FMP2_2

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Hereditary Colon Cancer Sunday, February 17, 2008 1:58 PM

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Week 9 Review Questions Thursday, March 06, 2008 5:59 PM

FMP 2008 week 09 review questions

Liver enzyme abnormalities 1. What are the different patterns of liver to injury? 2. What are the elements of “fibrotest”? 3. What are the tests that actually assess liver function? 4. How can liver fibrosis be diagnosed? 5. What liver enzymes can have their level elevated in the setting of hepatitis? 6. What are enzymes of cholestasis? 7. What causes “mild” hepatitis with ALT > AST? Of AST > ALT? 8. What are genetic causes of liver disease, what are the clinical features of each, and how can they be treated? 9. Which causes of viral hepatitis are vaccine-preventable? 10. Which causes of chronic viral hepatitis are treatable? 11. What is non-alcoholic fatty liver? 12. What are 36 drug causes of hepatitis? (just kidding) 13. What is autoimmune hepatitis? 14. What causes severe hepatitis? (What constitutes “severe” in this context?) 15. What causes cholestasis? 16. What is primary sclerosing cholangitis? 17. What is primary biliary cirrhosis? Viral hepatitis 18. What are the 5 major types of viral hepatitis? 19. What are the clinical features and clinical course of hepatitis A? 20. How is hepatitis A transmitted? 21. How is hepatitis A managed? 22. Who should receive the hepatitis A vaccine? 23. How is hepatitis B transmitted? 24. What are clinical features of hepatitis B? 25. How is hepatitis B infection diagnosed? What is the relevance of tests for hepatitis B e antigen and antibody? 26. What are the serologic patterns of infection with hepatitis B that recovers, and that stays chronic? 27. Who should receive hepatitis B vaccine? 28. What are sequelae of chronic viral hepatitis? 29. What are the available treatments for chronic hepatitis B? 30. Who should receive treatment for chronic hepatitis B? 31. How is hepatitis C transmitted? 32. What is natural history of hepatitis C infection? 33. What is treatment of chronic hepatitis C? 34. What is hepatitis D? 35. What is hepatitis E? 36. What is hepatitis G? Esophageal disorders 37. What is dysphagia? 38. What are the major causes of dysphagia? 39. What is a reasonable algorithm for the diagnosis of dysphagia? 40. What is odynophagia? 41. List three treatments for achalasia. 42. What is the mechanism of GE reflux in most cases? 43. How can the diagnosis of reflux be confirmed? 44. What are the major complications of GE reflux? 45. What is esophagitis? 46. What is Barrett’s esophagus? 47. What is the key element of treatment of GE reflux? 48. What is the mechanism of parietal cell acid secretion? 49. List 5 proton pump inhibitors. Dyspepsia and peptic ulcer 50. What is dyspepsia? 51. What is the commonest cause of dyspepsia:

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51. What is the commonest cause of dyspepsia: a. Overall b. That has an organic basis 52. What are other important causes of dyspepsia? 53. What laboratory tests are appropriate for work-up of patients with dyspepsia? 54. What are the two major underlying causes of peptic ulcer disease? 55. What is Zollinger-Ellison syndrome? 56. What are complications of peptic ulcer disease? 57. What is H. Pylori? 58. What are complications of H. pylori? 59. How is H pylori treated? 60. What are the potential effects of NSAIDs on the GI tract? 61. Why do NSAIDs lead to peptic ulcer? 62. What is the best way to diagnose peptic ulcer disease? 63. List four categories of drugs that can heal a peptic ulcer without the use of antibiotics. What is the chief benefit of adding antibiotics to this regimen? Gastrointestinal bleeding 64. What are the major causes of upper GI bleeding? 65. What are three high risk unusual causes of upper GI bleeding? 66. What do the following terms mean? a. Hematemesis b. Melena c. Hematochezia 67. What is the natural history of bleeding due to peptic ulcer disease? 68. What are the prognostic factors related to overall outcome in patients with upper GI bleeding? 69. What is the general mortality rate in patients with upper GI bleeding due to peptic ulcer? 70. What are endoscopic findings that predict an adverse outcome in patients with upper GI bleeding due to peptic ulcer? 71. What are general supportive measures related to management of patients with upper GI bleeding? 72. What are specific therapeutic measures for patients with upper GI bleed due to peptic ulcer? 73. What are indications for surgery in patients with upper GI bleeding? 74. What leads to esophageal varices? 75. What are risk factors for bleeding among patients with esophageal varices? 76. What are adverse prognostic factors for bleeding esophageal varices? 77. What specific therapeutic modalities are available for bleeding varices? 78. What is octreotide? 79. What is TIPS? 80. What are major causes of lower GI bleeding? 81. What are the major investigative modalities available for lower GI bleeding? 82. What is a Meckel’s diverticulum? Acute pancreatitis 83. What are the two major causes of acute pancreatitis? 84. What are the additional important causes of acute pancreatitis? 85. What do patients with acute pancreatitis complain of? 86. What are the major physical findings in a patient with pancreatitis? 87. What laboratory tests are most helpful in the diagnosis of acute pancreatitis? 88. What are other causes of hyperamylasemia? 89. What imaging tests are helpful in diagnosis of acute pancreatitis and its complications? 90. What are the local complications of acute pancreatitis? 91. What are the major elements of treatment? 92. What is the role of endoscopy in the therapy of acute pancreatitis? Diarrhea 93. What causes acute diarrhea? 94. What causes chronic diarrhea? 95. What are major causes of bloody diarrhea? 96. What tests are appropriate in a patient with chronic diarrhea? Inflammatory bowel disease 97. What are the major differences in the histopathology of Crohn’s disease versus ulcerative colitis? 98. What are the locations of Crohn’s disease in the GI tract? 99. How does IBD present? 100. What are intestinal complications of IBD? 101. What are the extraintestinal manifestations of IBD? 102. What items are appropriate to consider in the differential diagnosis of the patient with suspected IBD?

103.

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103. 104. 105. 106. 107. 108. 109. 110. 111. 112. 113.

What factors on history, physical exam and lab testing contribute to the assessment of disease severity in a patient with IBD? What are the major treatment options for patients with Crohn’s and those with UC? What is infliximab? What is azathioprine? What is 5-ASA? What are adverse effects of corticosteroids? What is cyclosporine? What is budesonide? What is methotrexate? What are indications for surgery in patients with IBD?

Liver failure What are the pathologic features of cirrhosis? What are the causes of cirrhosis? What are the physical findings of cirrhosis? What are the laboratory test abnormalities seen in patients with cirrhosis? What are the elements of the Child-Pugh-Turcotte prognostic scale? What are the major complications of cirrhosis? What is the pathogenesis of cirrhotic ascites? What are the elements of management of cirrhotic ascites? What is a paracentesis? What are the major indications for liver transplantation? What is fulminant hepatic failure? What are symptoms associated with jaundice, and how do they help to differentiate the causes? What are major differences between Crohn’s disease and ulcerative colitis: a. Pathologically b. Clinically c. In terms of treatment 127. What are the major complications of portal hypertension? 128. How is spontaneous bacterial peritonitis: a. Diagnosed b. Treated 129. What are the indications for liver transplantation? 130. What are the clinical features of sclerosing cholangitis? 131. What is the pathogenesis of cirrhotic ascites? 132. What is a TIPS procedure?

114. 115. 116. 117. 118. 119. 120. 121. 122. 123. 124. 125. 126.

GI cancer screening

133. What is appropriate screening for: a. Colon cancer b. Esophageal cancer

Pasted from <https://portal.utoronto.ca/courses/1/Fall-2007-FMP211Y1-Y-LEC0101/content/_913894_1/FMP%202008%20week%2009%20review%20questions.doc? bsession=11327372&bsession_str=session_id=11327372,user_id_pk1=501825,user_id_sos_id_pk2=1,one_time_token=>

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00 FMP 2008 Week 10 Intro Material Friday, February 22, 2008

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01 ALBERT 2008 Intro to Rheumatology Friday, February 22, 2008 5:24 PM

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Give an example of a non-inflammatory, non-immune rheumatoid disorder? Give an example of an inflammatory, nonimmune rheumatoid disorder? Give 3 examples of inflammatory, autoimmune rheumatoid disorders?(4)

Fibromyalgia and osteoarthritis are both categorized as: 1. Inflammatory, Non-immune; 2. Inflammatory, Nonimmune; or 3. Inflammatory, Immune? Some "non-articular" disorders and crystal arthritis (such as gout and CPPD) are (inflammatory or noninflammatory) and (immune or non-immune)? Give 4 examples of noninflammatory, non-immune diseases? Give 4 examples of inflammatory, immune diseases?

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Which of the following is an acute disease and which is a chronic disease?

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The unifying characteristic for most of the rheumatic diseases is ___? T/F: The inflammation in all rheumatic diseases represents an abnormal activation of the ADAPTIVE immune system?

Iin the absence of chronic infection, chronic inflammatory disease is the result of ___?

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Autoimmunity is usually benign because of ___ mechanisms?

With respect to the development of autoimmunity, Pro-T cells in the thymus may be categoriezed into which 3 groups?

Autoimmunity results from failure or breakdown of tolerance in ___, ___ or both? If self-reactive clones of pro-T cells escape the thymus because self-antigen is NOT expressed, then what are the 3 mechanisms in the periphery that may lead to peripheral tolerance?

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List the 3 main categories of autoimmune reactions?

List 3 different types of autoimmune reactions?

Autoimmune diseases may be either ___ or ___?

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Give examples of autoimmune disease that are organ specific? Give examples of autoimmune diseases that are non-organ specific? What does "epitope spreading" refer to?

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T/F: there are extra-articular features in RA?

List 4 serological indicators that may be positive in Reumatoid Arthritis?(5)

•

Polyclonal Gammopathy: A gammopathy in which there is a heterogeneous increase in immunoglobulins involving more than one cell line; may be caused by any of a variety of inflammatory, infectious, or neoplastic disorders. P asted from <http://w w w .nutritionperspectiv es.com/O ther/siteG lossary .cfm >

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In RA, there is edema of the ___ membrane with redundant folds and villi? In RA there is a (HYPO or HYPER) plastic synovial lining layer?

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Is a hyperplastic synovial membrane present in early or established RA?

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List 3 inflammatory mediators involved in RA?

The strongest evidence for a genetic link in RA comes from evidence that the ___ genes are associated with RA? List 3 environmental and/or lifestyle factors that have been implicated in the development of RA? What do DMARDS stand for? T/F: Flares and remissions DO NOT occur in RA since it is a chronic, progressive disease?

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List 2 Anti-TNF antibodies that are used in Arthritis management? Etanercept is a solube ___ used in Arthritis management? Anakinra is a popular ___ used in the management of Arthritis? In the management of Arthritis, drugs such as

methotrexate and lefluonmide counteract the actions of which cell in the pathogenetic progression of Arthritis? In the management of Arthritis, cytokine

neturalization drugs counteract the actions of which cytokines in the pathogenetic progression of Arthritis? In the management of Arthritis, Rutizimab counteracts the actions of which cells in the pathogenetic progression of Arthritis? While both Etanercept and Infliximab are both exert their effect through cytokine neutralization, one is a soluble TNF receptor while the other one is an Anti-TNF alpha antibody; which is which? Is Adulimumab a soluble TNF receptor or an antiTNF antibody? Apart from using a soluble TNF receptor or an anti-TNF antibody, which other drug mechanism is used for cytokine neutralization in the treatment of RA? IL-1 receptor blocker

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and Infliximab are both exert their effect through cytokine neutralization, one is a soluble TNF receptor while the other one is an Anti-TNF alpha antibody; which is which? Is Adulimumab a soluble TNF receptor or an antiTNF antibody? Apart from using a soluble TNF receptor or an anti-TNF antibody, which other drug mechanism is used for cytokine neutralization in the treatment of RA? IL-1 receptor blocker

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02 BOOKMAN 2008 Clinical Evaluation of Arthritis Friday, February 22, 2008 5:24 PM

What is seropositivity? Into which categories may inflammatory Arthritis be classified into? Into which categories may degenerative Arthritis be classified into? Into which categories may nonarticular Arthritis be classified into?

Seropositivity is the presence of a certain antibody in a blood sample. A pa ti ent with s eropositivity for a pa rti cular antigen or a gent is termed seropositive. It i s not a neutral term, a s in popular perception s eropositivity i s used most commonly i n reference to HIV s eropositivity. It i s also used (though l ess frequently) to refer to Rheumatoid factor. Pasted from <http://en.wikipedia.org/wiki/Seropositivity>

Polymyositis is a type of inflammatory myopathy, related to dermatomyositis and inclusion body myositis. Polymyositis means 'many muscle inflammation'. Polymyositis tends to become evident in adulthood, presenting with bilateral proximal muscle weakness, often noted in the upper legs due to early fatigue while walking. Sometimes the weakness presents itself by the person being unable to rise from a seated position without help, or inability to raise their arms above their head. The weakness is generally progressive, accompanied by lymphocytic inflammation (mainly cytotoxic T8 lymphocytes). The cause is unknown, but seems to be related to autoimmune factors, genetics, and perhaps viruses. In rare cases, the cause is known to be infectious, associated with the pathogens that cause Lyme

Scleroderma is a chronic disease characterized by excessive deposits of collagen in the skin or other organs. The localized type of the disease, while disabling, tends not to be fatal. Diffuse scleroderma or systemic sclerosis, the generalized type of the disease, can be fatal as a result of heart, kidney, lung or intestinal damage.[1] Pasted from <http://en.wikipedia.org/wiki/Scleroderma>

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be infectious, associated with the pathogens that cause Lyme disease, toxoplasmosis, and others. Polymyositis, like dermatomyositis, strikes females with greater frequency than males. The skin involvement of dermatomyositis is absent in polymyositis. Pasted from <http://en.wikipedia.org/wiki/Polymyositis>

List 4 different classifications for seropositive Arthritis?

List 3 characteristics of seropositive arthritis? How is seronegative Arthritis classified?

Which of the following has asymmetric spine involvement: Ankylosing spondylitis, or psoriatic arthritis?

• Spondylitis: inflammation of the vertebrae; called also rachitis.

What is podagra?

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Infectious arthritis may be classified into which two types?

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For the clinical evaluation of arthritis, draw a tree showing the classifications in the approach to making a diagnosis?

Is the duration of AM stifness less or more in a patient with inflammatory vs. degenerative arthritis?

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How does the pattern of arthritis different in symmetrical small joint polyarthritis vs. asymmetrical oligoarthritis?

How is the pattern of arthritis in monoarthritis different from that presented in degenerative joint disease?

What are tophi? In considering therapy for the clnical evaluation of Arthritis, what are the 5 factors that one must take into consideration?

List 4 extra-articular features of arthritis List 4 Activities of Daily Living (ADLs) that are used in the clinical evaluation of arthritis?(6)

calcium pyrophosphate deposition disease, (CPDD) an acute or chronic inflammatory arthropathy caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystals in the joints and characterized by chondrocalcinosis and the presence of the crystals in synovial fluid. Clinically, it may resemble numerous connective tissue diseases, including osteoarthritis, rheumatoid arthritis, and gout, or it may be asymptomatic. While most commonly idiopathic, CPDD can also be hereditary or associated with a variety of metabolic diseases. Acute attacks are sometimes called pseudogout. Called also CPPD d.

Pasted from <http://127.0.0.1:8080/rami? COMMAND=applyStylesheet(dor@doc.xsl,dor@d/12300762.pub)&sw ord=12301439>

Figure 123-20 Calcium pyrophosphate deposition disease (CPDD).Chondrocalcinosis of menisci, best shown anteriorly (black arrow), and characteristic distal femoral cortical notching (open arrow). P asted from <http://w iserw iki.com/D iagnostic_Imaging_of_Rheumatologic_D isorders>

A tophus (Latin: "stone", plural tophi) is a deposit of crystallised monosodium urate

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A tophus (Latin: "stone", plural tophi) is a deposit of crystallised monosodium urate in people with longstanding hyperuricemia. At this stage, most have already developed symptoms of the associated crystal arthopathy known as gout. Tophi form in the joints, cartilage, bones, and other places throughout the body. Sometimes, tophi break through the skin and appear as white or yellowish-white, chalky nodules. Without treatment, tophi may develop on average about ten years after the onset of the disease, although their first appearance can range from three to forty-two years. They are more apt to appear early in the course of the disease in people who are older in age. In the elderly population, women appear to be at higher risk for tophi than men. Pasted from <http://en.wikipedia.org/wiki/Tophus>

How is class I functional status different from class III functional status in the clinical evaluation of Arthritis? What is the distinguishing feature between class I and class II functional capacity, as it relates to the clinical evaluation of arthritis? What is the distinguishing feature between class Ii and class III functional capacity, as it relates to the clinical evaluation of arthritis? For the clinical evaluation of arthritis, Lab tests done for ___ blood include CBC, Urinalysis, ___, and ___?(2) For the clinical evaluation of arthritis, Lab tests done for ___ blood include ___?(1) For the clinical evaluation of arthritis, lab tests done to explore degenerative and non-articular rheumatism include ___?(1) For the clinical evaluation of arthritis, lab tests performed include ___ and ___?(2) For the clinical evaluation of arthritis, lab tests performed to investigate an infectious cause include ___ and ___?

Eburnation: e"b6r-na1sh6n) [L. ebur ivory] 1. the conversion of a bone into an ivory-like mass. â—‹ In osteoarthritis, the thinning and loss of the articular cartilage resulting in exposure of the subchondral bone, which becomes denser and the surface of which becomes worn and polished. 2. e. of dentin.

How are the xray changes different in the clinical evaluation of inflammatory vs. non-inflammatory arthritis? What does eburnation mean? Eburnation is a feature of inflammatory or non-inflammatory arthritis?

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List 4 characteristics of arthritis that are explored further in performing a history and physical?(7)

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03 UROWITZ 2008 Connective Tissue Disorders Friday, February 22, 2008 5:25 PM

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The pathogenesis of SLE can be broadly categorized into which 4 main categories?

(mea ning a ra sh with a round or oval shape)

List 9 criteria included in the 1997 Revised Criteria for the Classification of SLE?(11)

Serositis: Inflammation of the serous tissues of the body. The serous tissues line the lungs (pleura), heart (pericardium), and the inner lining of the abdomen (peritoneum) and organs within. P asted from <http://w w w .medterms.com/script/main/art.asp?articlekey =5467>

What is serositis?

A mnemonic for SLE diagnostic criteria Like many rheumatological diseases, systemic lupus erythematosus (SLE) is difficult to diagnose owing to the constellation of findings required. I offer a mnemonic that contains the 11 categories used by the American College of Rheumatology,1 from which four or more must be present to diagnose SLE:

A RASH POINts MD Arthritis Renal disease (proteinuria, cellular casts) ANA (positive antinuclear antibody) Serositis (pleurisy or pericarditis) H aematological disorders (haemolytic anaemia or leucopenia or lymphopenia or thrombocytopenia)

Photosensitivity Oral ulcers I mmunological disorder (positive LE cell, anti-DNA, anti-Sm, false positive serological test for syphilis) N eurological disorders (seizures or psychosis, in the absence of other causes) Malar rash Discoid rash Because the malar rash is the most easily recalled finding, this mnemonic uses that word and an accompanying message that it "points an MD to a possible diagnosis."

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accompanying message that it "points an MD to a possible diagnosis." Pasted from <http://ard.bmj.com/cgi/content/full/60/6/638a >

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List 3 manifestations of serositis that may found in SLE? (hint: pericarditis, ‌)

List 3 manifestations of neurological disorders that may found in SLE?(4)

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In SLE, leukocytes, lymphocytes, and thrombocytes are all (reduced OR increased)?

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•

•

•

•

Anti -Sm is an immunoglobulin s pecific a gainst Sm, a ri bonucleoprotein found in the cel l nucleus. Ra re i n UK; ma inly found in Wes t Indians with SLE. Not found in any other diseases, onl y i n SLE. However, only 30% of pa ti ents with SLE have a pos itive anti-Sm test. A pos i tive test means - A pos itive test usually means tha t l upus is present. A nega tive test means - Does not mea n that lupus is not pres ent. Most people with l upus have either a nti-DNA or a nti -Sm antibodies. Pasted from <http://www.uklupus.co.uk/antism.html >

List 3 manifestations of hematologic disorders that may be found in SLE?(4)

Apart from patient education, what are the 5 other components in the approach to SLE therapy?

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Is it active or inactive SLE that is associated with late deaths in SLE? Is it inactive or active nephritis that is associated with early deaths in SLE? Is infection or atherosclerosis more commonly associated with early deaths from SLE? Late deaths from SLE are associated more commonly with (atherosclerosis OR infection)?

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• What predisposes these people to have subclinical is severity of lupus (as evidenced by increased prevalence of vasculitis and npl) and also increased risk factors; steroids gives you htn, diabetes, hypercholesterolemia, etc. • So if there are two things in here, these women are susceptible because they had early lupus and secondly because they had other risk factors

An illness in which there's inflammation in only two organs; happens in children and adults Dermato/Polymyositis is a disease in which inflammation may be present in which 2 organs?

• Dermato/polymyositis is in mucle only or in skin only; separate illness • Usually associated with an underlying illness

•

Also a red, scaly flaky rash; different from luypus in that the nasolabial foold is NOT spared

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Upper eyelid in patients with dermatox/myox often has a

Nonspecific rash

purple discoloration; VERY PATHOGNOMONIC (THESE HELIOTROPE RASHES) of dermato/polx (dpx)

Gottren's papules: red rash over the knuckles themselves

• So characteristic rashes were:

purple heliotrope rash over eyelid and gottren's nodules on knuckles

Inflammation in muscles

• Also, shoulders and hips tend to be weak; when you do some blood tests, these inflamed muscles tkleak out their enzymes; one enzyme, CPK (creatine phosphokinase) leaks out of these muslce snad you have a high level CK in the blood; probably inflamed; if do EMG, find signs of irritability; inflamed; finally, if want to be absolutely sure, you do muscle biopsy and as in next slide, see inflammatory scells between muscle fibers

• So what causes this? ○ Dermatomyositis or the myositis by iteself may have 2 dfft mechs  Dermx - may be due to immune comlex's  Polymositis wihtout the skin,k seems imp mech is lymphocytes tat are cytotoxic agains the muscle

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Purple discoloration, or a purple heliotrope rash, on the upper eyelids of patients is very pathognomonic of which disease? T/F: Patients with dermato/polymy ositis have a typical malar rash?

Red rashes over the knuckles are called ____ papules and are characteristic of ___? In dermato/polymyositis is there symmetrical or asymmetrical muscle weakness? In dermato/polymyositis is there proximal or distal muscle weakness? T/F: In dermato/polymyositis the two regions of the body in which the muscles are characteristically weak are the hands and feet?

With respect to the pathogenesis of dermato/polymyositis, dermatositis is ___ mediated while polymyositis is ___ mediated? Is it dermatositis or polymyositis which is immune complex mediated? T/F: With respect to the pathogenesis of dermato/polymyositis, polymyositis is cell mediated.

Dermato/polymyositis is more common in males or females? Dermato/polymyositis is more common in patients over the age of ___?

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Major issues here:

Scleroderma = progressive systemic sclerosis

Scleroderma is essentially progressive ___? T/F: In scleroderma there's a great deal of skin inflammation? T/F: Patient with scleroderma DO NOT have inflammation but DO HAVE autoantibodies present in their blood?

• Everything we've talked about today is about the tissue getting

• Malignancies that occur are the common malignancies: man: lung, pancreas, stomach • Women: ovary, etc. • This underlying malignancy is more common in men, with dermato, and over 50 • So a man, over 50, with dermatocytis, will receive an intensive workup for an underlying malignancy

inflamed; in this condition, there's virtually NO inflmmation; there's progressive sclerosis; tighening, thickening, fibrotic reactions in the tissues; these patients do have autoantibodies but they don't lead to inflammation; they somehow lead to progressive inflammation through the tissues The mnemonic CREST, relating to the symptoms of scleroderma, stands for…?

R = reynaud's phenomenon • When go in cold, hands turn deep blue and then dead white, then n rewarming, turn red, this occurs in maybe 10% of the normal popultion; in scleroderma, happens in 95% of people indicates vascular instability

• Skin tightening can be so drastic that actual tissues are choked! Bone is even choked out!

• Sclerodactyly: tightening of tissues

in the fingers

• This pic is a picture of the T = telangiectasia: man on his lips see these red dots, on his palate, these telangiectasia; located on mucous membranes and skin; different from telangiectasia in liver disease; those have red dot and spider like arms coming out of them; these don't have spider arms, mjust red dot; these look loike hereditary teangiectasia; but patients with scelroderma you push on these telangx and they blanche; here these little blood vessels are being dilated and open up; so ge the picture that there's a blood vessel problem in scleroderma

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X-ray of calcinonsis

As tissue is being choked, there's a tendency to lay down calcinosis (laying down of calcium under the fingers

C=

Weakened Intima

E= esophagus: when you eat food, get peristalsis; patients with scleroderma and those with reynaud's henomenon in general tend to lose peristalsis so esophagus tends to become like a solid tube; you're pushing it down with gulping but the normal wave that you get in isn't pushing it down

• Here's an example of why this occurs: intima of the blood vessel is proliferating and intima is weakened; again coming back to the vascular story; blood vessel who's lumen is being obliterated T/F: patients with scleroderma and those with reynaud's henomenon in general tend to lose peristalsis in the esophagus?

• Here you see the lumen virtualy occluded by heaped up intimal proliferation • This is a problem of narrowing of blood vessel lumina

So heard now 3 different disease Lupus story: ○ Problem is autoantibodies which by 2 mechsnims discussed cause inflammation in every tissue of the body 2nd story: we've been real good in treating inflammation but created acceleratid athereosclerosis in 30 to 40 eyar sold women ○ Second inflmmation was also inflammation in skin and muscle, but this only a herald of skin and muscle problems Final disease: due to prorressive narrowing and obliteration of blood vessels

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04 ALBERT 2008 Seronegative Spondyloarthropathies Friday, February 22, 2008 5:25 PM

In the clinical evaluation of arthritis, there are 3 major categories; name them? What are the subsets of the inflammatory arthritis category? What are the subsets of the non-articular arthritis category? What are the subsets of the degenerative arthritis category? With respect to arthritis, a prime example of a seropositive disease is ___? Is it seroPOSITIVE or seroNEGATIVE arthritic diseases that have characteristic extraarticular manifestations?

Spectrum of Seronegative Diseases

Enteropathic Arthritis

List 4 subsets of the spondylarthropathies? There is an overlap between AS and which 3 other spondylarthropaties?

Psoriatic Arthritis Ankylosing spondylitis

Reactive Arthritis

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List 2 different types of enteropathic arthritis's?

• Spondyloarthropathy: disease of the joints of the spine. ○ seronegative spondyloarthropathies

Where is the entheses located? What is enthesitis?

spondyloarthropathy seronegative spondyloarthropathies, a general term comprising a number of degenerative joint diseases having common clinical, immunologic, pathologic, and radiographic features, including synovitis of the peripheral joints, enthesopathy, bony ankylosis of the large peripheral joints, lack of rheumatoid factor, and, in many cases, a positive status for the human leukocyte antigen HLA-B27. Included in this group are enteropathic arthritis, psoriatic arthritis, ankylosing spondylitis, and Reiter's syndrome. Pasted from <http://127.0.0.1:8080/rami?COMMAND=apply Stylesheet(dor @doc.xsl,dor@s/12751920.pub) &sword=12751926>

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Enthesitis is an inflammation of the entheses, the location

where a bone has an insertion to a tendon or a ligament. It is also called enthesopathy, or any pathologic condition involving the entheses. The entheses are any point of attachment of skeletal muscles to bone, where recurring stress or inflammatory autoimmune disease can cause inflammation or occasionally fibrosis and calcification. One of the primary entheses involved in inflammatory autoimmune disease is at the heel. Heel swelling and inflammation are therefore used to help diagnose certain inflammatory autoimmune diseases, including ankylosing spondylitis. Pasted from <http://en.wikipedia.org/wiki/Enthesitis>

Syndesmophyte a type of bone outgrowth of the spine occurring in various disease, including ankylosing spondylitis, alkaptonuria and enteropathic arthropathies (Crohns disease, ulcerative colitis, Whipples disease). In ankylosing spondylitis, ossification of the anulus fibrosus leads to development of a thin vertical outgrowth of bone that extends across the margin of the intervertebral disc. Syndesmophytes occur most commonly at the anterior and lateral aspects of thespine, particularly near the thoracolumbar junction. They can be differentiated from spinal osteophytes by their shape and site of attachment to the vertebral edges (spinal osteophytes are triangular in shape and arise several mm from the discovertebral junction) and from the nonmarginal paravertebral ossification of psoriatic arthritis and Reiters syndrome(located at a distance from the vertebral body and intervertebral disc). Extensive formation of syndesmophytes is termed syndesmophytosis. Pasted from <http://www.medcyclopaedia.com/library/topics/volume_iii_1/s/syndesmophyte.aspx>

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What is a syndesmophyte?

Schober's Test 1. Indication: Evaluation

of Lumbar Spine Range of Motion

1. Ankylosing Spondylitis 2. Technique 1. Patient stands erect with normal posture 2. Identify level of posterosuperior iliac spine 1. Mark midline at 5 cm below iliac spine 2. Mark midline at 10 cm above iliac spine 3. Patient bends at waist to full forward flexion 4. Measure distance between 2 lines (started 15 cm apart) 3. Interpretation 1. Normal: distance between 2 lines increases to >20 cm 2. Abnormal: distance does not increase to >20 cm 1. Suggests decreased Lumbar spine range of motion 2. May suggest Ankylosing Spondylitis Pasted from <http://www.fpnotebook.com/Rheum/Exam/SchbrsTst.htm>

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Pasted from <http://www.fpnotebook.com/Rheum/Exam/SchbrsTst.htm>

FABER stands for Flexion, ABduction, and External Rotation of the hip. 1. Ask the patient to lie supine on the exam table. 2. Place the foot of the effected side on the opposite knee. 3. Pain in the groin area indicates a problem with the hip and not the spine. 4. Press down gently but firmly on the flexed knee and the opposite anterior

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opposite anterior superior iliac crest. 5. Pain in the sacroiliac area indicates a problem with the sacroiliac joints.

Gaenslen's test is performed with the patient supine (on the back). The hip joint is maximally flexed on one side and the opposite hip joint is extended. This maneuver stresses both sacroiliac joints simultaneously. Pasted from <http://www.hughston.com/hha/a_15_1_1a.htm>

Pasted from <http://medinfo.ufl.edu/year1/bcs /slides/extrem/slide21.html>

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(7)

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The 2 most common extra-articular manifestations of AS are ___? RARE extra-articular manifestations of AS include ‌(list 3)?(5)

Approximately what percentage of patients who have ankylosing spondylitis are positive for HLAB27?

The association between HLAB27 and ___ is one of the strongest immunogenetic associations observed with any human disease? What is the risk of ankylosing spondylitis in patients who are positive for HLAB27? ESR and CRP are both acute phase reactants? Can the acute phase reactants ESR and CRP be used as diagnostic tests for ankylosing spondylitis?

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The KEY clinical symptom of ankylosing spondylitis is ___?

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A 35 year old patient comes to your office with a six month history of back pain that improves with exercise and is associated with morning stiffness. What is the MOST LIKELY diagnosis?

List the 4 New York criteria for the diagnosis of ankylosing spondylitis? T/F: One of the New York criteria for the diagnosis of ankylosing spondylitis is low back pain for more than 3 months that INCREASES with exercise? How many criteria must be positive bilaterally or unilaterally for there to be a positive diagnosis of ankylosing spondylitis? According to the New York Criteria, DEFINITE ankylosing spondylitis can be diagnosed if you have ____ + ___?

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What are the newly proposed criteria for inflammatory back pain in young to patients < 50 years old with chronic back pain (list the 4 criteria)?

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Asymmetric transient polyarthritis is a pattern common to which type of arthritis?

How do sacrolitis/spondyl itis vs. peripheral arthritis differ in their course in relation to the course of IBD?

Is it sacrolitis/spondyl itis OR peripheral arthritis that is associated with HLA B-27?

List 4 common patterns of psoriatic arthritis?

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Another name for reactive arthritis is ___ syndrome? How is reactive arthritis diagnosed (list the 3 criteria, ie. "Following a GI or GU infection the onset of ‌(3))?

List 2 organisms implicated in the gastrointestinal etiology of reactive arthritis?(4) List 3 extra-articular manifestations of reactive arthritis?(5) Campylobacter and Yersinia are both possible (GI or GU) causes of reactive arthritis?

• Balanitis is a term used to include all inflammation of the skin covering the head (glans) of the penis.

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With respect to therapy for ankylosing spondylitis, is sulfasalazine helpful for peripheral disease? With respect to therapy for ankylosing spondylitis, is sulfasalazine helpful for axial disease? List 2 drugs that can be used for anti-TNF therapy in treating ankylosing spondylitis? Indomethacin and Naproxen are both ___ that can be used in the treatment of ankylosing spondylitis? Indomethacin and Naproxen are both NSAIDs that can be used in the treatment of ___? What should you avoid in using corticosteroids to treat ankylosing spondylitis?

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List 3 possible treatments for Psoriatic arthritis?(5)

(ie. AS NOT responding to treatment using NSAIDs)

What do the CRA Consensus Guidelines state regarding the use of anti-TNG in ankylosing spondylitis (differentiate between recommendations for primary axial vs. primary peripheral disease)?

Sulfasalazine

is used to treat bowel inflammation, diarrhea (stool frequency), rectal bleeding, and abdominal pain in patients with ulcerative colitis, a condition in which the bowel is inflamed. Sulfasalazine delayed-release (Azulfidine EN-tabs) is also used to treat rheumatoid arthritis in adults and children whose disease has not responded well to other medications. Sulfasalazine is in a class of medications called anti-inflammatory drugs. It works by reducing inflammation (swelling) inside the body. Pasted from <http://www.nlm.nih.gov/medlineplus/druginfo/medmaster/a682204.html>

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List three drugs that are common between the treatments for enteropathic axial and peripheral disease? List 3 possible treatments for enteropathic PERIPHERAL arthritis?(5) List 3 possible treatments for enteropathic AXIAL arthritis?(4) List 2 therapies used to treat acute, reactive arthritis? How do you treat GI infections that lead to reactive arthritis? When should you treat GU infections in persons with reactive arthritis? Should you treat an active chlamydia infection leading to reactive arthritis or is it best to first see if it resolves on its own?

05 KEYSTONE 2008 Therapeutics in Rheumatic Diseases Friday, February 22, 2008 5:26 PM

The incidence of RA increases in persons between the ages of ___ and ___ years old? RA affects 3x as many (women or men)?

List 3 pharmacologic interventions for RA?

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List the 5 levels of treatment in the traditional "Pyramid" approach to therapy, as indicated for the treatment of RA?

List 4 drugs that are in current use for the treatment of RA? The goal of disease modifying antirheumatic drugs is to ____? Approximately how long do DMARDs used for the treatment of RA take to act? Do most patients taking DMARDs to treat arthritis achieve full remission?

Methotrexate is the GOLD STANDARD for the treatment of moderate/severe ___?

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What is the GOLD STANDARD for the treatment of moderate/severe RA? When should you initiate DMARDs following the initial diagnosis of RA?

Compared to methotrexate, leflunomide has a more direct effect on ___ cells?

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___ is a pivotal cytokine in RA?

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List 3 potential safety issues with the use of TNF antagonists in the treatment of RA?(6)

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06 CARETTE 2008 Vasculitis Friday, February 22, 2008 5:26 PM

1. 2. 3. 4. 5. 6. 7. 8.

Skin Joints/muscles Kidneys Nervous system Heart/Lungs Gastro-Intestinal ENT/EYES Other

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List 2 medium artery vasculitis's? List 2 small artery vasculitis's?(3) List 2 large artery vasculitis's? List 2 arteriole/capillar y venule related vasculitis's?

List 3 signs of small vessel vasculitis that can be found on physical exam?(6) List 3 signs of medium vessel vasculitis that can be found on physical exam?(5)

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Giant cell arteritis is more common in females or males?

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07 HAWKER 2008 Osteoarthritis and Low Back Pain Friday, February 22, 2008 5:27 PM

• Distal and proximal IP joints most common (rarely involvement of MCP joints) • Knees are by far most common join involved in OA

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• NOT just a cartilage problem!

T/F: Osteoarthritis is a natural consequence of aging that occurs secondary to superficial fissuring, erosions and loss of cartilage?

• Decreased bone mass and proteoglycans lead to fissuring, leading to exposed bone

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Each risk factor exlpored in slides below • OA challenges very different from RA

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• It's clearly been shown that people with knee OA had it BEFORE they started to develop knee OA

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T/F: Exercise is an economic and effective though underprescribed therapy in osteoarthritis?

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08 MCDONALD-BLUMER 2008 Osteoporosis Friday, February 22, 2008 5:28 PM

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Fra cture of the di s tal ra dius bone

List 4 common locations for fragility fractures?

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09 JUURLINK 2008 Pharmacologic Treatment of Rheumatic Diseases Friday, February 22, 2008 5:28 PM

• At highest risk of getting in trouble

• Has hepatotoxicity ○ But only becomes toxic when becomes converted to NAPQI; usually gets metabolized to glutathione or sulphate ○ NAPQI binds to the first thing it sees

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• Many people take more than one product with acetaminophen

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Aspirin also is an antiinflammatory (these doses that you'd give to patients with ‌ is about 80mg)

• Not that uncommon that you start someone on NSAIDS

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Misoprostol: at doeses of even 600mg, caused diarrhea; people couldn't tolerate it; remember this is the same Misoprostol we learned in FMP1, which is a teratogen

• Celecoxib, robacoxib (Vioxx): became blockbuster drugs; several large clinical trials more than 10,000 patients; clear that they were safer but they got used in people who were never even considered for traditional NSAIDS in the first place

• How sticky your platelets are (sticky = thromboxane; non-sticky = prostacyclin)

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• At least now 10,000 lawsuits re: Vioxx

It appears that all NSAIDs (selective AND nonselective) may sligthtly increase the risk of vascular events, WITH THE POSSIBLE EXCEPTION OF ___? T/F: it appears that all NSAIDs (selective AND non-selective) may sligthtly increase the risk of vascular events?

Podagra: gouty pain in the great toe.

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Podagra refers to …? The end product of purine breakdown is ___?

ASA is NOT used in the treatment of gout because …? In the treatment of acute gout, NSAIDs are genereally the preferred treatment unless the risk of adverse effects is deemed too high, such as (list 2)?

Indomethacin: [USP] a nonsteroidal antiinflammatory drug; used in the treatment of rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, acute gouty arthritis, other rheumatic and nonrheumatic inflammatory conditions, and dysmenorrhea, and the treatment and prophylaxis of vascular headaches; administered orally or rectally. It is also applied topically to the conjunctiva to prevent miosis during cataract surgery and to reduce the severity and occurrence of postoperative cystoid macular edema.

What is the mechanism of action of colchicine?

2 important side effects of colchicine are ___ and ___?

Really is very dangerous in large amounts; interferes with metaphase not just in neutrophils

3 potential treatments for the treatment of acute gout are …?(4) Generally speaking, the two drugs that are used to treat acute gout are ___ and ___? List 3 cautions for colchicine prescription?

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T/F: In the prevention of gout attacks, ___ decreases the frequency of gout episodes by about 75%?

KNOW THIS LIST FOR EXAM!

T/F: dietary modifications are generally effective for the prevention of gout? List 3 drugs that should be avoided in persons with gout because they increase uric acid levels?(6)

A common drug used to treat gout is ___? For the prevention of gout attacks, one should avoid or minimize drugs that can increase uric acid levels, such as ‌ (name 4)?(6) Colchicine is ONLY added as a treatment if a(n) ____ is added to the regimen?

Does allopurinol stimulate or block xanthine oxidase? List 2 adverse effects of allopurinol?(4)

T/F: Allopurinol hypersensitivity is a common, mild reaction to allopurinol that is mainly manifested as diffuse petichiae over the abdomen and chest areas? List 2 features of allopurinol hypersensitivity?

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The KEY drug interactions with allopurinol are ___ and ___?

T/F: Corticosteroids suppress inflammatory responses regardless of their etiology? T/F: In using corticosteroids, pain, erythema, warmth, and swelling often DO NOT occur? What effect do corticosteroids have on scar formation and wound healing? What effect do corticosteroids have on the synthesis of prostaglandins and leukotrienes? What effect do corticosteroids have on WBC migration and function? Corticosteroids impair (list 2)?(3)

A very serious ACUTE adverse effect of corticosteroids is ___? List 3 chronic adverse effects of corticosteroids?(9)

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Steroid-associated osteoporosis may occur because glucocorticoids increase the rate of bone loss by ‌(list 2 ways)?(4)

If patients are taking prednisone >5mg/d for 3 or more months, then 3 other medications should be given to prevent steroidassociated osteoporosis, namely‌?

(ni trogen narcosis)

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In avascular necrosis, there is death of ___ and progressive ___? Avascular necrosis is far more common in (men/women)? Most patients with avascular necrosis have ___ pain; a minority have ___ pain? Risk factors for avascular necrosis include (name 3)?(7)

Which group of patients have the highest risk for developing steroid avascular necrosis? Lots of sclerotic bone with radiolucency

Treatment for Addisonian Crisis secondary to abrupt cessation of steroid administration is to …? Symptoms of acute Addisonian Crisis include (list 3)?(6) • If you stop the steroid purposefully or not, person goes into period of abrupt or severe period of steroid withdrawal called Addisonian Crisis (complain of nausea, vomiting, hypotensive, potassium a little high); similar to an autoimmune adrenalitis • Treatment for Addisonian Crisis is giving more steroids

EXAM QUESTIONS!

HPA axis suppression (Addisonian Crisis) commonly occurs during which 2 common conditions?

Prior to an operation, a patient with adrenal insufficiency should receive (more or less) steroids?

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10 TUES Acute Monoarthritis Seminar Notes Friday, February 22, 2008 5:39 PM

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Name 3 synovial lined spaces?

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What is the best way to treat acute monoarthritis?

Does inflammatory synovial fluid have high or low viscosity? What is the cutoff for WBC #'s for noninflammatory synovial fluid? What is the range for inflammatory vs. septic synovial fluid? Noninflammator y and normal synovial fluid is comprised of what percentage of PMNs? Inflammatory vs. Septic arthritis is composed of what percentage of PMNs?

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Which of the following crystal depositions are known as "Gout": Momosodium Urate or Calcium Pyrophosphate Dihydrate?

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List 3 systemic therapy options for acute gouty arthritis? In which 2 categories of patients should colchicine be avoided? In which 3 cateogires of patients should you avoid NSAID treatment of acute gouty arthritis?

What are the 2 categories of septic arthritis? Which is more serious? What are the two steps in treatment of septic arthritis?

• Gonococcal responds great to 3rd generation ceph • Non-gonococcal- need treat with IV Abx

Colchicine Indications Systemic Gouty arthritis, chronic (treatment) or Gouty arthritis, acute (prophylaxis and treatment) Colchicine is indicated to reduce the frequency and severity of acute attacks of gouty arthritis in patients with chronic gout. Complete remission of such attacks may occur in some patients. Prophylactic administration of colchicine may be especially important during the first several months of treatment with an antihyperuricemic agent (allopurinol, probenecid, or sulfinpyrazone) because the frequency of acute attacks may be increased when such therapy is initiated. Although colchicine is also indicated to relieve the pain and inflammation of acute attacks of gouty arthritis , it has generally been replaced by less toxic medications for this purpose . Nonsteroidal anti-inflammatory drugs (NSAIDs) or corticosteroids (preferably via intrasynovial injection) are recommended for relief of an acute attack. Therapeutic doses of colchicine should be reserved for patients in whom these other agents are contraindicated or ineffective . Intravenous administration of colchicine may be considered for treatment of acute attacks of gouty arthritis when oral administration is ineffective, gastrointestinal side effects limit administration of effective oral doses, or an especially rapid response is needed . Although the risk of gastrointestinal toxicity is considerably lower with intravenous administration than with oral administration , the risk of other forms of toxicity is very high , especially in patients with renal and/or hepatic function impairment ; fatalities have been reported . It is recommended that the medication be administered intravenously with caution, in low doses, and only to carefully selected patients , if at all . Pasted from <http://www.pharmgkb.org/do/serve?objId=475&objCls=DrugProperties>

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What two things must be of short duration to ensure better outcomes in the case of septic arthritis? How long should antibiotic therapy continue for the management of septic arthritis?

• The sooner you treat the better but don't treat until you have that culture

• Not every joint problem is arthritis; sometimes may have periarticular • When thinking about mono or polyarthiritis, always think about inflammatory vs. noninflammatory • Criitical cell count: 2000 x 10x6 per liter

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What is the difference between Type A vs. Type B Synovytes?

Synovial fluid is an ultrafiltrate of plasma to which _____ and other factors are added locally by synoviocytes?

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List the 4 categories of differential diagnoses for shoulder pain (hint: articular, ‌)?

• Joint problems can arise in the acromioclavicular or glenohumeral joints

How recognize non articular problems? â—‹ Can be chronic low grade repetitive trauma or acute low inflamamtion; generally if you move the patients arm and move it passively then they won't have pain; if they voluntariy move; pain with esistant or active morvement in certain planes is characteristic of non-articular

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List 3 signs of inflammatory arthritis?(4)

• Limitation of range of motion is common to both inflammatory and noninflammatory arthritis

• If patients have bursitis, 3 important things to recognize • Pain arising in one joint area, eg. Hip joint pain referred to knee

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• If do experiemnt and stimulate diff cervical levels can se pain in the for example peri-scapular area originating in the lower cervical elements

• Persistent knawing pain, for example, subphrenic abscess causing shoulder pain, may not be MSK pain anyway

Now, in this paritcular patient, not worriesd about arthiritis or referred pain, but focusing on rotataor cuff tenditinitsis

Tendons around the shoulder

• rotator cuff pain is felt at the shoulder!!!

• Even if you forget what a particular tendon's name is , just rmember you're looking for tenderness along lentght of tendon by palpating or put tendon under stretch or stress • So locla tenderness on plapation, stretch or stress then • If palpate along head of humerus by arm going back then can feel insertion on humerus; is hard however to stretch the tendons; most often therefore stress

• • • •

Can palpate supraspinatus by moving arm back Subscapularis: internal rotation Supraspinatus: early part of abduction Teres minor and infraspinatorus

• Can test impingement at full abduction • Two other tests: a. Palm down, hold down scapula and try to bring rotator cuff tendon forcibly against acromioclavicular ligament; may produce pain if jhas impingement b. Thumb down, internally rotate bent arm

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Rotator cuff pain is referred to the ___?

•

tendonitis, bursitis and impingement syndrome, often go together

• Forced forward flexion

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•

Common extensor tendon: lateral epidcondyle

We're going to focus on tennis elbow

No swelling, • If had olecranon bursistis, see bag of fluid hanging off tip of elbow

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• • • •

Articular Nonarticular Referred Non-MSK

• Sometimes patients with seronegative aarthtiritis have Very common problems with achilles tendon

List of differentials are important to keep in back pocket; these are the commonest things that people come in with and if you havea list of ddx, then it reminds you of the other things to check for

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• Commonly caused by flat feet or bad footwear

• Anteromedial portion of the calcaneus • DORSIFLEX TOES CAN STRESS PLANTAR FASCIA

Hip pain means difft things to difft people; if at the side, then from the spine;

TRUE HIP PAIN IS FELT IN THE GROIN REGION!

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• Sometimes osteoporotic patients can come in with pubic ramus fracture

• Abducting or adducting leg puts pressure on trochanteric bursae

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• In general management of these conditions is fairly similar • If repetitive movement that can change then change the person's mechanics - physiotherapist can help with this

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A joint is an articulation between … or …? The three different types of joints are …?

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The most frequent crystal induced arthritis is ___?

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Extracted pages - seminar Sunday, February 24, 2008 12:59 PM

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Gout chiefly affects middle-aged and elderly (men or women)?

Gross urate crystal deposits are also known as ____?

Allopurinol is a xanthine oxidase inhibitor which decreases ___ synthesis?

In the treatment of acute gout, ___ such as indomethacin and ___ are the drugs of first choice? Colchicine is rarely used in the treatment of acute gout because of its‌?

Allopurinol is a ___ inhibitor which decreases uric acid synthesis? Allopurinol is the preferred ___ lowering drug?

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The LEAST common type of microcrystalline arthritis is ___?

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11 THURS Special Tests in Rheumatology Seminar Notes Friday, February 22, 2008 5:40 PM

Go to smhrheumatology.com and see presentations • Then go to lab presentations; little panel, orange card that you carry around in pocket • In screening looking for sensitivity not specificity; since the tests are not diagnostic; merely support our clinical impression; so if you have a postiive ana and you feel perfectly okay then likely that you don't have lupus

• HOW DO WE KNOW RHEUMATOID FACTOR DOESN'T CORRELATE WITH CLINICAL FINDINGS OF ACTIVITY? Not all patients with RA have rheumatoid factor; tells you that it's a marker of disease of how active it is, not of RA itself • So pick the tests that ARE GOING TO HELP YOU TO MAKE DECISION S ABOUT TREAMTNET, NOT ABOUT DIAGNOSIS; YOU'VE ALREADY MADE THAT!

• Extractable nuclear antigens: everything that DNA isn't • Eg. Staff doctor says work patient up for VASCULITIS ○ Website gives expalantion of every test

• CRP, ESR • Screening test is rheumatoid factor so doesn't matter if goes up or down; value of rheumatoid factor is whether or not it's positive; if treat, their rhumatoid factor may or may not go away; it doesn’t' really matter because once positive then it's positive

• There are conditions however when the rhumatoid factor does go away, namely, infection • Tests of rpatients in known rheumatic dises: only those • Sedimentation rate is a marker of inflammation • So want to look for the MARKERS OF THE ACTIVITY OF DISEASE; ONCE YOU HAVE THE DISEASE THEN UNFORTUNATELY YOU HAVE THE DISEASE; BUT IF YOU HAVE MESAURES THAT TELL YOU HOW ACTIVE THIS IS THEN YOU CAN FOLLOW THE DISEASE APPROPRIATELY

T/F: There are conditions, such as in some infections, in which rheumatoid factor levels decrease markedly? What is the main way in which RA and SLE are screened for?

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• If have penumonia, your ESR or CRP will both be above average

In IgM multiple myeloma get very low ESR; if see sedimentation rate of 0 then think multiple myelome of IgM multiple myeloma • So anythign that makes it go faster is a cuase of inflammation • In polycythenmia vera get clumping of RBCs ○ polycythemia ve1ra, a myeloproliferative disorder of unknown etiology, characterized by abnormal proliferation of all hematopoietic bone marrow elements and an absolute increase in red cell mass and total blood volume. The skin of the face is often ruddy and swollen, and ecchymoses are common. Most patients have splenomegaly, leukocytosis, and thrombocythemia. Hematopoiesis is also reactive in extramedullary sites (liver and spleen), and in time myelofibrosis occurs. Called also erythremia, p. rubra or p. rubra vera, myelopathic or splenomegalic p., and Osler's, Osler-Vaquez, Vaquez', or Vaquez-Osler disease. Cf. secondary p. Pasted from <http://127.0.0.1:8080/rami?COMMAND=apply Stylesheet(dor @doc.xsl,dor@p/12656167.pub) &sword=12656269>

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• Hepatitis B can present with a prodrome of polyarthritis; so can malignant conditions; so if have ESR in a patient with other findings, you have to look even though may not fiind anything • Case in point, last week, 60 yo fatigue, achiness, made diagnosis PMR; pah didn't get better; in process of doing reast of workup, found multiple malignant nests • POSITIVE TESTS HAVE VALUE; NEGATIVE TESTS JUST MEAN THAT YOU HAVEN'T RULED SOMETHING OUT!

• IN RHEUMATIC DISEASES, CRP is a marker for inflammation • In RA, crp is an indicator of more aggressive jiont damage over time

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• Rheumatoid factor can also be IgG • IgG is a measure of chronicity • Whatever was the stimulus, IgG is the body's reaction to it

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• Note that it's binding to the common structural element so it can do so non-spcifically; only lookking for that portion of the IgG • Certain types of infection that are classically associate with rehumatoid factor ○ Endeocarditis, Hep C • If take rheumatoid factor and inject it into a normal individaul, LIKELIHOOD IS THAT THEY DO NOT GET RA, OR LUPUS • Antibodies are a mesareu fo the disease being there indicator of the undderlyoing pathogenesis of the disease but so it's necessary but not sufficient

• complement control protein, (CCP) any of a superfamily of proteins involved in complement regulation, encoded in a closely linked gene cluster, and having one or more stretches of a common short consensus repeat encoding a 60 amino acid domain. Included are factor H, C4 binding protein, decay accelerating factor, membrane cofactor protein, and several complement receptors . Called also regulator of complement activation. • Citrulline: alpha-amino delta-carbamido normal valeric acid; it is formed from ornithine and is itself converted into arginine in the urea cycle. • Citrullinated = arginine been replaced with serine

• Problem with these tests: great in the investigation of disease • So when no clinical features, no point to ordering tests

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T/F: Rheumatoid factor is not diagnostic of Rheumatoid arthritis?

Almost all patients with SLE have a positive ___? T/F: The ANA test is NOT specific for SLE?

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T/F: The set ANA titre above which persons DEFINITELY have SLE is 1:40?

When should you order an ANA?

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Anti-Ro (SS-A) and Anti-La (SSB) is associated with which disease (though it can be seen in SLE)?

Anti-Jo-1 is specific for myositis associated with _______ and __________?

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T/F: ANA is recommended as a screening test?

Which test VIRTUALLY RULES OUT SLE if negative?

What are ANCAs? What does P-ANCA stand for? What does C-ANCA stand for? Which disease is C-ANCA associated with? Which disease is P-ANCA associated with? The major target antigen of C-ANCA is __________? The major target antigen of P-ANCA is __________?

The major target protein of cANCA is ___? The major target protein of pANCA is ___?

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In a usual patient with lower back pain, would you test HLA-B27?

Is a positive ANCA diagnostic of vasculitis? What is the approximate sensitivity of HLAB27 in patients with ankylosing spondylytis?

When is HLA-B27 testing useful?

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What is fibromyalgia syndrome?

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Is fibromyalgia syndrome more common in males or females?

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In terms of how they are DIAGNOSED, fibromyalgia syndrome and major depressive disorder are similar in that they are both ‌? Diagnoses of exclusion

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Myositis/Myopathies are characterized by (proximal/distal) muscle weakness? Bloodwork of a patient with myositis/myopathies would reveal high levels of which enzyme?

What value of ESR must be present (mm/hr) to suggest PMR (Polymyalgia Rheumatica)? What does PMR stand for? What does GCA stand for?

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In considering the diagnosis of fibromyalgia, which 5 other diagnoses would you consider in order to arrive at this diagnosis of exclusion?(6)

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What Did You Learn This Week? Lecture by Dr. Bookman, MD FRCPC Friday, February 29, 2008

Case 1 • • • • • • • • •

History 32 year old female Pain/swelling hands wrists x 6 mo Morning stiffness x 2hrs Right knee both wrists tender warm swollen, red Weaker by mid morning Exhausted painful feet by 3:30 pm Ibuprofen 8 tablets per day helped 5lb weight insomnia down in the ?

Physical Normal general physical exam • Tender swollen wrists all mcps pip and right knee • Small subcutaneous nodule, extensor right ulna • Weak grip • Normal back, neck, skin, mucous membranes, neurological

1. Which pattern characteristic this patient's illness in terms of anatomic distribution and historic evolution a. b. c. d. e.

Acute inflammatory monoarticular arthritis Subacute symmetrical inflammatory oligoarthritis Chronic symmetrical inflammatory ? ?

Answer c): Chronic symmetrical inflammatory Clinical evaluation of arthritis

2. Which most likely process causing this patient's illness a. b. c. d. e.

Hla b27 associated seronegative arthritis Crystal induced inflammation Infection Immune mediated connective tissue disease Trauma

Answer d): Immune mediated connective tissue disease

3. Which of the following blood test most likely to clinically dx a. b. c. d. e.

Rheumatoid factor Hlab27 antigen Sedimentation rate Uric acid Blood sugar

Answer: a) rheumatoid factor

4. Which additional test would be necessary to establish a dx? Lab results Hb. 100 gm/L WBC 8x109/L Platelets 580x109/l Complete normal Urinalysis, uric acid, calcium phosphate, kidney, CK Which additional test would be necessary to establish a dx?

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a. b. c. d. e.

Biopsy of elbow nodule Synovial fluid analysis Chest x-ray All the above None the above

Answer e): None of the above

5. What treatment would be most appropriate at this stage of her disease? a. b. c. d. e.

Naproxen 500 mg bid and prednisone 10 mg every morning Naproxen 375 mg twice a day and observe Cyclophosphamide, 2mg/kg intravenous Naproxen 500 mg b.i.d. and methotrexate 15 mg weekly Etanercept 25 mg sc twice weekly and naproxen 500 mg bid

Answer: d): Naproxen 500 mg b.i.d. and methotrexate 15 mg weekly • Naproxen twice a day wouldn't be sufficient to treat her and cyclophosphamide would be overkill; methotrexate is the gold standard now for management • Etanercept use if your more modest treatments failed • No prednisone because no DMARD added Radiographic profusion of joint erosion and deformity in RA patients • Most DMARDS we use today actually retard development of erosions of join

Case 2 70 Year old female, presents with aching in shoulders, hips upper arms legs , sudden onset after flu, 2-3 hours morning stiffness, 5 kg weight loss past 2 months, cannot comb hair, reach or use toilet, aunt with rheumatoid

On exam, tender muscles, trapezius delts, extreme pain, strength cannot be assessed due to pain, afebrile

1. What disease? a. b. c. d. e.

Local non-articular rheumatism Crystal induced arthritis Degeneration General non-articular Seronegative arthritis, B27 positive

Answer: d): General non-articular

2. Which investigation would be least helpful a. b. c. d. e.

Muscle nexumes (???) An electromyogram Serum uric acid X-ray of chest Sedimentation rate

Answer: C) uric acid Lab test results ESR 120, Hb low, white count normal, platelets elevated, normal urine creatinine, alt 25, alp increased somewhat, TSH normal, ANA negative, chest X-ray normal

3. What' most worrisome possible complication in this patient a. b. c. d. e.

Pneumonitis Peripheral neuropathy septic arthritis Blindness Myocarditis

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Answer: d) blindness • Because someone presenting this way with negative serology , older patient most things ruled out, presenting with polymyalgia rheumatica and biggest complication is GCA and blindness

(showed picture of temporal arteritis and pathology, disruption of internal elastic lamina

Case 3 34 man, sever knee pain 24 hours, twisted knee and scraped elbow; pain severe at night; bad with movement, hx of diabetes juvenile onset 15 year insulin dependent On exam Distress, painful immovable knee because of pain, tense warm, has effusion, mild left inguinal lymphadenopathy, and he has normal general physical exam, and abrasion on left elbow • Lost dimple in knee medially

Questions:

1. What problem most likely: a. b. c. d. e.

An acute inflammatory polyarthritis. A degenerative monoarthritis A localized non-articular rheumatism An acute inflammatory monoarthritis A generalized non-articular rheumatism

Answer: d) an acute inflammatory mono Yes, monoarthritis Lab results: Hb good, WBC 20, poly: 70% platelets elevated, Glucose 18, not well controlled, creatinine Somewhat elevated; no cells, protein, ketones

2. Which best diagnostic test to order a. b. c. d. e.

x-ray of knee Uric aid Culture elbow abrasion Arthrocentesis X-ray SI (sacro-iliac) joints

Answer: d) Arthrocentesis

• • • • •

Results of investigation: x-ray of knee : effusion only Swabs culture sent X-ray of sacroiliac joints normal Uric acid elevated Arthrocentesis showed 50 cc fluid, yellow and cloudy and culture pending

3. What's the best diagnosis? a. b. c. d. e.

Diabetic neuropathic joints RA Septic arthritis Medial meniscus tear Acute gout

Answer: c) Septic arthritis AND acute gout most likely dx's

4. Which of the following lab results NOT expect in the synovial fluid sample? a. WBC…? b. WBC…?

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b. c. d. e.

WBC…? WBC…? Negative birefringent needle shaped crystals Positive birefringent …?

Answer: ?) WBC 500 x 106/L with 80% monocytes

Birefringence

A calcite crystal laid upon a paper with some letters showing the double refraction Birefringence, or double refraction, is the decomposition of a ray of light into two rays (the ordinary ray and the extraordinary ray) when it passes through certain types of material, such as calcite crystals or boron nitride, depending on the polarization of the light. This effect can occur only if the structure of the material is anisotropic (directionally dependent).

Applications of birefringence It is also utilized in medical diagnostics: needle aspiration of fluid from a gouty joint will reveal negatively birefringent urate crystals. Pasted from <http://en.wikipedia.org/wiki/Birefringence>

Case 4 50 y.o. female painful right knee, worse on golf course, good health, normal general exam; antalgic gait, favoring right, cool effusion in right knee, stress pain in right knee Physical: atrophy of right quads; varus alignment soft knees, means bowlegged Hard bumps of DIPS in both hands QUESTIONS

1. What was the probable course of evolution of her arthritis a. b. c. d. e.

Chronic slowly progressive Axax. (?) And remiss. With accumulation of deformity Acute with rapid progression to deformity Evolution of Crohn's disease? Repeated acute exacerbations …?

Answer: a) Chronic slow progressive course, because diagnosis was RA Gradual accumulations

2. Which 2 tests most helpful a. b. c. d. e.

EMG quads bilaterally Weight bearing x-ray both knees Bone scan Serum uric acid Arthrocentesis of right knee

Answer: B, E (I'm almost positive this is what was written but a little less sure of this) B would say joint space, loss degree of E would tell you that there's bland fluid (showed x-ray of knees, on right side medial compartment narrowed) So patients blood tests all normal, fluid clear, etc.

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So patients blood tests all normal, fluid clear, etc.

3. What least significant risk factor in the patient a. b. c. d. e.

She walks 3 miles a day She has genu varus She is overweight She is female She is 72 years old

Answer: a) point being least sign risk factor

Case 5 • 56 year old lady abrupt onset thoracolumbar junction back pain • Bed confined for 3 days • Muscle spasms on physical

1. Which of these risk factors is least significant? a. b. c. d. e.

She weights 90 points She smokes Her mother had kyphosis She is sedentary She golfs

Answer: e) she golfs • Smoking predisposes her, mother had bone problem, and she's sedentary • She had osteoporosis with fractured spine vertebral collapse; risk of fracture increases the t-score falls in patients with osteoporosis; in women fractures more common with men with ecter(?)

2. T-score -2.5; which best improve: a. b. c. d. e.

Estrogen supplementation Calcium carbonate talest (?) Vitamin d Risedronate Calcitonin spray

Answer: d) risedronate bisphosphonate Risedronate is used to prevent and treat osteoporosis (a condition in which the bones become thin and weak and break easily) in women who have undergone menopause (change of life; end of menstrual periods) and in men and women who are taking glucocorticoids (corticosteroids; a type of medication that may cause osteoporosis). Risedronate is also used to treat osteoporosis in men. Risedronate is also used to treat Paget's disease of bone (a condition in which the bones are soft and weak and may be deformed, painful, or easily broken). Risedronate is in a class of medications called bisphosphonates. It works by preventing bone breakdown and increasing bone density (thickness). Pasted from <http://www.nlm.nih.gov/medlineplus/druginfo/medmaster/a601247.html>

Osteoporosis Health Centre -

Treatment

Calcitonin

Calcitonin is a hormone secreted by the thyroid gland. It binds to receptors on the osteoclasts and decreasing their ability to break down bone. Calcitonin: • may prevent bone loss in the hip • may maintain or increase bone mass in the spine • can decrease the risk of fractures to the spine • can provide some pain relief from bone pain, especially if related to a spinal fracture Calcitonin is derived from salmon. It is available in Canada as both a drug that is injected under the skin (subcutaneously) and as a nasal spray.

Calcitonin Nasal Spray Calcitonin nasal spray is now available in Canada as Miacalcin® nasal spray. It is currently approved for the treatment of osteoporosis in women who have been postmenopausal for AT LEAST five years. The nasal spray has also been shown to reduce pain related to spinal fractures. The dose of Miacalcin® Nasal Spray is ONE spray (200iu) into one nostril per day. Women are advised to alternate nostrils from one day to the next (eg. LEFT nostril on EVEN days of the month, RIGHT nostril on ODD days). Possible side effects of the nasal spray include: local irritation, dryness or inflammation in the nose

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• local irritation, dryness or inflammation in the nose • nose bleeds Other side effects similar to the injection such as facial flushing nausea, chills or skin and allergic reactions may occur, but RARELY do with the nasal spray. Bottles of calcitonin nasal spray should be stored in the fridge before use. Women should 'prime' the pump before the first squirt is used. Each bottle contains 14 full doses. It can be kept at room temperature for one month. The cost of Miacalcin® Nasal Spray is approximately $600 per year. Miacalcin® Nasal Spray is covered by most extended (private) health care plans. It is currently NOT covered by the Ontario* Government plan for seniors. *note: Coverage of Miacalcin® varies for each province

Calcitonin Injection Calcitonin injection is currently not approved for the treatment of osteoporosis but is prescribed for people who have fractures of the vertebrae, mainly to relieve pain. When the subcutaneous injection is used, it is first given as a test dose to check for an allergic reaction to the medication. Usual treatment is for three to five days in a row, initially, followed by maintenance therapy three times a week. It is used for up to about six months. Long-term use may decrease its effectiveness. Possible side effects of the injection include: • local pain or irritation at the site of the injection • facial flushing, nausea and chills • rarely, skin and allergic reactions These side effects are temporary and may decrease with a lower dose. Pasted from <http://www.womenshealthmatters.com/centres/osteo/treatment/calcitonin.html>

3. What's her prognosis? a. Her relative risk of subsequent fractures increased 25 fold b. A hip fracture as she ages and a 20% mortality following c. She has only 25% …?

Answer: All above are true

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Week 10 Review Questions Thursday, March 06, 2008 6:00 PM

FMP 2007-2008 REVIEW QUESTIONS - WEEK 10 – RHEUMATOLOGY Approach to arthritis 1. What are major categories of rheumatic disease? 2. What are the seropositive diseases? 3. What are the seronegative diseases? 4. What is meant by symmetrical versus asymmetrical? 5. What joints are affected by osteoarthritis? 6. What are non-articular causes of rheumatism? 7. What are features of degenerative versus inflammatory arthritis? 8. What is a useful fourfold classification of functional capacity? 9. What does “avocational activities” mean? Monoarthritis 10. What are the major causes of mono-arthritis? 11. What tests should joint fluid be sent for in the investigation of a patient with monoarthritis? 12. What tests are available for viscosity? 13. What are the characteristic patterns of findings in the joint fluid for each major category of monoarthritis? 14. What is birefringence? 15. What is chodrocalcinosis? 16. What infectious cause of monoarthritis is most threatening for the joint? 17. What are the features of gonococcal arthritis? 18. What crystals cause arthritis? 19. How is gout treated in the: a. Acute phase (list four possible treatments) b. Prevention phase Connective tissue diseases 20. What is the immunopatogenesis of SLE? 21. What are the 11 criteria for the diagnosis of SLE? 22. What is responsible for deaths in patients with SLE early and late in the course of the disease? 23. What are the clinical features of dermatomyositis and polymyositis? 24. What is the most concerning underlying illness in patients with polymyositis? 25. How is the disease diagnosed? 26. What are the clinical features of scleroderma/CREST/PSS? 27. What is the pathology of scleroderma? Localized non-articular disorders 28. What is a classification of causes of shoulder pain? 29. What are the major causes of shoulder pain? 30. What is differential diagnosis of elbow pain? 31. What is the differential diagnosis of foot pain? 32. What is an enthesopathy? 33. Where does disease of the hip cause pain? 34. What are the differential diagnoses of hip pain? Spondyloarthropathy 35. What is spondyloarthropathy? 36. What are the major diseases that are spondyloarthropathies? 37. What are typical extra-articular features of spondyloarhropathies? 38. What is HLA-B27? 39. What are clinical findings in a patient with ankylosing spondylitis? 40. What are radiographic findings in a patient with AS? 41. What is amyloidosis? 42. What are the two major categories of causes of chronic low back pain? Which is more common? 43. What are the key features of inflammatory back pain? 44. What are the New York criteria for diagnosis of AS? 45. What are the two major enteropathic arthritidites? 46. What are 5 patterns of psoriatic arthritis? 47. What is reactive arthritis? What is Reiter’s syndrome? 48. What are extra-articular manifestations of reactive arthritis? 49. What are the major elements of therapy of AS?

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Pharmacologic issues 50. What is the safe limit of dosing for acetaminophen? 51. What are the toxicities of acute acetaminophen excess? 52. What are the mechanism of action and effects of NSAIDs? 53. List four categories of side effects of NSAIDs. 54. What are risk factors for NSAID gastropathy? 55. What are cox-2 antagonists? 56. Are they safer? What specific concern is there about cox-2 antagonists? 57. What strategies can be used to reduce the risk of gastric complications in patients taking NSAIDs? 58. What is the value of colchicine in treatment of gout? Side effects? 59. What are the major side effects of allopurinol. 60. List 14 side effects of corticosteroids. 61. What is avascular necrosis? 62. When does acute adrenal insufficiency occur in the context of glucocorticoid therapy, how can it be avoided, and how should it be treated when it occurs? 63. List 4 DMARDs, used most commonly for patients with RA? What are their side effects? 64. What is a treatment algorithm for mild RA? For severe RA? 65. When should DMARDS be started? 66. What are three biological agents used for treatment of RA, and what are their major side effects? 67. What is the target of these biological agents? 68. What is the impact (in general terms) of these various agents on disease outcome in RA? 69. What is rituximab? Rheumatoid arthritis 70. What are pathological features of a rheumatoid arthritic joint? 71. What joints are affected in a patient with rheumatoid arthritis? What joints are seldom affected? 72. What are the criteria used to make a diagnosis of RA? 73. What problems may a patient with RA develop related to the cervical spine? 74. What are typical abnormalities in the blood tests of patients with RA that reflect systemic inflammation? 75. What are the radiographic abnormalities seen in a patient with chronic RA? 76. What is the typical evolution of joint problems in a patient with RA? Autoimmunity 77. What are three pathways that lead to autoimmune reactions? 78. What is meant by organ-specific autoimmune versus non-organ specific autoimmune diseases, and what are examples of each? 79. Which organs tend to be affected by non-organ specific autoiimune reactions? 80. What is tolerance? 81. What is a rheumatoid factor?

Vasculitis 82. What is the overall classification of vasculitides? 83. How does vasculitis affect each of the following: a. Skin (medium versus small vessel) b. Kidneys c. Nervous system d. Heart e. Lungs f. ENT g. Eyes 84. What are the clinical features of giant cell arteritis? 85. What are the two major diagnostic tests for giant cell arteritis? 86. What is the treatment for GCA? 87. What are clinical features of PAN? 88. What underlying viral illness is associated with PAN? 89. What are three types of vasculitis associated with ANCA? 90. What are renal manifestations of ANCA-associated vasculitis? 91. What are the therapeutic strategies used for ANCA-associated vasculitis? Blood tests in diagnosis of rheumatic disease 92. What are “routine� blood tests that may be helpful in the diagnosis of rheumatic disease? 93. What is the main particular use of ESR? 94. What is CRP? How is it helpful? 95. When should rheumatoid factor be ordered? 96. What other than RA is associated with rheumatoid factor? 97. When should ANA be ordered? 98. What are the sensitivity and specificity of RF for RA, and of ANA for SLE?

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98. 99. 100. 101. 102. 103.

What are the sensitivity and specificity of RF for RA, and of ANA for SLE? What else causes elevated levels of ANA? What form of ANA is most useful for monitoring SLE disease activity? What forms of ANA are associated with scleroderma and with Sjogren’s syndrome? What is the utility of serum complements? What are ANCA? What are their antigenic targets?

Generalized pain syndromes What is fibromyalgia? What are associated complaints in a patient with fibromyalgia? What is the basis for fibromyalgia (probably)? What are elements of therapy for fibromyalgia? What is PMR? How is it diagnosed and treated? What are other causes of generalized pain?

104. 105. 106. 107. 108. 109.

Osteoarthritis and low back pain Which joints are most frequently affected by osteoarthritis? What is the pathogenesis of OA? What are clinical manifestations of OA? What are risk factors for OA? What are the elements of management of OA? What medications are available for the management of nociceptive and neuropathic pain in OA? What are red flags in a patient with low back pain? What is appropriate workup of a patient with low back pain with no red flags? What is appropriate treatment of a patient with acute low back pain?

110. 111. 112. 113. 114. 115. 116. 117. 118.

Osteoporosis What is osteoporosis? What determines bone strength? What are the frequency and consequences of hip fracture in women? What about men? What is a fragility fracture? Where do they occur? What are consequences and physical findings of vertebral compression fracture? What are major risk factors for fracture? What are risk factors for low bone mass? What are minor risk factors for osteoporosis? List 4 pharmacological agents useful in the treatment of osteoporosis. With respect to osteoporosis, what is a “T-score� and what level of a T-score is diagnostice of: a. Osteoporosis b. Osteopenia 130. What is appropriate intake of calcium at various ages (principles)? 131. What strategies are available in the management of osteoporosis? 132. What are anti-resorptive agents? What is an anabolic agent?

119. 120. 121. 122. 123. 124. 125. 126. 127. 128. 129.

Pasted from <https://portal.utoronto.ca/courses/1/Fall-2007-FMP211Y1-Y-LEC0101/content/_919091_1/FMP%202008%20week%2010%20review%20questions.doc? bsession=11327372&bsession_str=session_id=11327372,user_id_pk1=501825,user_id_sos_id_pk2=1,one_time_token=>

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0_Intro Friday, February 29, 2008

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2_Pre-Op Eval and Prep Friday, February 29, 2008

In deciding whether or not you should operate on a patient, what should you consider? (hint: _____ vs. _____?)

• Here that we need to have some sort of rational system to decide whether or not patient will benefit from surgery

What does APACHE II stand for? What is its utility? Which 3 factors does the APACHE II scoring system take into consideration?

• Assessing benefits usually much easier and more straightforward than asessing risks • Acute physiology and chronic health evaluation (APACHE) semi-quantitative way of assessing risk • APACHE II 3 factors: ○ How sick patient is when comes in ○ Patient's chronic health status ○ Indepent of how sick acutely or chronically, AGE is a huge factor; 80 year old will not tolerate surgery as well as 20 year old

• Most of patients we deal with have variety of illnesses that don't fit into these easy schemes (APACHE II) • Instead, see how many organ systemsdysfunctional ; assess each one to determine whether or not workinga nd the number not working properly giv eyou guesstimate fo risk

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APACHE-acute physiology and chronic health evaluat...[Crit Care Med. 1981] - PubMed Result http://www.ncbi.nlm.nih.gov/pubmed/7261642 Screen clipping taken: 3/3/2008, 9:42 AM

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Apart from history and physical, how would you assess endocrine organ dysfunction? Apart from history and physical, how would you assess coagulation status? Apart from history and physical, how would you assess renal dysfunction? Apart from history and physical, how would you assess respiratory system dysfunction? Apart from history and physical, how would you assess cardiovascular system dysfunction? Apart from history and physical, how would you assess hepatobiliary dysfunction?

• Renal: use serum creatinine to tell you whether or not kidneys working • Toronto historically lead centre in world for assessment of nutritional readiness of patients for surgery • Endocrine: history: are you a diabetic, do you take insulin, etc.

What kind of help do we have?

• What you do to prepare depends on urgency

T/F: Patients who are hypothyroid react poorly to general anesthesia and surgery but not patients who are hyperthyroid? • Amazing how many patients suffer from pulmonary emboli and DVT's after surgery (now that we have CT's commonly, see this commonly) • Most patients in post-op MI simply drop dead • When patient falls asleep, don't have ANY gag reflex • Patients may get pneumonia post-operatively

• Patients who are hypo or hyper thyroid react very poorly to general anesthesia and surgery

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List 2 cardiovascular system conditions and their associated treatments that you can prevent post-surgical cardiovascular complications for? • Use of anticlotting agents such sc heparin decrease sig. chance of dying from pulmonary embolus ○ If look in journal CHEST every couple of years send out special supplement describing how do DVT prophylaxis in which patients ○ Similary neurosurgical patients with tumors; hypercoagulable and more prone to get DVT and pulmonary embolus but thing you have to prevent after neurosurgery is prevent bleeding! So trickly to prevent this

Which drug class is used for ulcer prophylaxis prior to surgery?

"An ounce of prevention is worth a pound of cure"

• NOT feeding the patients is the WORST thing you can do to patients! ○ Been shown to decrease the length of time of ileus ○ Stress GI bleeding one of complications of srugery or being ill in general ○ Ulcer prophylaxis will eliminate stress bleeding or stress ulceration

List 4 preventative actions that could be undertaken to prevent postsurgical cardiovascular system complications?(6)

(Ie. How do we prevent post-operative infections?)

• To avoid kidney damage, make sure kidney is well perfused • To avoid renal damage also avoid nephrotoxins • IV contrast for CT is nephrotoxic as is genatmycin Ab

List 4 preventative actions that could be undertaken to prevent post-operative infections?(4) • OR's are cold; even a degree or two of hypothermia will result in poor outcomes • Blood is like an immunosuppresant drug; if give blood transfusion, the infection rate is higher ○ Patient who did NOT get blood transfusion during surgery is more likely to survivie cancer surgery! ○ Also in renal transplatn operation; patient who has already had multiple transfusions are less likely to reject kidney s  So can be used to one's adv., the fact that blood transfusions cause immunosuppresion ○ Prophylactic antibiotics: endless studies: will decrease rate of surgical site infection

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List 2 preventative actions that could be undertaken to prevent post-operative endocrine system complications?

• Some very influential papers in NEJM from western europe showing in ICU pop. Tight control of blood glucose greatly decreased morbitidy and mortality rates • Reasonable blood glucose control therefore improves outcomes • Problem with oriignal papers: in reality, too many episodes of hypoglycemia

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3_Pain Mgm Friday, February 29, 2008

Pain Assessment: • VAS - Visual analogue scale (impracticall at bedside) • VRS - Where is your pain 1/10 (10 worst) ○ Studies correlating VAS and VRS; correlate extremely well ○ Very important to ask for pain with movement! Not just at rest! • Grimace shown to be very accurate reflection of pain degree

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What is multimodal analgesia?

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• Pain pathway is complex but even this is an oversimplification of the pathway

• When we have tissue damage, inflammation occurs; interleukins and cytokines released; cyclooxygenase 2 is induced; makes prostaglandin E, which is necessary to activate nervous system via lowered threshold of nocicceptors and allows to fire via stimulation by substances such as bradykinin

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Gabapentin and Ketamine block the transmission of pain along which arm of the pathway of the pain pathway? Celecoxib blocks the transmission of pain along which arm of the pathway of the pain pathway? Opioids block the transmission of pain along which arm of the pathway of the pain pathway? Acetaminophen blocks the transmission of pain at which site of the pain pathway?

Which nociceptive factors does dexamethasone prevent the release of? Which is the primary nociceptive factor that is blocked through the use of celecoxib? Local anesthetic blocks the transmission of pain along which arm of the pathway of the pain pathway?

• Dexamthasone: prevents release of interleukins and cytokines • Celecoxib: block production prost. E • Can use local anesthetic to prevent it from travelling to the spinal cord • Also can put epidural or spinal in to prevent further entry to the spinal cord by blocking the nerve roots • Acetaminophen acts on COX-3; prevents on • Can use drugs like gabapentin and Ketamine: prevents sensitization of the nervous sytem; thus, prevents amplification of the pain signal • Finally, opioids, prevent transmission from spinal cord to the brain • Therefore multiple drugs, preventing pain transmission

In thinking conceptually about the prevention of acute pain, which 3 points in the patin pathway can be targeted with drugs? (hint: Initiation, …)

PREVENT ACUTE PAIN TO PREVENT CHRONIC PAIN!

Pasted from <http://www.alphachimp.com/clients/blog/pain-map.jpg>

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T/F: Preventing acute pain is a minor risk factor in the prevention of post-operative chronic pain?

• Calculated chronic pain rates correlating with surgeries • Preventing acute pain will not necessairly prevent chronic pain; not ONLY risk factor but certainly MAJOR RISK FACTOR! ALSO important to treat pain before come to hospital

• Eg. Often before do surgeries, need to make sure pain maangment is intact • COXIB'S do not affect platelet function • Eg. Patients come in for knee surgery, but taken off pain relief two weeks before surgery because of effect of NSAIDs on platelet function; so patients in pain when come into OR; nervous systems are revved up • Usually only in hosptial for 5 days and doing great analgesic regiments but then after 5 days go home on Tylenol 3's and that's the weak link; POOR MANAGEMNT AT HOME!

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T/F: Coxib's DO NOT affect platelet function?

Name 6 drugs and/or drug classes involved in multimodal analgesia?

• So if have someone on acetaminophen and ibuprofen then additive effects

What effect does acetaminophen administration have on opioid consumption? What effect does acetaminophen admnistration have on the effectiveness of NSAIDs? Does acetaminophen have any adverse effects? What effect does acetaminophen have on opioid related sideeffects?

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What effect does NSAID administration have on opioid consumption? What is CELECOXIB? What effect does CELECOXIB have on platelets? What effect does CELECOXIB have on bone fusion? What effect does CELECOXIB have on thrombosis rates? By approximately how much do NSAID/COXIBs improve pain scores?

• We know in high risk patients, increase in thrombosis and with certain NSAIDs so not a class effect but specific drug effect

• Improves movement associated pain • If go up to 1200, 1400 mg. then have to consider greater side effects

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In addition to being an analgesic, Gabapentin is also a(n) _______? The optimal dose of gabapentin is ______mg?

What effect does Gabapentin have on opioid consumption? What effect does Gabapentin have on opioid-related sideeffects? Gabepentin has additive effects with which class of analgesics? Is it Dexamethasone, Gabapentin, or Ketamine, which has anxiolytic effects? T/F: Using Gabapentin results in NO increase in adverse effects?

• No adverse effects from single dose of dexamethasone

• Speed recovery • No adverse effects from single dose

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In using dexamethasone as an analgesic, which other analgesic does it reduce the consumption of? T/F: Dexamethasone and pregabalin are in the same drug class?

• • • •

The technique that gives best movement associated pain relief Eg. Continuous femoral nerve blocks also good after knee arthroplasty Goal of nerve blocks: JUST enough nerve blocks to eliminate pain; want to keep sensory and nerve pathways Remember pain carried by C fibers, very small, unmyelinated; bigger ones responsible for motor and sensory

Oxycodone: Absorption About 60% to 87% of an oral dose of oxycodone reaches the central compartment in comparison to a parenteral dose. This high oral bioavailability is due to low pre-systemic and/or first-pass metabolism. In normal volunteers, the t½ of absorption is 0.4 hours for immediate-release oral oxycodone. In contrast, OxyContin Tablets exhibit a biphasic absorption pattern with two apparent absorption half-lives of 0.6 and 6.9 hours, which describes the initial release of oxycodone from the tablet followed by a prolonged release. P asted from <http://w w w .rxlist.com/cgi/generic/ oxy contin_cp-page2.htm>

• Major problem after colon surgery: get reflex ileus • When give someone sympathetic epidural, doesn't block vagus nerve; mean bowel is working; if block sypathetic activity and do n't block parasympathetic, then shows that the use of throacic epidurals can reduce stays in hospital down to 2 days ○ So ambulating and drinking and eating helps people get out of hospital; with epidural can start feeding and walking immediate ly • Best way to give opioids: pain/sedation cycle ○ Whereas if give constant amount of opioid, then get just enough twith therapeutic efeect and don't get side efefct; oxycontin and hydrocontin 2 oens we use; oxycontin has biphasic release profile, meaning most contins have slow time to

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Which analgesic method gives the best movement associated pain relief? Does oxycontin have a biphasic or monophasic release? The duration of oxycontin release is ___ hours?

Ketamine or Clonidine consumption will decrease the consumption of which other class of analgesics? What is a downside to the use of ketamines?

List 5 multimodal analgesics that have additive effects?

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What does PCEA stand for? List 2 drugs that reduce PCEA use?

•

PCEA: Patient controlled epidural analgesia

•

Means get an initial bolus of epidural and local anesthetic, then patient can manage extra boluses of analgesia, as needed

If use multimodal analgesia, can elminate opioids completely! Why is it advantageous to give analgesics prophylactically rather than after surgery has started?

• Advantage to giving drugs before!! Because if you give after, then cytokines and interleukins have already been produced! If give these drugs beforehand, then can prevent the relaese of these substances

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List 5 multimodal analgesia agents that improve outcomes? • Gabapentin: with ACL patients had better knee flexion and less anxiety: with breast surgery: lower incidence chronic pain at 6 months • Dexamethasone: laproscopic cholecystecomies; better outcomes, better return to function • Epidurals: less length of stay after colon surgery • Use of long acting opioids: less length of stay after knee surgery LES = lower extremity surgery

What prof would do for most surgeries

If you could use Ketamine OR Gabapentin, which would you use for intraoperative analgesia, if both were equally indicated? Why? Pre-operatively, list 4 medications and one optional medication that you would give for preoperative analgesia? Intra-operatively, list 3 medications/techniques and one optional medication that you would give for intra-operative analgesia?

• Ketamine has a higher side effect profile and gabapentin does basically the same thing so best to use gabapentin if you can

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• HAVE TO CONTINUE MULTIMODAL ANALGESIA when patient goes home!

Post-operatively, list 5 medications/techniqu es that you would consider for postoperative analgesia?(7)

: TOTAL HIP ARTHROPLASTY (usually takes 2 hours for peak effect of these drugs when given orally)

• Put spinal in to decrease sensitization of the CNS

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Give an example of dosages and medications for 4 drugs one would use for preoperative (2hr) total hip arthroplasty?(5) Out of the following 4 drugs, which one would be administered with the highest dosage preoperatively (ie. 1000 mg) and which one with the lowest dosage preoperatively (ie. 8mg): celecoxib, acetaminophen, gabapentin, dexamethasone?

Intra-operatively, which mediation would a surgeon administer via local infiltration?

• PCA: patient controlled analgesia: eliminating for most surgeries now for total hip; basically eliminated because if can manage pre-operatively then don't need postoperative PCA

Give an example of dosages and medications for 3 drugs one would use for post-operative (2hr) total hip arthroplasty?(5)

Post-operatively, 1000mg acetaminophen would be approximately every ___ hours? Post-operatively, 100-200mg gabapentin would be approximately every ___ hours?

Out of the following 4 drugs, which one would be administered with the highest dosage pre-operatively (ie. 1000 mg) and which one with the lowest dosage preoperatively (ie. 5-10mg): celecoxib, acetaminophen, gabapentin, oxycontin, oxycodone?

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IL-1 Monday, March 03, 2008 10:44 AM

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Gabapentin Monday, March 03, 2008 10:43 AM

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Cox-2 Inhibitors Monday, March 03, 2008 10:45 AM

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Oxycodone / Oxycontin Monday, March 03, 2008 10:50 AM

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Ketamine Monday, March 03, 2008 10:56 AM

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PCA Monday, March 03, 2008 10:58 AM

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5_Gallbladder & Biliary Tree Friday, February 29, 2008

List 4 factors that predispose to gallstone formation? Why does gallstone incidence increase with age? Ultimately, the 3 factors that result in gallstone incidence increasing with age are due to the fact that they all lead to ________ and thus lead to stone formation?

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List 2 populations in which there is a clear correlation between increased gallstone risk and family history? Why is there an increased risk of gallstones in patients who are morbidly obese?

List 5 diseases which are risk factors for gallstone formation?

• These risk factors are key to know • Long TPN: see in the ICU: patients who are starved are on TPN; not eating or drinking anything • Why does resecting the terminal ileum lead to formation of gallstones - because terminal ileum is area of small bowel that bile acids are absorbed from; if you don't have absorption of bile acids, then the the enterohepatic circ of bile depends on reabstorption of bile from this circulation but if don't have it then liver keeps pumpting out bile

HOW DO GALLSTONES FORM?

What are the 3 critical phases in the formation of gallstones? T/F: Prophylactic cholecystectomy is indicated in 1% of asymptomatic patients over 20 years? When is surgery recommended for patients suffering from gallstones?

• US very common now; almost always find gallstones; before, tradition was to take gallbladder out but after landmark study, found that you should not take gallbladder

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List 4 symptom complexes that patients with gallstones commonly present with? Acute cholecystitis is associate with the signs and symptoms of _____? The pain from Acute cholecystitis usually last more than ___ hours? Which well known clinical sign is positive in acute cholecystitis? In which percent of patients suffering from Acute cholecystitis is there a palpable mass and in which percent is jaundice present?

found that you should not take gallbladder

http://rezidentiat.3x.ro/eng/litbiliaraeng.files/image002.gif Screen clipping taken: 3/5/2008, 9:29 AM

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Acute cholecystitis is associate with the signs and symptoms of _____? The pain from Acute cholecystitis usually last more than ___ hours? Which well known clinical sign is positive in acute cholecystitis? In which percent of patients suffering from Acute cholecystitis is there a palpable mass and in which percent is jaundice present?

List 2 treatments that are indicated for biliary colic?

• Explainging what are the different type of symptom complexes that patients can present with.

What is bilary colic? Where is the pain from biliary colic usually felt? Where does the pain from biliary colic radiate to? After which type of meal does the pain from biliary colic usually start?

• Biliary colic is CONSTANT pain!

How can cholecystitis be picked up on ultrasound (ie. What do you look for)? List 4 diagnoses that are implicated in acute cholecystitis?(6) T/F: LFT's DO NOT increase in acute cholecystitis but do in chronic cholecystitis?

• In biliary colic, the stone obstructs the cystic duct, but here, the stone stays stuck (in acute cholecystitis), then get secondary infection; MUST TREAT WITH ANTIBIOTICS

• Positive murphy's: patient takes in big breath, and you palpate the right upper quadrant, then as the patient breathes IN, you may feel the gallbladder coming down

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Treatment of acute cholecystitis involves the administration of ___, ___, and ___? Approximately which percentage of patients with acute cholecystitis improve without surgery? When is early laparoscopic cholecystectomy indicated for patients with acute cholecystitis?

• Sympx: acute attacks of acute cholecystitis

• Means a patient will complain of vague abdominal pain that is very hard to pin down! Will say "doctor, I feel very bloated"

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• Gallbladder wall is very thin; 1mm in diameter

• Advantage of MRCP is that you avoid ERCP and thereby avoid ERCP and it gives you the DIAGNOSIS and if has stones THEN you can do the ERCP

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Generally speaking, how do the complications of gallstones present (ie. Complications related to …, complications related to …, etc.)? Are abnormal Liver Function Tests (LFTs) pathognomonic of gallstones?

If in the presence of gallstones, LFTs are abnormal, then one must determine whether they are …(3)?

What is the incidence of acute acaclculous cholecystitis as a complication of gallbladder disease? acute acaclculous cholecystitis is commonly seen after which conditions/situations? What is the presentation of acute acaclculous cholecystitis on ultrasound? What is the treatment of acute acalculous cholecystitis?

• Gallbladder performation is RARE, except for severe diabetics; 95% • Gallbladder carcinoma: a complication of chronic gallstones; almost never get unless if have stones in gallbladder; stones irritate the gallbladder of time, even with severe cholecystitis, won't have perforation wall; gallbaldder CA is a terrible disease; 1% of the gallbladders that • AIR IN THE BILIARY TREE IS NOT NORMAL! Treatment is to take out surgeons send to the pathologist contain gallbladder cancer stone from gallbladder

T/F: While in non-diabetic patients, prophylactic cholecystectomy IS NOT recommended in asymptomaic patients, the reverse is true in diabetic patients (ie. Patients who are diabetic AND asymptomic for gallstone disease should still have prophylactic cholecystectomies)? Diabetics with acute cholecystitis have a higher incidence of which 2 complications?

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How is alcohol consumption related to gallstone formation? Why should cholecystectomies be very carefully considered AGAINST in patients with cirrhosis?

• Most common cause of pancreatitis: gallstones and alcohol • Best treatment here is to get rid of the stones using endoscopic means (ERCP)

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List 3 complications of CBD stones? Transient gallstone blockage of the Ampulla of Vater leads to ___? What is another name for cholangitis? What is another name for biliary sepsis?

What is the etiology of cholangitis?

Within the context of cholangitis, what is charcot's triad?

After which surgical procedure is there an increased risk for cholangitis to develop?

Fever, Jaundice, and RUQ pain together are known as ___? How common is Charcot's triad in patients with cholangitis? What is Reynaud's Pentad?

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List 3 steps in the management of cholangitis?

List 3 different methods of biliary decompression? Within the context of biliary decompression, what does ERCP stand for? Within the context of biliary decompression, what does PTC stand for? What are the advantages of laparoscopic cholecystectomy (list 3)?(4) What are the disadvantages of laparoscopic cholecystectomy (list 2)?(3) Are cholecystectomies in Canada now done more often as open surgical procedures, as laparascopic procedures, or approximately the same? What is the treatment of cholelithiasis?

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6_Abdominal Infection Friday, February 29, 2008

Some terminology...

• Inflamatory response not only kills bacteria but inflammation sets off coagulation fibre and deposition; localization: whwerever there's it is and coagulation, a sticky goo is deposited; purpose is to prevent spread of micro-organisms • Absorption: bacteria are absorbed via lymphatics under the diaphragm • What's connecteed o the bloodstream that sucks out and kills bactera? Reticuloendothelial system

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• Diverticular disease is a benign condition of the colon; characterised by outpouchings of colon • In this case patient has perforation (pinpoint) • Left alone, this patient dies!

• Barium + stoll is LETHAL! • Other ones have PAQUE at the end

If leave alone, bacteria will accumulate and perforate; leak out and kill a person • Up to 50% depends on not the condition but for older people or immunosuppressed (such as on steroids for arthritis), then get high death rate

• Perforated diverticulitis: most likely diagnosis for pain starting in left lower quadrant rebound tenderness, generalized abdominal pain severe after 5 minutes, pain now radiating up to upper right • Fistula: abnormal connection between two epithelial lined surfaces ○ Eg. Leak from the gut to bladder or another site of the body • Renal failure one of multiple organ failures that can occur; if sustain this and survive, then will be on dialysis for the rest of your life Ileus is a disruption of the normal propulsive gastrointestinal motor activity from non-mechanical mechanisms [1][2]. Motility disorders that result from structural abnormalities are termed mechanical bowel obstruction. Some mechanical obstructions are misnomers, such as gallstone ileus and meconium ileus , and are not true examples of ileus by the classic definition [3]. Pasted from <http://en.wikipedia.org/wiki/Ileus>

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• Had small bowel lymphoma; got chemo; shrinked tumor so fast that now hole in part of bowel; feels fine; next day after chemo ends, temp goes • Age is like an immunosuppressant; also don't feel/complain about as much pain down; on high doses of steroids, immune suppresents; they don't send him • Ischemic gut: common in older people; may thrombose to a vessel supplying home; on day 5 he gets short of breath; do chest xray and see gross free air; part of the gut

What is a PEG tube?

• PEG: Percutaneous Endoscopic Gastrostomy

• Common enough that in the ICU you'll learn that when patient going sour in the icu, abdominal infection is always on the differential dx

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• Really, these are the diagnostic signs!

• Abd operation followed by organ failure, think of leaked anastomosis • NOT PICKED UP OFTEN ENOUGH! • DELAY IN DIAGNOSIS AND TREATMENT IS THE PRIMARY REASON FOR POOR OUTCOME!

• Need LOTS OF FLUID - UP TO 20L - because capillaries leak • 7 day rule: if the patient will not get meaningful nutrition for a week, needs TPN or some other kind of supplementation or else will get immunosuppressed

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7_Bowel Obstruction Friday, February 29, 2008

What is anotehr name for colonic ileus?

Ogilvie's syndrome, colonic distention resembling that caused by obstruction, but without evidence of mechanical obstruction; it is usually due to a defect in the sympathetic nerve supply. Called also false colonic obstruction.

• Intramural causes of small bowel obstruction • Crohn's disease can go on to cause stricturse ○ One common example of an intramural benign inflamatory cause of bowel obstruction ○ Another one: radiation stricturs  Thrownthis in because a number of benign inflamatory problems that can cause this; mentioned ulcers; typically in women who have been treated with a combination of external beam radiation and internal seed radiation with carcinoma of the cevix; get rctal stricturse because of proxilmity and terminal ileum also sitting behind it so get radiation enteritis  So ther are multiple benign lesions that can affect the bowel • Extramural causes of small bowel obstruction: dhesions: usually the result of a surey; wheneer operate on the stomach, in the process of healing, patients often left with fibrous bands from one arae of the body to the other; this allows a fixed point of the small bowel to kink or herniate • Basic idea is always the asme: adhesions sually from surgery; maybe also had appendicitis • Adhesive bowel obstruction therefor quite common in ER • 2nd to that and worldwide same order of magnitude: incarcerated hernias: can have a femoral aor groin hernias: cough vigorously and the neck of the henia would be pinched by the contours of the hernia: px: painful groin mass and signs and syplmtomsp of bowel obsturcution • Incarceration: • Peirtoneal carcinomatosis: many cancers in the perineal cavity: thesecan grow up and twist off any portion of bowel ○ Usually metastases: caells on the serosal aspect of the stomach will go off and break off; most common with overian cancer; usulally very diff. to treat, esp. if tumor dsn' respond to chemox • Large bowel ○ Intralumnial  Very uncommon; since bowel is so large;  Typically see what appears to be large bowel obstruction due to constipation; usually hard stool in distal ends of the rctum ○ Intramural  Number of posibilities

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Give an example of an intraluminal cause of large bowel obstruction? Give 2 examples of intramural causes of large bowel obstruction?(3) Give an example of an extraluminal cause of large bowel obstruction? Give 2 examples of intraluminal causes of small bowel obstruction? Give an example of an intraluminal cause of stomach and duodenal obstruction? Give 3 examples of intramural causes of small bowel obstruction? Give 3 examples of extramural causes of small bowel obstruction? Give an example of an extramural cause of stomach and duodenal obstruction?

□ Benign  Ibd - particularly crohn's diseaseradiation strictursre (women radiated for carx of the cervix) □ MALX:  Most common: ADENOCARCINOMA: commonly prsents with large bowel obstruction ○ Sigmoid volvulus: • So if you get bowel obstruction, what happens to you? • Clinical presenation varies somewhat as to level of obstruction and cause of obsutciton

• Early satiety: Eat breakfast okay but not much lunch or dinner; don't get hunger pangs; sometimes may compalin of vomiting

• CLASSIC PX (PRESENTATION):

List 2 common signs/symptoms of gastric outlet obstruction? List 3 common signs/symptoms of small bowel obstruction?

• Typcially presnts very acutely ; typically come to emerg within a few hours of theonset of obstruction; ason is that most of the cuases of smal bowel obstruction present suddenly: get incarcrated in a chernia , for example; raction of bowle is to peristalse with an even stronger magnitude of • Pain is felt from incrasted wasll tension in the small bowel; terrible crampy pain is mediated by the autonomic nervous sytstem so can't pinpoint location of pain because mediated by ANS

(PASSAGE OF NOTHING PER RECTUM)

• If wall tension in your colon does incrase suddenly • Should NOT have periteonale signs such as tenderness or guarding ○ Should laso not have fever or white count ○ If do see patient in emerg with bowel obstruction, want to lok for signs fo groin hernias: often miss dx of incarcerated henia

How does small bowel obstruction typically present? What is the definition of obstipation?

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With respect to laboratory findings, prolonged gastric outlet obstruction leads to ___? (in bowel obstruction)

• One exception to what mentioned: gastric outlet obstruction; vomiting gastric acid; contain slots of hcl ; so get hypochlromeic, hypolkelemic metabolic alkalosis; because of this, kidney wastes potassium to conserve othe electrolytes • Fav. For MCQ: patient comes in with bowel obstruction, give electrolytes, then what does the patient have? If has hypochloremic, hyochalemic metabolic alkalosis, then is gastric outlet obstruction

• Nowadays, don't even really do 3 views of abdomen; do CT scan; if suspecting obwel obstuction because of clnical presentation, etc. then just go straight to ct scan • CT very good at showing rare obturator hernia • Strange abdominal wall hernia: spigelian hernia

A Spigelian hernia (or lateral ventral hernia) is a hernia through the spigelian fascia, which is the aponeurotic layer between the rectus abdominis musclemedially, and the semilunar linelaterally. These hernias almost always develop at or below the linea arcuata, probably because of the lack of posterior rectus sheath. These are generally interparietal hernias, meaning that they do not lie below the subcutaneous fat but penetrate between the muscles of the abdominal wall; therefore, there is often no notable swelling. Most of these hernias are small, and, as such, there is a high risk of strangulation. Most of them develop around age 50 (4th-7th decade of life). As an entity, they are rare,[1] when compared other types of hernias. Pasted from <http://en.wikipedia.org/wiki/Spigelian_hernia>

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The laboratory finding of hypochloremic, hypokalemic metabolic alkalosis is pathognomic of ___? What is the treatment for a malignant obstruction? What is an incarcerated hernia?

If make a diagnosis of malx obstruction, then never going to get beter if you just lleave them alone; typically fixing done surgically • Nowadays, particularly, if in rctum, then can do stent placed in • Occassionally perioteneal carcinosis due to carcinoma of the ovry, then can treat with radiation ○ Not often can do this though

• Radiation enteritis: no particular treatment for it; often treat non-operatively in the hopes that it does get better on its own; often does get better • Incarcerated hernias: in children works to push on the hernia; in adults doesn't work

• Don't operate on adhesive bowel obstruction unless if it doesn’t get better • If bowel dies, then may get some form of inflamation in the area: then may get • DEAD BOWEL IN A PATIENT MAKES THEM VERY SICK VERY FAST

Closed loop bowel obstruction

Pasted from <http://www.radiologyassistant.nl/images/thmb_4543054d4a4b9cecal-volvulus4.jpg>

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Closed loop bowel obstruction Tuesday, April 01, 2008 8:48 PM

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8a_Abdominal Infections Friday, February 29, 2008

• Ulcer, appendix, diverticulum, inschemic bowel, all can perforate • Another mechanism of perforation: penetrating injury (stab wound) • Also can peforate as a result of intestinal surgery as the anastomases created by even the best surgeons can leak What do CAPER and HOPER stand for?

• Primary: ○ underlying serositis and ascites is common complication; may result in abupt change in general condition; primary means there is no obvious perforation • Secondary: ○ large number of bacteria normally present in bowel at hat level infect peritoneal spaces  CAPER: Community acquired peritonitisk  HOPER: HOSPITAL AQUIRD PERITONITIS: tend to be due to mor drug resistanct or abx rseistant bacteia; may influence management

• From the microbiological point of view, it's logical that the cause of the inffection is not going to be homogeneous • Because the gut has large numbers of different organisms, then these infections are suuslaly polymicrobial; very commonly and typically will have mixture of anaerobic organisms

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Where in the GI tract are the number of anaerobes approximately equal to the number of aerobes? Secondary peritonitis can be categorized into ___ and ___? Localized intraabdominal abscess (localized) can be categorized into which two categories?

• Begin with proximal bowel: stmach, duodenum, and proximal small bowel, number of bacteia tends to be low (10^4 per mL of fluid and most are aerobic; usually organisms that we swallow; therefore consequeces of peeforation there are far less sever and dramatic than in the distal bowel • In the small bowel: 10^8; aerobes roughly equal anaeobes but as get to colon, now 10^12 per gram of stool and there the anerboc pop outnumber the aeobic population 1000:1 or so • Most of the organisms in the proximal bowle will be aerobic; distal anaerobic

Which are the antimicrobials of choice for single agent therapy for abdominal infections?

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Approximately how long before surgery should prophylactic antibiotics be started (preoperatively)? Why may you need a second dose to be administered?

Antibiotic prophylaxis for abdominal surgery on the surgical sites of the colon and appendectomy include which two antibiotics? Antibiotic prophylaxis for abdominal surgery on the surgical sites of the biliary tract, stomach/duodenum, and small bowel include which two antibiotics?

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Is abdominal infection usually the result of perforation of the GI tract or does it more commonly sponatenously present? How can the incidence of surgical site infection following abdominal surgery be lowered?

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8b Abdominal Infections Notes Friday, February 29, 2008

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9_Intro to Anesthesiology Friday, February 29, 2008

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What are the 5 A's of anesthesiology?

• Propofol: makes people go to sleep; doesn't do anything for pain control; not part of any major drug group

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• Most common benzo is midazolam: has prominent amnesia effects ○ Story of the wimpy football player :-) • Rohipnol: what they call midazolam in the UK; most chemically resembles midazolam

• Koran patient diagnosed with pancreatic cancer; tried to kill himself stabbing with kitchen knife • ANY OPERATION IS CONTROLLED TRAUMA • Job of anesthesiologist is to keep vital signs stable

In the process of preparing someone for surgery and during the surgery is itself, when is sympathetic tone the highest?

• Stres axis is euphamism for sympathetic tone (body's esponse to stress or pain) • Opiates, muscle relaxants, propofol, have to give to counteract stress rseponse

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• NOT GOOD TO DO ANESTHESIA IN THIS PATIENT BECAUSE WILL VOMIT IN RESPONSE TO ANESTHESIA ADMINISTRATION • Jaundice: suspicious: perhaps prolems with absorption and elminiation of anesthetics • Chest pain: remember have stress rseponse with surgical sitmulus • Best therefore get all these issues rsolved before operation or at least bette managed

• Here do a ring block • If on area of the body you can't do a ring block, then just put a little lidocaine around area of wound

What is the distinction between a regional and local never block? • Distinction between a local and rgional block ○ If neve has name, then it's regional ○ In this case would do an ankle block

• Takes five needle punctures around area of the foot • All the complications of a general anesthetic can be avoided by doing spot neve blocks

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Another example of regional anesthetic

• • • •

• In this case, rathe rthan blocking small neve, block at level of the spinal chord • Diff between spinal and epidural: ○ Epidural: insert eedle patient back, just outside the dura; princple ther is that if you inject lidocain, eg. Passive diffusion into dura and into csf which pabthes spinal chord; so if you block at right level, won't feel labour pains ○ Classically use it for labour, but also for circumcision in little bbies or anything in • Spinal the lower body ○ Same procedure, through skin, ligaments, between spines, and then actually ○ Why not higher? C345 Local anesthetic options: specific nerve blocks around the cervix through the dura; much smaller needle, then give a much lowr dose, and keeps the diaphragm one shot (because don't have to worry about diffucison of meds); principle is Early in labor most of pain coming from cervical dilation alive..put patient in rsep the sam though, blocking nerve impulses General anesthesia is too much for labor failure  What's the highest you can do this at? Midline solution is the epidural (spinal) ○ Can do an epidural □ Sinal tap is L1 or L2: where the spinal chord ends thorugha big enough lneedle and can put tubing into needle, so that can have contninuous infusion of anesthetic meds; handy because duration of nedle is unknown

What is the difference between an epidural and a spinal? What effect does ketamine have on sleep? • Ketamine causes TERRIBLE NIGHTMARES

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Skipped everything until here (from gen. anesth. Slide)

Malignant hyperthermia typically occurs in response to administration of which anesthetics?

KNOW MALIGNANT HYPETHERMIA FOR EXAM!

Ventricular fibrillation

• Classic description of MALIGNANT HYPERTHERMIA!

• Mechanism of action: due to a mutation in the ryanodine rceptior which is responsible for calcium uptake in SR in skeletal muscle, so what winds up appening is that the raynodine rceptor is mutated and these patients end up having an enormous amount of intracellular calcium; body is constantly spending ATP to equalize the intracellular calcium; so atp pumps draining calcium from intracellular calcium and this is exothermic, so get hypethemia • Calcium metabolism causes rhabdomyoliysis, ATN, (see below)

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Is malignant hyperthermia autosomal dominant or recessive? T/F: The penetrance of malignant hyperthermia IS NOT variable? What is the approximate incidence of malignant hyperthermia? What is the incidence of malignant hyperthermia caused secondary to nitrous oxide administration?

NMS DOES NOT EQUAL MHS (MALIGNANT HYPERTHERMIA SYNDROME)

• Dantrolene blocks the ryanodine receptor

• Should differentiate this from malignant hyperthermia

• 2.5mg/kg is usually a large dose but it comes in small volumes so have to usually open up 5 bottles and it comes in poder and it comes like sand; takes a while; dilutes like sand; very difficult to administer

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What is malignant hyperthermia? What is NMS (neuroleptic malignant syndrome)? How are malignant hyperthermia and neuroleptic hyperthermia syndrome different? What is the treatment for malignant hyperthermia? Prior to the use of Dantrolene as a treatment for malignant hyperthermia, what was the mortality rate from malignant hyperthermia? T/F: Malignant Hyperthermia is the modern name of Neuroleptic Malignant Syndrome?

Propofol Friday, March 07, 2008 10:23 AM

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Halothane Friday, March 07, 2008 10:24 AM

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Midazolam Friday, March 07, 2008 10:30 AM

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Digital Ring Block Friday, March 07, 2008 10:42 AM

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Obstetric Anesthesia Friday, March 07, 2008 10:50 AM

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Malignant Hyperthermia Friday, March 07, 2008 10:56 AM

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11_Pre-Op Prep Friday, February 29, 2008

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• Diverticulitis very uncommon in young patients so would do CT to confirm diagnosis and assist in preoperative planning

• What are the downsides of doing a CT ○ CT is not insignificant radiation ○ Time

• LFT is so low in healthy people that it wouldn't be useful to do • Would you give fluid? Depends on whether hypotensive or hypertensive - 100cc an hour for a normal 70 KG male, maintenance • Antibiotics preoperative - against gram negatives, anaerobes, and gram postiives (on skin) ○ Once the appendix is out, we don't really need give more Abx's ○ NPO before surgery  Because of risk of aspiration; general anesthetic with layngyscope then will vomit and aspirate ○ Analgesia - morphine • INFORMED CONSENT! ○ Risks - if I need blood, they can give me blood ○ What is chance I can get HIV? About 1/10^6 ○ 1/50,000 risk for hepatitis C ○ Risks associated with srugery bleeding and need for transfusion and then transmission of viral illness, ABO incompatibility, hypoethermia ○ Risks of the general anesthesia: infection: Wound infection: 5 to 10% of patients who have appendectomies

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 Wound infection: 5 to 10% of patients who have appendectomies  Will likely heal secondarily  Perforation during surgery: cecum, terminal ileum  Also talk about complications that are rare but important ○ Talk about risks and benefits ultimately then: risks of not having operation ○ If it hasn't perforated, then will have risk of perforation  Appendix will perforate and get gram negative bacteria and develop intraabdominal abscess and then travel through portal vein and settle into liver abscesses

• What would you do differently if patient was a 12 week pregnant 19 year old woman? ○ No CT US instead ○ 10-11,000 normal WBC for woman

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•

Colonoscopy: Find other lesions as 5-10% will have synchronous tumors

• Jehova witness Sign consent that Absolutely would not want to be trasnfused with any blood or blood products • Get factor VIII concentrate intraoperatively

• What if guy is 82, diabetic, leg amputation, dbtc, tumor in rectum ○ Ablation! Can do endoscopic ablation; or cryotherapy (don't have seame durative bneefit); so other options besdies abdominal curative resection

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• No good chemotherapy for gastric carcinoma • No survival benefit for stage IV gastric carcinoma

palliation

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truss truss (trus) an elastic, canvas, or metallic device for retaining a hernia reduced within the abdominal cavity.

Referral, second opinion; tell them that you won't do it but they have the right to choose another surgeon

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12_Post-op Care & Complications Friday, February 29, 2008

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• Mnemonic for post op order is DAVID • Crepitus for wound is feeling of subcutaneous emphysema

D: Diet A: Acitivity • V: Vitals • I: Investigations/nursing orders • D: Drugs • •

• Physical exam: start with vitals; temp: 39.2; looks sick • Resusitative fluid (100cc saline is maintanenance so neeed more than that) • Examine the wound: pinkish erythema; sore on touch, crepitus ○ Comes with comunciation with organ that has air in it or gas filling organisms (this is for creptisu) ○ Gas forming organisms cause necrosis and thrombosiss, necrotiszing fasciitis ○ So if you feel this, ALAWAYS OPEN THE WOUND ○ If you feel fluctuance and you feel erythema, then prob. Subcu. Abscess; no point to being trapped under skin ○ Open wound and get foul smelly think darksih tissue fluid;  Irrigate really well then culture it! Want to know what this is! • Send culture to lab: send gram stain in 12 hours • Also listen to chest and send a urine specimen

• Post-op: hypotensive with oligouria:

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Abdominal perineal resection

• Hypovolemia: related to bleeding • Cardiogenic shock: maybe patient having an MI • Maybe having PE: pulmonary embolism (can cause hypotension and oligouria)) ○ Post-op diff:  Bleeding  Third space loss  Sepsis □ Cardiogenic (MI) □ Obstructive (PE)  Transfusion reaction □ If Hb post-op was low • 1st thing: bang in 2L of ringer's lactate to resuscitate ○ Ask patient questions:  Chest pain? SOB? When did this start? Any pain anywhere? □ Says no chest pin, breathing fine, lightheaded  Maybe anemic □ Had MI two years ago on aspirin since; got betablocker pre-operatively  O/E: check JVP □ Don't mix up fluid status with intravascular volume □ Auscultate; listen to chest for crackles □ CBC, HB check stat □ INR, PTT takes 30 to 40 minutes; CBC 10 min if stat!  3rd space: capilaries become leaky in surgery: absorb third space loss after leaked out of capillaries

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(from Tuesday case)

• NPO, NG tube stays in! • Will have significatn gastric ileus

• DDx: PE, PE, PE! • H&P • Priority: bring up O 2 sats; low O 2 causes lots of anxiety; make sure IV's are secure ○ May go into R. ventricular failure ○ V/Q scan can make dx of (ventilation perfusion scan) nuclear med study; gas venilated to perfusion ○ Angiography ○ CT/A (ct angiography)  Of chest, in 2008 this is most senstiive way; will see pulm onary arteries and tributaires and will see an abrupt defect □ So what do now? Normal cx, sinus tachycardia, bp 100,  Thrombolysis ◊ Indications ► Time ► What lowers their clotting capacity more: TPA ► Want to make sure therefore that patient's clot burdern is significant enough ; then give TPA ◊ Contraindications ► Pregnant ► Just had surgery (unless acdcept risk that she'll bleed); with heparin,  Heparin (tradiitonal common lytic therapy) - prevents further clot proposation from wherever clot coming from; clots most likely in pelvic veins so heparin would prevent clots from travelling to lungs; this would be routine post-op  Remember this person has CA ○ Chest Xray  Most common finding in PE is no blood going to parts of lung; see NO VASCULARE MARKINGS on x-ray  Most common finding: NORMAL, doing cx to exclude pneumonia, CHF, pneumothorax, lung collapse…other dx's that cuase these findings ○ Cardiac enzymes and EKG on every patient short of breath!  On cardiogram: have SINUS TACHYCARDIA (rhytm is normal bur rate is up)  Make sure has no electrophysiological abnormalities □ in MI will have depressed segments  Also want blood gas  MUST do cardigram and MSUT do chest xray

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Answers to Pre- Post- Op Scenario Seminars

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Week 11 Review Questions

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1_Intro Trauma Friday, March 14, 2008

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2_Mgm Airway Breathing Friday, March 14, 2008

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3_Hypotx in Trauma Friday, March 14, 2008

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4_Thracic and Abd Trauma Friday, March 14, 2008

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• Can get lots of false positives and negatives

• Injury to spleen often accumulates between spleen and kidney • Usual way assess abdomen in trauma room

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• Never used to diagnose specific injury; looking for free fluid (blood)! • Need 400cc of blood in abdomen for it to be seen on FAST; so what you can do is repeat it

• CT: SHOULD NEVER BE IN A CT SCAN WITH A HYPOTENSIVE patient

• Excellent for solid organ; not that good for hollow organ injuries • May see extravasation of contrast; need to go to OR or do angio suite since surgeon can embolize it

• If gunshot has penetrated peritoneum, then the patient needs surgery; incidence of intra bdominal surgery to some structure is very high so need surgery

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(and you have an indication that there's blood in the abdomen)

• Ful laparotomy; pack all 4 sponges and take out one at a time to see if bleeding from any 4 quadrants; can get liver bleeding stopped, etc.

• If you stay there and try to fix all injuries, then patient gets lethal triad, and patients die • Bleeding from a liver (can't take liver out) the more you touch it, the more it bleeds; for a bleeding spleen the spleen can take it out • One downside to damage control laparotomy: bowel will be more restrictive; if do all this and close the abdomen, presure will be very high; if have ongoing oozing, then the pressure goes swso high that you get renal failure and bowel ischemia and more acidosi s; increased pressure to thoracic cavity and collapse aof lung and get hypoxemic and hypercarbic; all this if you close it up; so instead leave abdomen open and put special expanisve dressing on it ○ Increased pressure of abdomen following this called abdominal compartemtn syndrome

• Become now a role for non-surgical manamgent; if hemodynamically stable, then can admit to icu • Usually leave packs in abcomen in damage control lapartotomy

• Increased abdomeinal pressure: usually 20-25 mmHg • And end organ dysfunction • Treatment for ACS is open abdomen, fasciaand skin and put some dressing on it

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5_Cerv Spine and Spinal Cord Trauma Friday, March 14, 2008

• In blunt trauma, the overall incidence of inuries to the cspine specifgically is about 2 to 3 percent • Includes fender benders s and all other kinds of trauma • If look at fender benders, fall from low height, etc, then about 1% have c-spine; in high energy, 1 in 10 chance • ANY injury above the clavicles high chance of c-spine injuries

• Missing an injury to c-sine: disastrous consqcs

Common reasons why people miss c-spine injuries

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• Incidence of patients worsening neurologically after reaching hospital is 2 to 10%

• Chin lift or jaw thrust DO cause movement of cspine; if doing this, MUST immobilize the spine still; have to hold head to s that neck doesn't flex or extend when do jaw thrust or chin lift

• NOT ENOUGH to simply put a soft collar on neck • Patients who have hard collar put on can still felx, rotate and laterallly flex; need to put more than just a hard collar on; need to put sand bags or iv bags beside neck • LOG ROLL AT ALL TIMES UNTIL PATIENT DETERMINED TO HAVE NO INJURIES

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If meet all 4 criteria, then can say have cleared the c-spine

• No pain with rotation, flexion, extension of the c-spine

• Remember CT scan is done IN AXIAL PLANE; cuts maybe in the same plane as cuts or between cuts; but can now reconstruct images; so if have qualified neurosurgeon or orthopedic or radiologist, then radiologically, that spine doesn't have any bony injuries; BUT you can have a normal CT scan but can have a ligamentous injury; SO NOT ENOUGH TO JUST DO A CT scan

• What about patients who don't have normal sensorium? Keep the collar on until have normal sensorium; what about if they have a head injury? If not normal sensorium; because the incidence of a ligamentous injury is so low, most neurosurgeons if patient has normal CT scan then a lot of neurosurgeons will take the collar off; if leave on then many problems can occur; imapir venous drainage from brain, ulcers on occiput, etc. • NEVER DO FLEXION OR EXTENSION VIEWS ON NECK • MRI is fantastic for soft tisues so if patient has bad head injury, then will most likely get MRI • If a patient even has minor injuries, but have lot so fnarcotics, then will still image the c-spine

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If CT scan normal, can still have a ligamtneous injury; must examine again to make sure don't have any ligamentous injury; this is not common but big problem is that the consequences of missing it is that the consequences are disastrous

• Complete: spinal cord function below level of injury is TOTAL; the impulses from above are NOT getting past area of injury

Level of lesion;

• Sacral nerves are spared (sacral sparing); may be indication of incomplete injury

key is loss of reflexes; with complete inuries, have the reflexes but are overactive often

• With vulvar cavernosus reflex, lose the reflex of

• If you have a C6 injury, you lose all motor and sensory below

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If CVP is higher than CSF pressure then use CVP pressure

• Eg. If have T8 lesion and have full bladder, the sympathetics below T8 will be stimulated; all the sympathetics above will hvave some kind of modulation from higher function; if have c-spine injury, get refelxf rom t1 to l2 so get hypertension below and bradycardia above

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Intercostals can helps you draw air in; if only have diaphragm; under normal circumstance may be adequate but if have asthma attack

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6_Neurotrauma - Brain Injuries Friday, March 14, 2008

• Google brain trauma foundation for great resources related to this lecture

Don't have to know actual numbers; appreciate drastic nature of TBI

• It strips the dura off inside of skull but held in place because the dura is very adeherent all around • Therefore, looks like a lens • Classically have lucid interval here • In older people, because brains have atrophied, can accommodate more injuries to skull • Usually MMA temporal bone injury: high risk for epidural hematoma

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CONTUSION; really hematomas in the brain

SUBDURAL HEMATOMA

• Look at diff: instead of being lens shaped, here dura is still attached to inner table of cortex; usually due to bridging veins; from inner table of skull into brain; get torn and you get subdural hematoma

White: skull (bone), blood, or contrast • So if you're doing an abdominal CAT scan, do head ct first because…

Diffuse axonal injury

• Diffuse axonal injury: shearing of the brain; disrupt millions of axons; CT scan can be very normal • Normal CT with bad neuro

• GCS: devised in 70's • Very useful to follow patient's progress • Also great for communication

• CRUCIAL TO KNOW THIS; use it not only for brain injuries BUT ANY NEUROLOGICAL IMPAIREMENT, IE. STROKE • Supraorbital pressure best to assess pain; sternal rub leaves marks

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Ie. GCS drops from 12 to 8, then ct head

• Hypoxemia and hypotension together in a patient with severe TBI, then 80 to 100% death • By the time see them in the hospital, they've already had their injury • Maintain CPP (Mean arterial presure - ICP); normal CPP = 90 mmHg; normal ICP about 10mmHg

• How opitimize cerebral perfusion pressure?

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If ICP increases, you can herniate

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Veins of skull drain into internal jugular (mainly right) • If spine not clear and hypotensive patient • Trandellenburg is head down; reverse trandellenburg is head up

• If you're hyperthermic, then need to prevent and treat hyperthermia • Remember CAN HAVE NON-CONVULSIVE SEIZURES!

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7_Organ_Tissue Donation Friday, March 14, 2008

Within the context of organ donation, what do NDD and DCD stand for? Can tissue donations come from organ donors? Organ donation can result from which two types of death? How long after cardiocirculatory death must tissue be acquired in order to be used for tissue donation?

• Hospitals DON't accept spinal cord donations following death • Donation can come from anyone who dies from any cause

List 3 conditions associated with Neurological Death Donation?(4) In order for Neurological Death to be diagnosed, which 3 conditions must absolutely be met?

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Canadian medical standard for the neurological determination of death (NDD) require that which 6 factors be fulfilled? If the 6 factors from the minimum clinical criteria CANNOT be fulfilled, then what types of ancillary tests can be done?

Clinical examination for NDD requires that there be bilateral absence of ‌(4)? Clinical examination for NDD requires that there be absence of ‌(3) (list the NON-bilateral absences )? T/F: There are NO additional requirements for the clinical examination for NDD in very elderly patients (>90 years old) OR infants (under 1 year)? How is the apnea test performed?

T/F: Ancillary testing is done IN CONJUNCTION WITH and NOT AS A SERIES OF STANDALONE CONFIRMATORY TESTS for NDD?

What 2 types of cerebral imaging studies could one do to investigate neurological death?

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TGLN = Trillium Gift of Life Network

• These patients still have reflexes; can blink back and forth and can answer yes and no; can be very ethically challenging when have these kinds of situations; • Next of kin therefore usually decision makers • What that involves: they decide to withdraw life suppolt; first and foremost decision has to be firmly made then the decision can be made for donation; decision made with the attending team! • If the family do decide to go forward with donation then wait the adequate amount of time depending on which hospital you were in and it 's very fast and diff. process from most of regular donors (for those after cardiac death (maintained right up to withdrawal process)

• Use the person's name in expressing sorrow/regret over their death; avoid medical jargon; often times patients don't understand; if they did get the message, you can ask ○ "so what is your understanding of what just happened?" ○

"We are very sorry that [John] has died"

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8_Tues Sem Friday, March 14, 2008

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List 3 muscle groups that are involved in the mechanics of inspiration? Which muscle groups are involved in NORMAL expiration?

Central chemical control of breathing is via pCO2 or PO2? Peripheral control of breathing is via PO2 and H+ or pCO2?

List 3 common reasons for malfunction of the central nervous system components of the respiratory system?(4) List 3 common reasons for malfunction of the neuromuscular system components of the respiratory system?(5) List a common reason for malfunction of the chest wall and diaphragm components of the respiratory system?(3) List 2 common reasons for malfunction of the airway components of the respiratory system?(4) List 3 common reasons for malfunction of the pulmonary parenchyma components of the respiratory system?(4) List a common reason for malfunction of the blood vessel components of the respiratory system?(2)

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The horizontal fissure is located on the right or left lung?

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09 FMP 2008 THURS Trauma Radiology Seminar Notes.pdf

<file://C:\Documents and Settings\Mr. Intensity\My Documents\1Medicine\2ndYearFiles\1FMP-2007\Week12\09 FMP 2008 THURS Trauma Radiology Seminar Notes.pdf>

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FMP 2008 Trauma Week Q & A - PART 1.pdf Tuesday, April 01, 2008 10:20 PM

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FMP 2008 Trauma Week Q & A - PART 2.pdf Tuesday, April 01, 2008 10:20 PM

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FMP 2008 Trauma Week Q & A - PART 3.pdf Tuesday, April 01, 2008 10:20 PM

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Week 12 Review Questions Saturday, March 22, 2008 5:30 PM

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00 FMP 2008 Week 13 Intro Pages.pdf

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Pain Week Student Manual 2008 Saturday, March 22, 2008

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T/F: almost all acute and cancer pain can be relieved? T/F: a patient's self-report of pain should be used whenever possible?

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T/F: while there many different types of pain, such as acute, recurrent, chronic noncancer and cancer related pains, most people usually have more than one type.

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