ear drum anatomy
Wonder Me!

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carvenous sinus thrombosis
Wonder Me!
Patients generally have sinusitis or a midface infection (most commonly a furuncle) for 5-10 days. In as many as 25% of cases in which a furuncle is the precipitant, it will have been manipulated in some fashion (eg, squeezing, surgical incision).
The clinical presentation is usually due to the venous obstruction as well as impairment of the cranial nerves that are near the cavernous sinus.
Headache is the most common presentation symptom and usually precedes fevers, periorbital edema, and cranial nerve signs. The headache is usually sharp, increases progressively, and is usually localized to the regions innervated by the ophthalmic and maxillary branches of the fifth cranial nerve.
In some patients, periorbital findings do not develop early on, and the clinical picture is subtle.
Some cases of CST may present with focal cranial nerve abnormalities possibly presenting similar to an ischemic stroke.[2]
As the infection tracts posteriorly, patients complain of orbital pain and fullness accompanied by periorbital edema and visual disturbances.
Without effective therapy, signs appear in the contralateral eye by spreading through the communicating veins to the contralateral cavernous sinus. Eye swelling begins as a unilateral process and spreads to the other eye within 24-48 hours via the intercavernous sinuses. This is pathognomonic for CST.
The patient rapidly develops mental status changes including confusion, drowsiness, and coma from CNS involvement and/or sepsis. Death follows shortly thereafter.


Tx:

source: http://emedicine.medscape.com/article/791704-clinical#b1
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metronidazole
Wonder Me!
http://patient.info/medicine/metronidazole-for-infection-flagyl

Metronidazole is used to treat a wide variety of infections caused by anaerobic bacteria and micro-organisms called protozoa. These types of organisms often cause infections in areas of the body such as the gums, pelvic cavity and abdomen because they do not need oxygen to grow and multiply. It is commonly prescribed to treat an infection called bacterial vaginosis. It is also prescribed before gynaecological surgery and surgery on the intestines, to prevent infection from developing. Metronidazole can safely be taken by people who are allergic to penicillin.

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physical exam resources
Wonder Me!
http://www.stethographics.com/main/physiology_ls_vesicular.html
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Dysphagia
Wonder Me!

DYSPHAGIA MNEMONIC (DIFFICULTY SWALLOWING):

Having trouble remembering all the important questions to ask during your patient encounter? Then try this Dysphagia Mnemonic (difficulty swallowing) for USMLE Step 2 CS.

Institution
PHYSICAL EXAMINATION for Dysphagia Mnemonic
NOTE: Make sure to wash your hands or wear gloves before you start physical examination. Make sure to ask for permission before you start each physical exam. Make sure to use proper draping(don’t forget to tie back patient’s gown). Make sure to explain each physical examination in layman’s term to your patient. Do NOT repeat painful maneuvers.
  • HEENT: Check throat for erythema and exudate
  • Neck exam: Check for lymphadenopathy, thyromegaly
  • Cardiovascular exam: Auscultation
  • Pulmonary exam: Auscultation
  • Abdominal exam: Inspection, auscultation, palpation, percussion.
  • Skin: check for signs of scleroderma/CREST.
DIFFERENTIAL DIAGNOSIS for Dysphagia Mnemonic
  • Esophageal cancer (Dysphagia starts with Solids and progresses to liquids. Hx of chronic alcoholism, smoking & weight loss )
  • Achalasia (Dysphasia for BOTH solid and liquids)
  • Esophagitis (Pain on swallowing. Immunocompromised “e.g. HIV, Corticosteroids”)
  • Systemic Sclerosis (Look for CREST syndrome)
  • GERD (Cough at nights, Hoarseness, sore throat)
  • Plummer-Vinson syndrome (Iron deficiency anemia, sore throat, craving ice, dirt, clay…)
  • Zenker diverticulum (Halitosis, regurgitation)
  • Pill-induced esophagitis (e.g. Bisphosphonates)
  • Mitral Stenosis (look for an immigrant or a pregnant female)
DIAGNOSTIC WORKUP for Dysphagia Mnemonic
  • CBC
  • Serum iron, ferritin, TIBC
  • Throat culture
  • HIV antibody and viral load, CD4 count
  • Chest X-ray
  • Barium swallow
  • Endoscopy
  • Esophageal manometry 
  • Chest CT
http://www.medical-institution.com/dysphagia-mnemonic-difficulty-swallowing-usmle-step-2-cs-mnemonics/
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GI mnemonics
Wonder Me!
Bowel Segments
"Dow Jones Industrial Averages Closing Stock Report" is a good one, even though it misses the Cecum...
Dow
Jones
Industrial
Averages
Closing
Stock
Report		Duodenum
Jejunum
Ileum
Appendix
Colon
Sigmoid
Rectum
Liver Lobes
The four lobes of the liver: caudate, quadrate, left and right, bring to mind the newspaper headline of the wheelchair bound fellow who left a party right after his ugly girlfriend departed: "QUAD LEFT RIGHT after COW-DATE"

Pertoneum Facts
The idea is to relate key letters of related parts...
stOMach and OMentum (which lays over the stomach)
The bacterium e. coLI is found in the Large Intestine
The OMentum covers the stOMach
The Lesser OMentum holds the Liver and stOMach
The Mesentery holds the sMall intestine
The mesoCOLON attaches the large intestine (COLON) to the posterior abdominal wall.
The periTONEa, which prevents the intestines from kinking, TONES the GI tract.

Sphincters of the Ailmentary Canal
APE OIL initials the five of them...
A
P
E
O
I
L		Anal
Pyloric
(Lower) Esophageal
Oddi
Ileocecum
iLeocecum

Stomach Parts
"The CAR is FUN 'til the BODY PILES" relates the four parts of the stomach: Cardiac, Fundus, Body, Pylorus. The pylorus is where the food piles waiting for the sphincter to open.
Ulcerative colitis: definition of a severe attack A STATE:
Anemia less than 10g/dl
Stool frequency greater than 6 stools/day with blood
Temperature greater than 37.5
Albumin less than 30g/L
Tachycardia greater than 90bpm
ESR greater than 30mm/hr

Vomiting: extra GI differential VOMITING:
Vestibular disturbance/ Vagal (reflex pain)
Opiates
Migrane/ Metabolic (DKA, gastroparesis, hypercalcemia)
Infections
Toxicity (cytotoxic, digitalis toxicity)
Increased ICP, Ingested alcohol
Neurogenic, psychogenic
Gestation

Pancreatitis (acute): causes GET SMASHED:
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune (PAN)
Scorpion stings
Hyperlipidemia/ Hypercalcemia
ERCP
Drugs (including azathioprine and diuretics)
· Note: 'Get Smashed' is slang in some countries for drinking, and ethanol is an important pancreatitis cause.

IBD: surgery indications "I CHOP":
Infection
Carcinoma
Haemorrhage
Obstruction
Perforation
· "Chop" convenient since surgery chops them open.

Hereditary Nonpolyposis Colorectal Cancer (HNPCC) cause is DNA mismatch repair DNA mismatch causes a bubble in the strand where the two nucleotides don't match.
This looks like the ensuing polyps that arise in the colon.

IBD: extraintestinal manifestations A PIE SAC:
Aphthous ulcers
Pyoderma gangrenosum
Iritis
Erythema nodosum
Sclerosing cholangitis
Arthritis
Clubbing of fingertips

Digestive disorders: pH level With vomiting both the pH and food come up.
With diarrhea both the pH and food go down.

H. Pylori treatment regimen (rough guidelines) "Please Make Tummy Better":
Proton pump inhibitor
Metronidazole
Tetracycline
Bismuth
· Alternatively: TOMB:
Tetracycline
Omeprazole
Metronidazole
Bismuth

Bilirubin: common causes for increased levels "HOT Liver":
Hemolysis
Obstruction
Tumor
Liver disease

Ulcerative colitis: complications "PAST Colitis":
Pyoderma gangrenosum
Ankylosing spondylitis
Sclerosing pericholangitis
Toxic megacolon
Colon carcinoma

Cholangitis features CHOLANGITITS:
Charcot's triad/ Conjugated bilirubin increase
Hepatic abscesses/ Hepatic (intra/extra) bile ducts/ HLA B8, DR3
Obstruction
Leukocytosis
Alkaline phosphatase increase
Neoplasms
Gallstones
Inflammatory bowel disease (ulcerative colitis)
Transaminase increase
Infection
Sclerosing

Charcot's triad (gallstones) "Charge a FEE":
Charcot's triad is:
Fever
Epigastric & RUQ pain
Emesis & nausea

Haemachromatosis complications "HaemoChromatosis Can Cause Deposits Anywhere":
Hypogonadism
Cancer (hepatocellular)
Cirrhosis
Cardiomyopathy
Diabetes mellitus
Arthropathy

Pancreatitis: criteria PANCREAS:
PaO2 below 8
Age >55
Neutrophils: WCC >15
Calcium below 2
Renal: Urea >16
Enzymes: LDH >600; AST >200
Albumin below 32
Sugar: Glucose >10 (unless diabetic patient)

Pancreatitis: Ranson criteria for pancreatitis: at admission "GA LAW" (GA is abbreviation for the U.S. state of Georgia):
Glucose >200
AST >250
LDH >350
Age >55 y.o.
WBC >16000

Pancreatitis: Ranson criteria for pancreatitis: initial 48 hours "C & HOBBS" (Calvin and Hobbes):
Calcium < 8
Hct drop > 10%
Oxygen < 60 mm
BUN > 5
Base deficit > 4
Sequestration of fluid > 6L

Pancreatitis: Ranson criteria for pancreatitis at admission LEGAL:
Leukocytes > 16.000
Enzyme AST > 250
Glucose > 200
Age > 55
LDH > 350

GIT symptoms BAD ANAL S#!T:
Bleeding
Abdominal pain
Dysphagia
Abdominal bloating
Nausea & vomiting
Anorexia/ Appetite changes
Lethargy
S#!ts (diarrhea)
Heartburn
Increased bilirubin (jaundice)
Temperature (fever)

Crohn's disease: morphology, symptoms CHRISTMAS:
Cobblestones
High temperature
Reduced lumen
Intestinal fistulae
Skip lesions
Transmural (all layers, may ulcerate)
Malabsorption
Abdominal pain
Submucosal fibrosis

Dysphagia: differential DISPHAGIA:
Disease of mouth and tonsils/ Diffuse oesophageal spasm/ Diabetes mellitus
Intrinsic lesion
Scleroderma
Pharyngeal disorders/ Palsy-bulbar-MND
Achalasia
Heart: eft atrium enlargement
Goitre/ myesthenia Gravis/ mediastinal Glands
Infections
American trypanosomiasis (chagas disease)
21

Dry mouth: differential "DRI":
·2 of each:
Drugs/ Dehydration
Renal failure/ Radiotherapy
Immunological (Sjogren's)/ Intense emotions

Liver failure: decompensating chronic liver failure differential HEPATICUS:
Haemorrhage
Electrolyte disturbance
Protein load/ Paracetamol
Alcohol binge
Trauma
Infection
Constipation
Uraemia
Sedatives/ Shunt/ Surgery

Cirrhosis: causes of hepatic cirrhosis HEPATIC:
Hemochromatosis (primary)
Enzyme deficiency (alpha-1-anti-trypsin)
Post hepatic (infection + drug induced)
Alcoholic
Tyrosinosis
Indian childhood (galactosemia)
Cardiac/ Cholestatic (biliary)/ Cancer/ Copper (Wilson's)

Hepatic encephalopathy: precipitating factors HEPATICS:
Hemorrhage in GIT/ Hyperkalemia
Excess protein in diet
Paracentesis
Acidosis/ Anemia
Trauma
Infection
Colon surgery
Sedatives

Diabetic ketoacidosis: precipitating factors · 5 I's:
Infection
Ischaemia (cardiac, mesenteric)
Infarction
Ignorance (poor control)
Intoxication (alcohol)

Whipple's disease: clinical manifestations SHELDA:
Serositis
Hyperpigmentation of skin
Eating less (weight loss)
Lymphadenopathy
Diarrhea
Arthritis

Celiac sprue gluten sensitive enteropathy: gluten-containing grains BROW:
Barley
Rye
Oats
Wheat
· Flattened intestinal villi of celiac sprue are smooth, like an eyebrow.
Liver failure (chronic): signs found on the arms CLAPS:
Clubbing
Leukonychia
Asterixis
Palmar erythema
Scratch marks

Splenomegaly: causes CHIMP:
Cysts
Haematological ( eg CML, myelofibrosis)
Infective (eg viral (IM), bacterial)
Metabolic/ Misc (eg amyloid, Gauchers)
Portal hypertension

Source: http://www.valuemd.com/gastro.php
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Pancreatitis
Wonder Me!
Source: http://webcache.googleusercontent.com/search?q=cache:7OvEopugpDkJ:unmhospitalist.pbworks.com/f/31.1-24%2520to%25201-30%2520Resident%2520Pancreatitis%2520Module.doc+&cd=20&hl=en&ct=clnk&gl=us

Resident Version






Acute and Chronic Pancreatitis Module
Created by Dr. Teodora Konstantinova







Objectives:

1.  List two differences in the diagnosis of acute and chronic pancreatitis.
2.  Name 4 risk factors for developing pancreatitis
3.  List two differences between treatment approaches to acute and chronic pancreatitis
4.  Use Ranson criteria to predict severity of acute pancreatitis.





References:

1.  Whitcomb D. C., Acute pancreatitis, N Engl J Med 2006, 354:2142-2150
2.  Steinberg W, Tenner S, Medical Progress: Acute pancreatitis, NEnglJMed 1994, 330:1198-1210
3.  Michael L. Steer, MD, Irving Waxman, MD and Steve Freedman, MD,  Medical progress: Chronic Pancreatitis, N Engl J Med 1995, 332:1482-1490
4.  Ranson JH, Diagnostic Standards for Acute Pancreatitis World J Surg 1997, 21:136-42









CASE:

HPI: A 60 yo female presents to the ER with severe mid-epigastric pain with radiation to the back, nausea and vomiting that started after lunch the previous day.  Vomiting did not relieve the pain.  The patient also reports coughing with yellow sputum for about a day.  She doesn’t report fever, but states she has “chills” post emesis.  

PMH:
HTN, depression, GERD, and menopausal symptoms requiring hormone replacement therapy (HRT).  The patient also recently completed a course of nitrofurantoin for cystitis. 

PSH: cholecystectomy 6 months ago.
 
Social hx: Patient has no history of alcohol abuse. 

Medications: Lisinopril, Paxil, cimetidine, estrogen and completed course of nitrofurantoin 2 days ago.

Physical exam: VS: 100/60,  P- 110,  R-16,  T-37.0 C, P02 - 87 % on RA.
The exam is significant for left lower lung field rales and egophany.  The patient also had moderate mid-epigastric and RUQ tenderness without rebound or guarding. The rest of the exam is unremarkable.

Labs:
wbc: 16.5, H/H: 12/45
electrolytes are WNL
SGOT/SGPT: 500/400 U/l, alkaline phosphatase  400 U/l , total Bi 2.0 mg/dL
LDH:  860 IU per liter, serum lipase-5000, serum amylase- 2000, TG- 300
UA which is neg for LCE, nitrites, bacteria, WBCs or RBCs.




1.  At this point in your evaluation, what should you initially be concerned about? 


2. What could be the etiologies of this patient’s pancreatitis?


3.  What radiologic studies should you consider obtaining? 


4.  Are you able to calculate your patient’s Ranson’s score? 


Discussion Outline:

I. Differences between acute and chronic pancreatitis:

Acute and chronic pancreatitis are distinguished from each other on the basis of structural and functional criteria.

1.  Acute pancreatitis is an inflammatory condition of the pancreas. Acute disease is characterized by a normal pancreas that becomes inflamed prior to the attack and once the attack resolves the pancreas returns to normal.
2.  Chronic pancreatitis is a progressive disorder of the pancreas that causes destruction of the pancreas. It involves long-term inflammation and scarring of the pancreas that is irreversible.


II. Pathogenesis:

Acute pancreatitis:

1.  It relates to inappropriate activation of trypsinogen to trypsin (the key enzyme in the activation of pancreatic zymogens and a lack of prompt elimination of active trypsin inside the pancreas.
2.  Activation of digestive enzymes causes pancreatic injury and results in an inflammatory response that is out of proportion to the response of other organs to a similar insult.
3.  The acute inflammatory response itself causes substantial tissue damage and may progress beyond the pancreas to a systemic inflammatory response syndrome, multiorgan failure and death.


Chronic pancreatitis:

1.  The hypersecretion of protein from acinar cells in the absence of increased fluid or bicarbonate secretion from duct cells is characteristic of chronic pancreatitis.
2.  Plugs formed by the precipitation of protein within the interlobular and intralobular ducts are an early finding.
3.  The plugs contain multiple proteins (digestive enzymes, glycoproteins, and acidic mucopolysaccharides).
4.  The precipitation of calcium carbonate in the plugs results in the formation of intraductal stones (this is more common in patients with alcohol-induced or tropical pancreatitis).
5. Patients with idiopathic chronic pancreatitis frequently have an elevated pressure in the pancreatic duct.



III. Causes of pancreatitis:

1.  Gallstones (45 % of cases)
2.  Alcohol (35 % of cases)
3.  Drugs: Azathioprine, Mercaptopurine, Valproic acid, Estrogen, Tetracyclines, Metronidazole, Nitrofurantion, Pentamidine, Lasix, Sulfonamides, Methyldopa, Cimetidine, Ranitidine, Salicylates, Erythromycin                                               
4.  Metabolic abnormalities: Hypercalcemia, Hypertriglyceridemia
5.  Trauma: accidental or iatrogenic (ERCP, postoperative, endoscopic sphincterotomy)
6.   Infections:
Parasitic (ascariasis, clonorchiasis)
Viral (mumps, rubella, Hepatitis A, B, non-A, non-B, coxsackievirus B, Echo virus, adenovirus, varicella, Epstein-Barr virus, HIV virus)
Bacterial: (mycoplasma, Campylobacter jejuni, Mycobacterium tuberculosis, Legionella, Leptospirosis)
7. Miscellaneous causes: penetrating PUD, Crohn’s disease, Reye’s syndrome, cystic fibrosis)
8.  Idiopathic (10% of cases)


IV. Diagnosis

Diagnosis of acute pancreatitis:

1.  Characteristic abdominal pain (begins in the upper abdomen and spreads through the back)
2.  Nausea and vomiting (usually the vomiting doesn’t relief the pain)
3.  Elevated serum levels of pancreatic enzymes (amylase and lipase)
4.  Both enzymes remain elevated with ongoing pancreatic inflammation, with amylase level typically returning to normal shortly before lipase levels in the resolution phase.
5.  Imaging:
-  Ultrasound of the abdomen remains the most sensitive method of evaluating the biliary tract in acute pancreatitis. It has a sensitivity of 67% in the urgent diagnosis, and a specificity of 100%.
-  CT scan is the imaging method of choice in delineating the pancreas, as well as in determining the severity and complications.
-  ERCP plays a part in diagnosis in patients in whom no definite cause is found. Abnormalities revealed by this study include small pancreatic tumors, pancreatic ductal strictures, gallstones, pancreas divisum, sphincter of Oddi dysfunction.

Diagnosis of chronic pancreatitis:

1.  In developed countries, most patients with chronic pancreatitis have a history of prolonged and heavy alcohol use.  They typically have recurrent attacks of upper abdominal pain, which may radiate to the mid-back, nausea and vomiting.
2.  10-20 % of patients have “painless” pancreatitis.  They may present with DM, jaundice, malabsorption, steatorrhea with weight loss.
3.  Malabsorption resulting from exocrine insufficiency may cause fecal fat excretion to be elevated. Undigested fat is qualitatively detected by Sudan staining of feces.
4.  Routine blood studies (such as amylase, lipase) do not necessary show elevations.
5.  Plain film of the abdomen: The finding of pancreatic calcification is virtually diagnostic of chronic pancreatitis, but often this is not found.
6. There are several other tests: US, CT scan of the pancreas, ERCP, EUS, MRCP, MRI
7.  ERCP is the gold-standard imaging procedure for the diagnosis of chronic pancreatitis and planning treatment.


V. Treatment:

Acute pancreatitis:

1. Supportive therapy, vigorous IVF hydration, possible use of NG (especially with ileus and severe vomiting), correction of electrolytes.
2.  Immediate endoscopic removal of impacted stones in patients with severe disease appears to reduce mortality.
3.  Use of antibiotics: A potential role for prophylactic use of antibiotics in severe acute pancreatitis was initially given support by a randomized trial demonstrating that imipenem reduces infection complications.
Recent randomized trial failed to demonstrate differences in outcome among patients treated with Cipro and Flagyl, as compared with placebo, leading some experts to recommend against routine use of prophylactic antibiotics.
4.  Nutritional support: ensuring adequate nutrition is important in patients with severe or complicated pancreatitis.  Recent meta-analysis of 6 randomized trials involving a total of 263 patients demonstrated improved outcomes with enteral nutrition, including decreased rate of infections and surgical interventions, reduce length of hospital stay, reduced costs.
5.  Decision on the appropriateness of surgical management of sterile necrotic tissue should be made on a case-by-case basis, however, infected necrotic tissue and infected collections of fluid are best treated by surgical debridement.

Chronic pancreatitis:

1.  Pain:  abstinence from alcohol, administration of analgesic medications, and nerve blocks.  Exocrine insufficiency may lead to increased cholecystokinin-mediated stimulation of the pancreas.  This process theoretically could be interrupted by administration of digestive enzymes (trypsin, cholecystokinin receptor antagonists, or somatostatin).
2.  When the pain persists in spite of aggressive noninvasive therapy, patient should undergo ERCP to define the caliber and morphologic characteristic of the pancreatic ducts.
3.  Malabsorption:  when > 90 % of exocrine pancreatic function is lost, clinically overt malabsorption occurs. Treatment consists of low-fat diet. Medium chain triglycerides may be useful because their absorption depends on minimal amounts of pancreatic enzymes and does not require bile salts.
For persistent symptoms pancreatic-enzyme replacement should be given orally just before meals. Neutralization of gastric acid with orally administration bicarbonate, inhibition of acid secretion, or enteric coating of enzyme preparation may prevent degradation of these enzymes as they traverse the stomach.
4.  Pseudocysts: develop in 10 % of patients.  Most resolve spontaneously but hemorrhage into a pseudocyst, rupture or infection can occur.
Treatment is indicated for those who persist for 6 weeks or are either enlarging or cause symptoms. Treatment is resection, external or internal drainage.
5.  Pancreatic ascites or pleural fistulas. Diagnosis is made if paracentesis or thoracentesis yields fluid high in protein and amylase. Currently the treatment is surgery.


VI. Predicting severity of acute pancreatitis:
Many models exist although none are ideal and most of them take about 48 hrs to complete assessment. They also do not have high sensitivity or specificity, although relying on routine clinical assessment identifies only 30-40% of patient with severe acute pancreatitis.  These models are usually based on:
1. Presence or absence of organ failure, and local complications.
2. Systems that assess inflammation or organ failure (Ranson criteria)
3. Findings on imaging studies


Ranson criteria to predict severity of acute pancreatitis

At 0 Hours
Age > 55 yo                                                                       
Wbc> 16 k                                                                          
Glucose> 200 mg/dL                                                          
LDH> 350
SGOT (AST) > 250                                                    Mortality per positive criteria:
0-2 <5% mortality
3-4 20% mortality
At 48hours                                                                 5-6 40% mortality
Hct fall by > 10%                                                       7-8 100 % mortalit
BUN increase > 5 mg/dl despite fluids
Ca < 8 mg/dL
PO2 < 60 mm/Hg
Base deficit > 4mEq/L
Fluid sequestration > 6L

11 total criterias in Ranson scoring. The presence of 1 to 3 criteria represents mild pancreatitis; as the number of criteria increase, the severity of pancreatitis increase and so does the mortality associated with it.

Review Questions:

1.  A 27 yo patient is admitted with acute pancreatitis. Four days after admission patient develops high fever with worsening abdominal pain. The examination reveals a T of 102F and marked upper abdominal tenderness without rebound. A CT scan of the abdomen with contrast shows a solid mass and gram stain of the aspirate is positive for gram-negative organism.
Based upon the above information you will now recommend:

A)  IV broad spectrum antibiotics.
B)  IV antibiotics plus insert a CT –guided percutaneous drainage tube.
C)  IV antibiotics plus surgical debridement.





2..  A 60 yo man with known chronic pancreatitis caused by alcohol  reports  a 25 lbs weight loss in the past several months and frequent, greasy, and malodorous stools. A 72- hour fecal fat collection confirms steatorrhea. The patient no longer consumes alcohol and reports no abdominal pain.
Which of the following is the most appropriate first-line treatment for this patient?

A)   Administration of enteric-coated pancreatic enzyme replacement tablets with meals and snacks and concurrent use of a calcium containing antacids.
B)  Administration of non-enteric-coated pancreatic enzyme replacement tablets with meals and snacks with concurrent dosing with a histamine2 blockers.
C)  Endoscopic placement of a pancreatic dust stent.
D)  Institution of a low-fat diet (less than 20 g fat/day).
E)  Subcutaneous administration of octreotide daily.

















Post Module Evaluation

Please place completed evaluation in an interdepartmental mail envelope and address to Dr. Wendy Gerstein, Department of Medicine, VAMC (111).


1) Topic of module:__________________________


2) On a scale of 1-5, how effective was this module for learning this topic? _________
(1= not effective at all, 5 = extremely effective)


3) Were there any obvious errors, confusing data, or omissions? Please list/comment below:

________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________


4) Was the attending involved in the teaching of this module? Yes/no (please circle).


5) Please provide any further comments/feedback about this module, or the inpatient curriculum in general:


6) Please circle one: 

Attending        Resident (R2/R3)                    Intern               Medical student



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Murphy's sign
Wonder Me!

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GI resources
Wonder Me!
Gallbladder dz (excellent basic texts on anatomy, lab, tx!): http://fitsweb.uchc.edu/student/selectives/Luzietti/Gallbladder_anatomy.htm
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GI case studies resources
Wonder Me!
http://www.mednet.gr/static_page/54
http://www.meddean.luc.edu/lumen/MedEd/MEDICINE/cpc/case27/case_f.htm
https://lutheranmeded.com/research/elearning/gastro/
http://www.proprofs.com/quiz-school/topic/gastroenterology#
http://www.hcplive.com/journals/resident-and-staff/2005/2005-04/2005-04_07

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