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132 Cards in this Set

  • Front
  • Back
Labrythine NT cause of N/V
GI NT causes of N/V
M1 and H1
GI: 5HT3
Area postrema receives following NT
5HT3, M1, H1, dopamine
Biliary colic causes N/V by
stimulating visceral afferent
Causes of gastroparesis
s/p vagotomy
pancreatic adenocarcinoma
messenteric vascular insufficiency
DM
scleroderma
amyloidosis
What is cyclic vomiting syndrome associated with?
migraine HA, adults with chronic weed use, mostly in children
Tx for chronic idiopathic nausea and functional vomiting
low dose TCAs
odansetron and granisetron act as
5HT3 antagonists
reglan acts as a
combined 5HT4 agonist and D2 antagonist
Treat H pylori with following 2 conditions
MALT and peptic ulcer
Conservative management of refractory GERD symptoms
TCAs, probiotics, exclusion of gas producing foods like legumes
How much fluid (avg) enters GI, large intestinesper day
9 L and 1L
What is the migrating motor complex
during fasting there is cyclic motilty taht seeks to remove nondigsestible material--lasts about 4min
Describe defecation
puborectalis muscle relaxes owing to sacral parasympathetic influence which straightens the rectoanal angle. Rectal distention causes passive relaxtion of the internal anal sphincter.
Sigmorectal contractions increase until the RS angle opens to >15 deg
diarrhea classifications
Acute<2 weeks
Persistant 2-4 weeks
Chronic >4 weeks
What are the Pathophysiologic mechanisms of Diarrhea
Secretory
Osmotic
Steatorrheal
inflammatory
Dysmotile
Factitial
Iatrogenic
What causes pancretic cholera AKA hypokalemia achlorhydria
VIPoma
What type of thryoid cancer causes diarrhea
medullary due to calcitonin
What causes uticaria pigmentosa and diarrhea
Systemic Mastocytosis mediated with histamine release or direct mast cell inflammation in the colon
What is translocation in the GI setting
Long term bowel rest especially in the ICU can lead to movement of enteric pathogens that normally live within the colon to move into the systemic circulation
WHy is enteral nutrition preferred over parenteral in the ICU setting
Translocation from bowel rest can lead to sepsis
enteral feed contraindications
circ shock, intestinal ischemia, complete mech bowel obstruction, ileus
What type of feeding is preferred in the setting of pancreatitis?
jejunostomy feedings
ICU feedings should include how many nonprotein calories and how many g of protein per kg body mass
25-30kcal/kg nonprotein and
1.2-1.6g/kg for hypercatabolic state and 0.8-1.0 for normal
Which antioxidant is not commonly found in parenteral or enteral feeds in the ICU patient
selenium
What is the difference between fermentable fiber and nonfermentable fiber
Fermentable fiber (cellulose, pectin, gums) degraded in intestines to short chain FA which are energy for large bowel mucosa and it slows gastric emptying and bile salts to alleviate diarrhea
Nonfermentable fiber (lignins): not degraded by intenstinal bacteria but creates osmotic force that absorbs water from lumen and reduces tendency for water diarrhea
Who should receive Branch chain FA supplements in enteric feeds
Trauma victims and hepatic encephalopathy
Compare gastric vs small bowel motility post op abdominal surgery
Gastric mobility is often hypomotile for 24-48 hours while the small bowel is often unimpaired
Name the three endoscopic techniqies used on the small bowel
capsule,
push-enteroscope is pushed down the small bowel, sometimes with the help of a stiffening overtube that extends from the mouth to the small intestine. The mid-jejunum is usually reached, and the endoscope's instrument channel allows for biopsies or endoscopic therapy
, double ballon-a long overtube and endoscope are both equipped with balloons that, when inflated, appose the intestinal wall and allow for pleating of the small intestine over the endoscope and overtube. The double-balloon enteroscope may be passed orally or anally, and the entire small bowel can be visualized in some patients when both approaches are used. Biopsies and endoscopic therapy can be performed throughout the visualized small bowel.
% of Post ERCP pancreatitis
5% and 25% if there is sphincter of oddi dysfunction
How do you prep for an urgent colonoscopy in presence of hematochezia
Rapid colonic purge with polyethylene glycol
Dieulafoy's Lesion
is a large-caliber arteriole that runs immediately beneath the gastrointestinal mucosa and bleeds through a pinpoint mucosal erosion (Fig. 285-17). Dieulafoy's lesion is seen most commonly on the lesser curvature of the proximal stomach, causes impressive arterial hemorrhage, and may be difficult to diagnose; it is often recognized only after repeated endoscopy for recurrent bleeding. Endoscopic therapy is typically effective for control of bleeding and ablation of the underlying vessel once the lesion has been identified Angiographic embolization or surgical oversewing is considered when endoscopic therapy has failed.
What endoscopic tx are available for Mallory-Weiss Tear
1. epinephrine injection,
2. coaptive coagulation,
3. hemoclips
4. band ligation
What are Vascular ectasias and how are they treated
flat mucosal vascular anomalies that are best diagnosed by endoscopy. They usually cause slow intestinal blood loss and have several characteristic distributions in the gastrointestinal tract (Fig. 285-19). Cecal vascular ectasias (senile lesions), gastric antral vascular ectasias ("watermelon stomach"), and radiation-induced rectal ectasias are often responsive to local endoscopic ablative therapy, such as argon plasma coagulation (APC). Patients with diffuse small-bowel vascular ectasias (associated with chronic renal failure and hereditary hemorrhagic telangiectasia) may continue to bleed despite endoscopic treatment of easily accessible lesions by conventional endoscopy. These patients may benefit from double balloon enteroscopy with endoscopic therapy, pharmacologic treatment with octreotide or estrogen/progesterone therapy, or intraoperative enteroscopy.
What is Charcot's Triad and what does it indicate
1. jaundice
2. abdominal pain
3. fever
Present in about 70% of patients with ascending cholangitis and biliary sepsis
Reynald's Pentad
1. jaundice
2. abdominal pain
3. fever
4. Shock
5. Confusion

Promptly restore biliary flow
Dysphagia: What is difference in swallowing between stricture vs motility d/o in esophagus
Esophageal strictures typically cause progressive dysphagia, first for solids, then for liquids
motility disorders often cause intermittent dysphagia for both solids and liquids.
Why should Colonoscopy be perfomed in men and postmenopausal women with Fe def anemia?
even in the absence of detectable occult blood in the stool, approximately 30% of patients will have colon polyps, 10% will have colorectal cancer, and a few additional patients will have colonic vascular lesions.
Chronic anemia with neg colonscopy and neg EGD, if small bowel is suspected then what is next step
Capsule endoscopy can provide a dx in 50% of cases which is most commonly mucosal vascular ectasias
Work up for Hematochezia?
trivial amounts of hematochezia should be investigated with flexible sigmoidoscopy and anoscopy to exclude large polyps or cancers in the distal bowel.
Blood on TP only vs blood in the toilet
Blood on the TP only indicates an anal lesion requiring external inspection, digital examination, anoscopy
What are the barium studies findings for motor d/o of the esophagus?
(1) Pharyngeal paralysis with tracheal aspiration
(2) Cricopharyngeal achalasia. the prominent cricopharyngeus, which is recognized by its smoothness and location in the posterior wall.
(3) Diffuse esophageal spasm: corkscrew appearance of the lower part of the esophagus.
(4) Achalasia: a dilated esophageal body with an air-fluid level and a closed lower esophageal sphincter.
(5) Muscular (contractile) lower esophageal ring. The asymmetric contraction visible in has disappeared in,
(6) Scleroderma esophagus: dilated esophagus with a stricture and reflux of barium from the stomach into the esophagus
Name and Describe the hypertensive esophageal d/o
In nutcracker esophagus, esophageal contractions are normally peristaltic but hypertensive.

In hypercontracting LES, the normal sphincter relaxation is followed by hypertensive contraction.

In hypertensive LES, basal LES pressure is elevated, but sphincter relaxation and contraction are normal
Differentiate the pathophysiology DES from the hypertensive d/o
Nonperistaltic contractions are due to dysfunction of inhibitory nerves. Histopathology shows patchy neural degeneration localized to nerve processes, rather than the prominent degeneration of nerve cell bodies seen in achalasia.
DES may progress to achalasia. Hypertensive peristaltic contractions and hypertensive or hypercontracting LES may represent cholinergic or myogenic hyperactivity.
What happens to the LES and peristaltic contractions in achalasia
the esophageal body loses peristaltic contractions and the LES does not relax normally in response to swallowing.

This mainly due to loss of intramural neurons
Primary sx of achalasia
Dysphagia, chest pain, and regurgitation
Describe the esophageal lesions in Sceleroderma
esophageal lesions in systemic sclerosis consist of atrophy of smooth muscle, manifested by weakness in the lower two-thirds of the esophagus and incompetence of the LES.
Erosive esophagitis may heal by (blank) leading to Barrett's esophagus, a risk factor for adenocarcinoma.
intestinal metaplasia
Simple dx of GERD can be made by __________ and ______
1. History
2. One week trial with 40mg omeprazole with relief of sx
Diagnostic studies are indicated in patients with persistent symptoms or symptoms while on therapy, or in those with complications. What are the 3 elements that we need to monitor?
The diagnostic approach to GERD can be divided into three categories:
(1) documentation of mucosal injury
(2) documentation and quantitation of reflux
(3) definition of the pathophysiology.
Name the PPIs, dosages,their use, and some side effects
The PPIs are comparably effective:
omeprazole (20 mg/d), lansoprazole (30 mg/d), pantoprazole (40 mg/d), esomeprazole (40 mg/d), or rabeprazole (20 mg/d) for 8 weeks can heal erosive esophagitis in up to 90% of patients.
The PPI should be taken 30 min before breakfast. Refractory patients can double the dose.
Since GERD is a chronic disease, long-term maintenance therapy is often required, and symptoms may relapse in up to 80% of patients within 1 year if therapy is discontinued.
PPIs are most effective in preventing recurrences. The side effects of PPI therapy are generally minimal. However, aggressive acid suppression may cause hypergastrinemia but does not increase the risk for carcinoid tumors or gastrinomas. Vitamin B12 and calcium absorption may be compromised by the treatment.
What is acid reflux and what is alkaline reflux
Acid Reflux is gastric acid
Alkaline reflux is bile salts which are often a reason for PPI, H2 tx failure.
Describe the esophagitis that can occur directly from HIV infection
acute esophageal ulceration associated with oral ulcers and a maculopapular skin rash, which occurs at the time of HIV seroconversion. Some patients with advanced disease have deep, persistent esophageal ulcers requiring treatment with oral glucocorticoids or thalidomide. Some ulcers respond to local steroid injection.
What meds are responsible for pill esophagitis
Antibiotics such as doxycycline, tetracycline, oxytetracycline, minocycline, penicillin, and clindamycin account for more than half the cases.
Nonsteroidal anti-inflammatory agents such as aspirin, indomethacin, and ibuprofen may cause injury.
Others: potassium chloride, ferrous sulfate or succinate, quinidine, alprenolol, theophylline, ascorbic acid, and pinaverium bromide. Bisphosphonates, particularly alendronate and pamidronate, are more common offenders.
Pill-induced esophagitis can be prevented by avoiding the offending agents or taking pills in the upright position with copious amount of fluid.
What do imaging studies of eosinophilic esophagitis show?
Barium esophagogram may show a small-caliber esophagus, isolated esophageal narrowing, or single or multiple esophageal rings.
Esophagoscopy may reveal one or more longitudinal fissures, fixed or transient concentric rings, proximal strictures, and focal white specks (abscesses).
Endoscopic ultrasound may show thickening of the esophageal wall.
hypopharyngeal webs and iron-deficiency anemia in middle-aged women suggests...
Plummer-Vinson Syndrome
Differentiate Lower esophageal mucosal ring vs a muscular ring
Mucosal ring or Schatzki ring is a thin, weblike constriction located at the squamocolumnar mucosal junction at or near the border of the LES. It may result from GERD or be congenital in origin. It invariably produces dysphagia when the lumen diameter is <1.3 cm. Dysphagia to solids is the only symptom, and it is usually episodic. A lower esophageal ring is one of the common causes of dysphagia. Asymptomatic rings may be present in ~10% of normal individuals. Symptomatic rings and webs are easily treated by dilatation.
lower esophageal muscular ring or contractile ring is located proximal to the site of mucosal rings and may represent an abnormal uppermost segment of the LES. These rings can be recognized by the fact that they are not constant in size and shape. They may also cause dysphagia and should be differentiated from peptic strictures, achalasia, and lower esophageal mucosal rings. Muscular rings do not respond well to dilatation.
What leads to a sliding hiatal hernia?
weakening of the anchors of the gastroesophageal junction to the diaphragm, from longitudinal contraction of the esophagus, or from increased intraabdominal pressure
Describe the pain experienced in esophageal rupture
esophageal perforation causes severe retrosternal chest pain, which may be worsened by swallowing and breathing.
Name 3 locations where foreign bodies most commonly become stuck
1. cervical esophagus just beyond the UES
2. near the aortic arch
3. above the LES
What serologic tests can be ordered for celiac sprue
IgA endomysial antibody and IgA tissueTransGlutaminase antibody tests, both of which have a 90% sensitivity and 95% specificity for the diagnosis
Antigliadin antibodies are no longer recommended because of their lower sensitivity and specificity.
What are three syndromes that occur with EtOH withdrawl
1. Tremulousness and Hallucinations:
2. Seizures:
3. DT:
When do tremulousness and hallucinations occur, the symptoms, and how are they treated?
within 2 days
tremulousness, agitation, anorexia, nausea, insomnia, tachycardia, and hypertension. Tx with diazepam, 5–20 mg, or chlordiazepoxide, 25–50 mg, orally every 4 hours
When do EtOH withdrawl seizures occur after withdrawl?
occur within 48 hours of abstinence, and within 7–24 hours in approximately two-thirds of cases. Roughly 40% of patients who experience seizures have a single seizure; more than 90% have between one and six seizures. In 85% of the cases, the interval between the first and last seizures is 6 hours or less.
What are some alarming signs that EtOH withdrawl seizures are due to another cause
focal seizures
prolonged duration of seizures (>6–12 hours)
more than six seizures
status epilepticus
prolonged postictal state
What is the treatment for EtOH withdrawl seizures
Nothing
Dilantin is usually not required but diazapam and chlorazapam should be given for DT prophylaxis
How many days after the last drink do DTs begin and how long does it last?
3–5 days after cessation of drinking and lasts for up to 72 hours.
Symptoms of DT
confusion, agitation, fever, sweating, tachycardia, hypertension, and hallucinations.
Causes of Death in DT
Death may result from concomitant infection, pancreatitis, cardiovascular collapse, or trauma.
Treatment of DT
diazepam, 10–20 mg intravenously, repeated every 5 minutes as needed until the patient is calm
correction of fluid and electrolyte abnormalities and hypoglycemia
The total requirement for diazepam may exceed 100 mg/h.
Concomitant beta-adrenergic receptor blockade with atenolol, 50–100 mg/d, also has been recommended.
Increased BUN with normal GFR
■Prerenal azotemia
■Catabolic states
■High-protein diets
■Gastrointestinal bleeding
■Glucocorticoids
■Tetracycline
Causes of Increased Albumin
Dehydration
shock
hemoconcentration
Causes of Decreased Albumin
Decreased hepatic synthesis (chronic liver disease, malnutrition, malabsorption, malignancy, congenital analbuminemia [rare]).
Increased losses (nephrotic syndrome, burns, trauma, hemorrhage with fluid replacement, fistulas, enteropathy, acute or chronic glomerulonephritis). Hemodilution (pregnancy, CHF).
Drugs: estrogens.
What causes NASH
Results from progression of macrovascular steatosis to steatohepatitis and fibrosis
Describe NASH histologically
Characterized histologically by macrovesicular steatosis of NAFLD with
– Focal infiltration by polymorphonuclear neutrophils
– Mallory's hyalin
– Histologic features are indistinguishable from alcoholic hepatitis
What are the causes of Nonalcoholic fatty liver disease (NAFLD)
DM, obesity, hypertriglyceridemia
Causes of microvesicular steatosis
Reye's syndrome
valproic acid toxicity
tetracycline
acute fatty liver of pregnancy


Women in whom fatty liver of pregnancy develops often have a defect in fatty acid oxidation due to reduced long-chain 3-hydroxyacyl-CoA dehydrogenase activity
Describe the lab tests for Nonalcoholic fatty liver disease (NAFLD)
There may be mildly elevated aminotransferase and alkaline phosphatase levels

In contrast to alcoholic liver disease,


– Ratio of alanine aminotransferase (ALT) to aspartate aminotransferase (AST) is almost always > 1 in NASH


– However, it decreases to < 1 as advanced fibrosis and cirrhosis develop
Differentiate the AST/ALT relationship between EtOH liver disease and NAFLD
In contrast to alcoholic liver disease,
– Ratio of alanine aminotransferase (ALT) to aspartate aminotransferase (AST) is almost always > 1 in NASH
– However, it decreases to < 1 as advanced fibrosis and cirrhosis develop
Differential Diagnosis of Nonpalpable purpura
■Trauma
■Senile or solar purpura
■Corticosteroid use
■Idiopathic thrombocytopenic purpura
■Thrombotic thrombocytopenic purpura
■Disseminated intravascular coagulation
■Other thrombocytopenia or platelet dysfunction
■Clotting factor defect
■Vitamin K deficiency
■Warfarin necrosis
■Amyloidosis
■Waldenström's macroglobulinemia
■Scurvy
■Ehlers-Danlos syndrome
Differential for palpable purpura
DDx
Vasculitis
■Polyarteritis nodosa
■Rheumatoid arthritis
■Wegener’s granulomatosis
■Churg-Strauss syndrome
■Henoch-Schönlein purpura
■Systemic lupus erythematosus (SLE)
■Hypersensitivity (leukocytoclastic) vasculitis


Infection or emboli
■Meningococcemia
■Gonococcemia
■Endocarditis
■Rocky Mountain spotted fever
■Aspergillus
■Candidiasis
■Ecthyma gangrenosum (neutropenic, pseudomonal)


Other
■Sarcoidosis
■Cryoglobulinemia
■Ulcerative colitis
■Crohn’s disease
■Medications
Types of Bruises
Bruises may be referred to by size
ecchymosis (1-3 cm)
purpura (3-10 mm)
petechia (<3 mm)
In the setting of chronic diarrhea, diarrhea that wakes up the patient would indicate which pathology
Crohns
In the setting of chronic diarrhea, post prandial diarrhea would inidicate
IBS
Effective initial treatment for diarrhea only IBS
Lamotil
3 types of polyps
mucosal neoplastic (adenomatous) polyps
mucosal nonneoplastic polyps (hyperplastic, juvenile polyps, hamartomas, inflammatory polyps)
submucosal lesions (lipomas, lymphoid aggregates, carcinoids, pneumatosis cystoides intestinalis)
Most common polyp removed at colonoscopy. #2
1. Adenoma 70%
2. Hyperplastic
Large hyperplastic polyps located in the proximal colon may evolve into a unique type of premalignant lesion called
a "serrated adenoma."
4 Histological Classifications of adenomas
tubular
villous
tubulovillous
serrated
From normal mucosa, it takes how many years to develop a medium sized polyp and a how many years to cancer
5 years to polyp
10 years to CA
Peutz-Jeghers syndrome
hamartomatous polyps throughout the gastrointestinal tract (most notably in the small intestine) as well as mucocutaneous pigmented macules on the lips, buccal mucosa, and skin.
Bethesda Criteria for Colon CA
(1) colorectal cancer under age 50
(2) synchronous or metachronous colorectal or HNPCC-associated tumor regardless of age (endometrial, stomach, ovary, pancreas, ureter and renal pelvis, biliary tract, brain)
(3) colorectal cancer with one or more first-degree relatives with colorectal or HNPCC-related cancer, with one of the cancers occurring before age 50
(4) colorectal cancer with two or more second-degree relatives with colorectal or HNPCC cancer, regardless of age
(5) tumors with infiltrating lymphocytes, mucinous/signet ring differentiation, or medullary growth pattern in patients younger than 60 years.
Follow up colonoscopy with polyps
– In 5–10 years for patients with 1–2 small (< 1 cm) tubular adenomas (without villous features or high-grade dysplasia)
– In 3 years for patients with 3–10 adenomas, an adenoma > 1 cm, or an adenoma with villous features or high grade dysplasia
– In 1–2 years for patients with > 10 adenomas; consider evaluating these patients for a familial polyposis syndrome
Types of GIST
spindle cell or epitheliod
MC Location of GIST
Stomach and proximal Small bowel
What immunohistochemical staining can be performed for GIST
80% express CD117 antigen,
Presenting symptoms of Small Bowel lymphoma
Obstruction
Bleeding
Perforation
SB Lymphoma occurs most commonly what two areas?
proximal jejunum-celiac
distal ileum-de novo.
Test for Carcinoid tumor
measure urinary 5-HIAA
Substances produced by Carcinoid tumors
serotonin
substance P
neurotensin
gastrin
somatostatin
motilin
secretin
pancreatic polypeptide
Given the GI physiology, how do you treat acute pancreatitis
NPO to prevent fat and protein from stim CCK release which will stimulate the pancreas
PPI to raise the pH of the starved stomach acid to prevent release of secretin which will stimulate pancreas to release bicarb
cholelithiasis caused by which two substances
80% cholesterol caused
the rest are bilirubin
In a study that looked at the autospy results of patients who had had cholecystectomy at some point in their lives, what abnormalities correlated with pain/without pain
Pain-adhesions of small bowel to gb site (9%); tumours, or tumour-like scars, in the cystic duct-stump and choledochal region found in 15 (15%)
No Pain:peptic ulcers, cystic remnants, or choledochal stones showed no association with the complaints
Treatment of constipation
Laxative stimulant: bisacodyl, docusate and senna, polyethylene glycol
Stool softener: docusate, senna
Laxative: magnesium hydroxide, mineral oil, methylcellulose
Osmotic laxative: glycerin, lactulose, polyethylene glycol, sorbitol
Bulk laxatives: psyllium, polycarbophil, methylcellulose
Enterokinetic agents: 5-HT agonists –tegaserod
GI agent, prokinetic: cisapride, domperidone, metoclopramide
Clues GERD rather than asthma
Adult onset
poor response to meds
nocturnal cough
nonallergic
related to meals
Precipatating factors for GERD
Large meals
Fatty Meals
peppermint
EtOH
caffeine
CCBs
SSRIs
obesity
prego(progesterone)
Meds to avoid in GERD
theophyline
anticolinergics
ccb
diazapam
morphine
barbs
a blockers
GERD resistant to PPI bid x 2 months
non-reflux esophagitis: pill, infection, eosinophilic, skin disease
dyspepsia: gastroparesis, PUD, NERD, NUD
rapid metabolizer
non-compliance
dysmotility: achalasia, spasm, nutcracker, g-paresis
IBD and thromboembolism
3 fold increased risk
Why is Nephrolithiasis so common in Crohns
caused by hyperoxaluria due to increased intestinal absorption of oxalate
Heptobiliary complications with Crohns
cholelithiasis
benign pericholangitis
sclerosing cholangitis
autoimmune chronic active hepatitis
cirrhosis.
Prevalence in Crohns vs UC
Crohns:7 cases per 100,000
UC:35-100 cases per 100,000
Age of Onset
UC: any age but peaks are 1-25; 55-65
Crohns: 15-30 mostly ileal and most cases; 60-80 mostly colonic
Serum immunochemistry test that can differentiate UC from Crohns
+ p-ANCA indicates UC
+ASCA indicates Crohns
Do contractions occur in achalsia with aperistalsis
Yes. vigorous achalasia has simultaneous contractions that are in sync but not coordinated therefore unable to properly to propel food.
Surgical technique used for achalasia
Heller Myotomy: requires PPI and will have long term GERD
Define long and short segment barret's
Long >3cm and short <3cm
Stages of Barrets to Cancer
Intestinal Metaplasia that is Negative for Dysplasia ==>indefinite for dysplasia==>Low Grade==>High Grade==> AdenoCA
Types of Esophageal Diverticula
Zenker's=Upper E
Traction=MidE
Epiphrenic=distal E
What Physical signs indicate necrosis in acute pancreatitis
Fever, Increased WBC
What is the first radiological test to order in setting of suspected acute pancreatitis
Ab US to r/o biliary stones, pseudocyst, CBD dilation, ascites
When should a CT be ordered in setting of acute pancreatitis
suspicion of necrosis
Organ Failure
failure to improve clinically
What does increased ALT indicate in the setting of CBD obstruction, gall stone pancreatitis
Hepatocyte compression
What lab value can determine severity of acute pancreatitis
CRP: >150 drawn within 48 hours of symptom onset indicates severe acute pancreatitis
What does the PANCREAS acronym stand for in acute pancreatitis treatment
P: Pain control usually demerol
A: Antibiotics
N: NPO; enteral feedings are better than TPN
C: Ca/Mg
R:Rest
E: electrolytes
A: Acid-PPI
S: Suction via NG
How many L of fluid are given in Acute pancreatitis
10L/day
Ransons Criteria at Dx
Age>55;
WBC>16;
Gluc>200;
AST >250;
LDH>350
Ransons Criteria at 48 hours
HCT decrease by 10%;
BUN increase >5;
Base Defecit>4;
Ca<8;
PaO2<60;
Fluid defecit >6L
What causes GI Bleed in acute pancreatitis
Splenic vein thrombosis
Hemosuccus pacreaticus: Bleed through the Pancreatic duct into duodenum due to erosion of pseudocyst into adjacent vasculature
Hormones that promote gastric emptying/inhibit gastric emptying
Promote: Motilin/Neurotensin
Inhibit (delay): Secretin/SCK
What is erythromycin MOA with Gastroparesis therapy
Motilin agonist which stimulates antral contractions
Mechansim for Bethanechol(urecholine) in Gastroparesis
cholinergic that stimulates muscarinics receptors
MOA of Cisparide(porpulsid) in gastroparesis
facilitates ACH release at myenteric plexus. Not available in US