe abd pain radiating to back
- -rigid, board like abd muscles
- -shallow, rapis rr and weak rapid pulse
- -no bowel sounds
- -n/v
- -hx of previous ulcer
- -bacterial peritonisis w/in 6-12 hours if untreated
-
gatric outlet obstruction: what is it
obstruction in distal stomach and duodoneum
-
gatric outlet obstruction is a result of
- edema
- inflammation
- pylorospasm
- -scar tissue
-
gatric outlet obstruction: S/S
- -long hx of ulcer pain
- -upper abd discomfort
- -pain worse at end of day
- -relif from belching of self induced vomit
- -projectile
- -emisi may contain food ingested hrs or days before
- -constipation from dehydration
- -buldging of stomacj in upper abdomen
-
PUD diagnostics
- edoscopy w biopsy
- -biopsy of stomach to test for urease
- -gold standard for h pylori
- -barium contrast studies(rule out gastric obstruction)
- -cbc for anemia
- -liver enzymes for cirrhosis
- -stools for blood
-
PUD pain
disappears in 3-6 days but ulcer healing takes 3-9 weeks
-
PUD drug therapy
- -AB
- -antisecretory
- -cytoprotecive
- -antacids-
- -antidepressants
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