fmp2-summary of all notes 2
TRANSCRIPT
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Hereditary Colon CancerSunday, February 17, 20081:58 PM
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FMP 2008 week 09 review questions
What are the different patterns of liver to injury?1.What are the elements of “fibrotest”?2.What are the tests that actually assess liver function?3.How can liver fibrosis be diagnosed?4.What liver enzymes can have their level elevated in the setting of hepatitis?5.What are enzymes of cholestasis?6.What causes “mild” hepatitis with ALT > AST? Of AST > ALT?7.What are genetic causes of liver disease, what are the clinical features of each, and how can they be treated?8.Which causes of viral hepatitis are vaccine-preventable?9.Which causes of chronic viral hepatitis are treatable?10.What is non-alcoholic fatty liver?11.What are 36 drug causes of hepatitis? (just kidding)12.What is autoimmune hepatitis?13.What causes severe hepatitis? (What constitutes “severe” in this context?)14.What causes cholestasis?15.What is primary sclerosing cholangitis?16.What is primary biliary cirrhosis?17.
Liver enzyme abnormalities
What are the 5 major types of viral hepatitis?18.What are the clinical features and clinical course of hepatitis A?19.How is hepatitis A transmitted?20.How is hepatitis A managed?21.Who should receive the hepatitis A vaccine?22.How is hepatitis B transmitted?23.What are clinical features of hepatitis B?24.How is hepatitis B infection diagnosed? What is the relevance of tests for hepatitis B e antigen and antibody?25.What are the serologic patterns of infection with hepatitis B that recovers, and that stays chronic?26.Who should receive hepatitis B vaccine?27.What are sequelae of chronic viral hepatitis?28.What are the available treatments for chronic hepatitis B?29.Who should receive treatment for chronic hepatitis B?30.How is hepatitis C transmitted?31.What is natural history of hepatitis C infection?32.What is treatment of chronic hepatitis C?33.What is hepatitis D?34.What is hepatitis E?35.What is hepatitis G?36.
Viral hepatitis
What is dysphagia?37.
What are the major causes of dysphagia?38.
What is a reasonable algorithm for the diagnosis of dysphagia?39.
What is odynophagia?40.
List three treatments for achalasia.41.
What is the mechanism of GE reflux in most cases?42.
How can the diagnosis of reflux be confirmed?43.
What are the major complications of GE reflux?44.
What is esophagitis?45.
What is Barrett’s esophagus?46.
What is the key element of treatment of GE reflux?47.
What is the mechanism of parietal cell acid secretion?48.
List 5 proton pump inhibitors.49.
Esophageal disorders
What is dyspepsia?50.
What is the commonest cause of dyspepsia:51.
Dyspepsia and peptic ulcer
Week 9 Review QuestionsThursday, March 06, 2008
5:59 PM
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Overalla.
That has an organic basisb.
What is the commonest cause of dyspepsia:51.
What are other important causes of dyspepsia?52.
What laboratory tests are appropriate for work-up of patients with dyspepsia?53.
What are the two major underlying causes of peptic ulcer disease?54.
What is Zollinger-Ellison syndrome?55.
What are complications of peptic ulcer disease?56.
What is H. Pylori?57.
What are complications of H. pylori?58.
How is H pylori treated?59.What are the potential effects of NSAIDs on the GI tract?60.
Why do NSAIDs lead to peptic ulcer?61.
What is the best way to diagnose peptic ulcer disease?62.
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?
63.
What are the major causes of upper GI bleeding?64.
What are three high risk unusual causes of upper GI bleeding?65.
Hematemesisa.
Melenab.
Hematocheziac.
What do the following terms mean?66.
What is the natural history of bleeding due to peptic ulcer disease?67.
What are the prognostic factors related to overall outcome in patients with upper GI bleeding?68.
What is the general mortality rate in patients with upper GI bleeding due to peptic ulcer?69.
What are endoscopic findings that predict an adverse outcome in patients with upper GI bleeding due to peptic ulcer?70.
What are general supportive measures related to management of patients with upper GI bleeding?71.
What are specific therapeutic measures for patients with upper GI bleed due to peptic ulcer?72.
What are indications for surgery in patients with upper GI bleeding?73.What leads to esophageal varices?74.
What are risk factors for bleeding among patients with esophageal varices?75.
What are adverse prognostic factors for bleeding esophageal varices?76.
What specific therapeutic modalities are available for bleeding varices?77.
What is octreotide?78.
What is TIPS?79.
What are major causes of lower GI bleeding?80.
What are the major investigative modalities available for lower GI bleeding?81.
What is a Meckel’s diverticulum?82.
Gastrointestinal bleeding
What are the two major causes of acute pancreatitis?83.
What are the additional important causes of acute pancreatitis?84.
What do patients with acute pancreatitis complain of?85.
What are the major physical findings in a patient with pancreatitis?86.
What laboratory tests are most helpful in the diagnosis of acute pancreatitis?87.
What are other causes of hyperamylasemia?88.
What imaging tests are helpful in diagnosis of acute pancreatitis and its complications?89.
What are the local complications of acute pancreatitis?90.
What are the major elements of treatment?91.
What is the role of endoscopy in the therapy of acute pancreatitis? 92.
Acute pancreatitis
What causes acute diarrhea?93.
What causes chronic diarrhea?94.
What are major causes of bloody diarrhea?95.
What tests are appropriate in a patient with chronic diarrhea?96.
Diarrhea
What are the major differences in the histopathology of Crohn’s disease versus ulcerative colitis?97.
What are the locations of Crohn’s disease in the GI tract?98.
How does IBD present?99.
What are intestinal complications of IBD?100.
What are the extraintestinal manifestations of IBD?101.
What items are appropriate to consider in the differential diagnosis of the patient with suspected IBD?102.
103.
Inflammatory bowel disease
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What factors on history, physical exam and lab testing contribute to the assessment of disease severity in a patient with IBD?103.
What are the major treatment options for patients with Crohn’s and those with UC?104.
What is infliximab?105.
What is azathioprine?106.
What is 5-ASA?107.
What are adverse effects of corticosteroids?108.
What is cyclosporine?109.
What is budesonide?110.
What is methotrexate?111.
What are indications for surgery in patients with IBD?112.
113.
What are the pathologic features of cirrhosis?114.
What are the causes of cirrhosis?115.
What are the physical findings of cirrhosis?116.
What are the laboratory test abnormalities seen in patients with cirrhosis?117.
What are the elements of the Child-Pugh-Turcotte prognostic scale?118.
What are the major complications of cirrhosis?119.
What is the pathogenesis of cirrhotic ascites?120.
What are the elements of management of cirrhotic ascites?121.
What is a paracentesis?122.
What are the major indications for liver transplantation?123.
What is fulminant hepatic failure?124.
What are symptoms associated with jaundice, and how do they help to differentiate the causes?125.
Pathologicallya.Clinicallyb.
In terms of treatmentc.
What are major differences between Crohn’s disease and ulcerative colitis:126.
What are the major complications of portal hypertension?127.
Diagnoseda.
Treatedb.
How is spontaneous bacterial peritonitis:128.
What are the indications for liver transplantation?129.
What are the clinical features of sclerosing cholangitis?130.
What is the pathogenesis of cirrhotic ascites?131.
What is a TIPS procedure? 132.
Liver failure
Colon cancera.
Esophageal cancerb.
What is appropriate screening for:133.
GI cancer screening
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 MaterialFriday, February 22, 2008
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01 ALBERT 2008 Intro to RheumatologyFriday, February 22, 20085:24 PM
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Give an example of a
non-inflammatory, non-immune rheumatoid disorder?Give an example of an
inflammatory, non-immune rheumatoid disorder?Give 3 examples of
inflammatory, autoimmune rheumatoid disorders?(4)
Fibromyalgia and
osteoarthritis are both categorized as: 1. Inflammatory, Non-immune; 2. Inflammatory, Non-
immune; or 3. Inflammatory, Immune? Some "non-articular"
disorders and crystal arthritis (such as gout and CPPD) are (inflammatory or non-inflammatory) and (immune
or non-immune)?Give 4 examples of non-
inflammatory, 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?
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?
Autoimmunity results from
failure or breakdown of tolerance in ___, ___ or both?
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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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List 4 serological
indicators that may be positive in Reumatoid Arthritis?(5)
T/F: there are
extra-articular features in RA?
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.
•
Pasted from <http://www.nutritionperspectiv es.com/O ther/siteGlossary .cfm>
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In RA, there is edema of the
___ membrane with redundant folds and vil l i?In RA there is a (HYPO or
HYPER) plastic synovial l ining layer?
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Is a hyperplastic
synovial membrane present in early or established RA?
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The strongest
evidence for a genetic l ink in RA comes from evidence that the
___ genes are associated with RA?List 3 environmental
and/or l ifestyle 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?
List 3
inflammatory mediators involved in RA?
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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 lefluonmidecounteract the actions of which cell in the pathogenetic progression of Arthritis?
In the management of
Arthritis, cytokine neturalization drugscounteract the actions
of which cytokines in the pathogenetic progression of Arthritis?In the management of
Arthritis, Rutizimabcounteracts the actions
of which cells in the pathogenetic progression of Arthritis?
While both Etanercept
and Infl iximab 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 anti-TNF antibody?
IL-1 receptor
blocker
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?
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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 anti-TNF antibody?
IL-1 receptor
blocker
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?
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Seropositivity is the presence of a certain antibody in a blood sample. A patient with seropositivity for a
particular antigen or agent is termed seropositive.
It i s not a neutral term, as in popular perception seropositivity i s used most commonly in reference to HIV
seropositivity. It i s also used (though less frequently) to refer to Rheumatoid factor.Pasted from <http://en.wikipedia.org/wiki/Seropositivity>
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>
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
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 non-articular Arthritis be classified into?
02 BOOKMAN 2008 Clinical Evaluation of ArthritisFriday, February 22, 2008
5:24 PM
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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?
What is podagra?
Spondylitis: inflammation of the
vertebrae; called also rachitis.
•
Which of the following
has asymmetric spine involvement: Ankylosing spondylitis, or psoriatic arthritis?
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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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A tophus (Latin: "stone", plural tophi) is a deposit of crystallised monosodium urate
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?
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 arthritisList 4 Activities of Daily
Living (ADLs) that are used in the clinical evaluation of arthritis?(6)
What are tophi?
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([email protected],dor@d/12300762.pub)&sword=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).Pasted from <http://w iserw iki.com/Diagnostic_Imaging_of_Rheumatologic_Disorders>
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A tophus (Latin: "stone", plural tophi) is a deposit of crystallised monosodium uratein 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?
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?
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.
○
Eburnation: e"b6r-na1sh6n) [L. ebur ivory] 1.
the conversion of a bone into an ivory-like mass.
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 ___?
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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 DisordersFriday, February 22, 2008
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(meaning a rash with a round or oval shape)
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. Pasted from <http://www.medterms.com/script/main/art.asp?articlekey =5467>
The pathogenesis
of SLE can be broadly categorized into which 4 main
categories?
List 9 criteria
included in the 1997 Revised Criteria for the Classification of
SLE?(11)
What is serositis?
A mnemonic for SLE diagnostic criteriaLike 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 MDArthritis
Renal disease (proteinuria, cellular casts) ANA (positive antinuclear antibody) Serositis (pleurisy or pericarditis) H aematological disorders (haemolytic anaemia or leucopenia or lymphopenia or thrombocytopenia)
PhotosensitivityOral 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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Anti -Sm is an immunoglobulin specific against Sm, a ribonucleoprotein found in the cel l nucleus.
•
Rare in UK; mainly found in West Indians with SLE. Not found in any other diseases, only in SLE. However, only 30% of patients with SLE have a pos itive anti-Sm test.
•
A pos i tive test means - A pos itive test usually means
that lupus is present.
•
A negative test means - Does not mean that lupus is not present. Most people with lupus have either anti-DNA or anti -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?
In SLE, leukocytes,
lymphocytes, and thrombocytes are all (reduced OR increased)?
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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 il lness in which there's inflammation in only
two organs; happens in children and adults
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
•
Dermato/Polymyositis
is a disease in which inflammation may be present in which 2 organs?
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Nonspecific rashUpper eyelid in patients with dermatox/myox often has a
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
•
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
•
Inflammation in muscles
Dermx - may be due to immune comlex's
Polymositis wihtout the skin,k seems imp mech is lymphocytes tat are cytotoxic agains the muscle
Dermatomyositis or the myositis by iteself may have 2 dfft mechs
○
So what causes this?•
Purple
discoloration, or a purple heliotrope rash, on the upper
eyelids of patients is very pathognomonic of which disease?
T/F: Patients with
dermato/polymyositis 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:
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
•
Scleroderma = progressive systemic sclerosisEverything we've talked about today is about the tissue getting
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
•
R = reynaud's phenomenonWhen 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
•Sclerodactyly: tightening of tissues in the fingers
•
Skin tightening can be so drastic that actual tissues are choked! Bone is even choked out!
• 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
•
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 auto-antibodies present in
their blood?
The mnemonic
CREST, relating to the symptoms of scleroderma, stands for…?
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As tissue is being choked, there's a tendency to lay down C = calcinosis (laying down of calcium under the fingers
X-ray of calcinonsis
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
•
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
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 womenSecond inflmmation was also inflammation in skin and muscle, but this only a herald of skin and muscle problems
○
Lupus story:
Final disease: due to prorressive narrowing and obliteration of blood vessels
T/F: patients with
scleroderma and those with reynaud's henomenon in
general tend to lose peristalsis in the esophagus?
Weakened Intima
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Spectrum of Seronegative Diseases
Ankylosing spondylitis
Enteropathic Arthritis
Reactive Arthritis
Psoriatic Arthritis
List 4 subsets of the
spondylarthropathies?There is an overlap
between AS and which 3 other spondylarthropaties?
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 extra-articular
manifestations?
List 2 different types
of enteropathic arthritis's?
04 ALBERT 2008 Seronegative SpondyloarthropathiesFriday, February 22, 2008
5:25 PM
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Where is the
entheses located?What is
enthesitis?
seronegative spondyloarthropathies○
Spondyloarthropathy: disease of the joints of
the spine.
•
spondyloarthropathy
Pasted from <http://127.0.0.1:8080/rami?COMMAND=applyStylesheet([email protected],dor@s/12751920.pub)&sword=12751926>
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.
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Syndesmophytea 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 the spine, 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 arthritisand 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>
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 pathologiccondition 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 diagnosecertain inflammatory autoimmune diseases, including ankylosing spondylitis.Pasted from <http://en.wikipedia.org/wiki/Enthesitis>
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Schober's Test
Ankylosing Spondylitis1.
Indication: Evaluation of Lumbar Spine Range of Motion 1.
Patient stands erect with normal posture1.
Mark midline at 5 cm below iliac spine1.Mark midline at 10 cm above iliac spine 2.
Identify level of posterosuperior iliac spine 2.
Patient bends at waist to full forward flexion3.Measure distance between 2 lines (started 15 cm apart) 4.
Technique 2.
Normal: distance between 2 lines increases to >20 cm1.
Suggests decreased Lumbar spine range of motion1.May suggest Ankylosing Spondylitis2.
Abnormal: distance does not increase to >20 cm 2.
Interpretation 3.
Pasted from <http://www.fpnotebook.com/Rheum/Exam/SchbrsTst.htm>
What is a
syndesmophyte?
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Pasted from <http://www.fpnotebook.com/Rheum/Exam/SchbrsTst.htm>
Ask the patient to lie supine on the exam table.
1.
Place the foot of the effected side on the opposite knee.
2.
Pain in the groin area indicates a problem with the hip and not the spine.
3.
Press down gently but firmly on the flexed knee and the opposite anterior
4.
FABER stands for Flexion, ABduction, and External Rotation of the hip.
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opposite anterior superior iliac crest. Pain in the sacroiliac area indicates a problem with the sacroiliac joints.
5.
Pasted from <http://medinfo.ufl.edu/year1/bcs/slides/extrem/slide21.html>
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>
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(7)
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The association
between HLA-B27 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 HLA-
B27?
ESR and CRP are both
acute phase reactants?Can the acute phase
reactants ESR and CRP be used as diagnostic tests for ankylosing spondylitis?
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 HLA-B27?
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The KEY clinical
symptom of ankylosing spondylitis is ___?
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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
____ + ___?
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?
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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 (l ist the 4
criteria)?
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Is it
sacrolitis/spondylitis OR peripheral arthritis that is associated with
HLA B-27?
How do
sacrolitis/spondylitis vs. peripheral arthritis differ in their course in
relation to the course of IBD?
Asymmetric
transient polyarthritis is a pattern common to which type of
arthritis?
List 4 common patterns of
psoriatic arthritis?
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Another name for
reactive arthritis is ___ syndrome?How is reactive
arthritis diagnosed (l ist 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 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?
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>
List 3 possible
treatments for Psoriatic arthritis?(5)
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)?
(ie. AS NOT responding to treatment using NSAIDs)
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List 3 pharmacologic
interventions for RA?
The incidence of
RA increases in persons between the ages of ___ and ___ years
old?RA affects 3x as
many (women or men)?
05 KEYSTONE 2008 Therapeutics in Rheumatic DiseasesFriday, February 22, 20085:26 PM
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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 anti -rheumatic 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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Skin1.Joints/muscles2.Kidneys3.Nervous system4.Heart/Lungs5.Gastro-Intestinal6.ENT/EYES7.Other8.
06 CARETTE 2008 VasculitisFriday, February 22, 2008
5:26 PM
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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/capillary 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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Distal and proximal IP joints most common (rarely involvement of MCP joints)
•
Knees are by far most common join involved in OA•
07 HAWKER 2008 Osteoarthritis and Low Back PainFriday, February 22, 2008
5:27 PM
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NOT just a cartilage problem!•
Decreased bone mass and proteoglycans lead to fissuring, leading to exposed bone
•
T/F: Osteoarthritis is
a natural consequence of aging that occurs secondary to
superficial fissuring, erosions and loss of carti lage?
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OA challenges very different from RA•
Each risk factor exlpored in slides below
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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 OsteoporosisFriday, February 22, 2008
5:28 PM
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Fracture of the dis tal radius bone
List 4 common
locations for fragility fractures?
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But only becomes toxic when becomes
converted to NAPQI; usually gets metabolized to glutathione or sulphate
○
NAPQI binds to the first thing it sees○
Has hepatotoxicity•
At highest risk of
getting in trouble
•
09 JUURLINK 2008 Pharmacologic Treatment of Rheumatic DiseasesFriday, February 22, 2008
5:28 PM
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Many people take more than one product with acetaminophen•
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Aspirin also is an anti-
inflammatory (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•
Podagra: gouty pain in the great toe.
It appears that all NSAIDs
(selective AND non-selective) 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?
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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.
Really is very dangerous in large amounts; interferes with
metaphase not just in neutrophils
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 (l ist 2)?
Podagra refers to …?The end product of purine
breakdown is ___?
What is the mechanism of
action of colchicine?
2 important side effects of
colchicine are ___ and ___?
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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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?
T/F: In the prevention of
gout attacks, ___ decreases the frequency of gout episodes by about 75%?
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?
Does allopurinol
stimulate or block xanthine oxidase?
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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 (l ist
2)?(3)
A very serious
ACUTE adverse effect of corticosteroids is ___?
List 3 chronic
adverse effects of corticosteroids?(9)
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(ni trogen narcosis)
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 steroid-associated osteoporosis, namely…?
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)
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Lots of sclerotic
bone with radiolucency
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!
Treatment for Addisonian
Crisis secondary to abrupt cessation of steroid administration is to …?Symptoms of acute
Addisonian Crisis include (list 3)?(6)
Prior to an operation,
a patient with adrenal insufficiency should receive (more or less) steroids?
Which group of
patients have the highest risk for developing steroid avascular necrosis?
HPA axis suppression
(Addisonian Crisis) commonly occurs during which 2 common conditions?
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10 TUES Acute Monoarthritis Seminar NotesFriday, February 22, 2008
5:39 PM
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Name 3 synovial
l ined 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 cut-
off for WBC #'s for non-inflammatory 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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Gonococcal responds great to 3rd generation ceph•Non-gonococcal- need treat with IV Abx•
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?
ColchicineIndicationsSystemicGouty 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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The sooner you treat the better but don't treat until you have that culture•
When thinking
about mono or polyarthiritis, always think about
inflammatory vs. noninflammatory
•
Criitical cell
count: 2000 x 10x6 per liter
•
Not every joint problem is arthritis;
sometimes may have periarticular
•
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?
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What is the
difference between Type A vs. Type B Synovytes?
Synovial fluid is
an ultrafi ltrate of plasma to which _____ and other factors are added
locally by synoviocytes?
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Joint problems can arise in the acromioclavicular or glenohumeral joints•
List the 4
categories of differential diagnoses for shoulder pain
(hint: articular, …)?
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
○
How recognize non articular problems?
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If patients have bursitis, 3 important things to recognize•Pain arising in one joint area, eg. Hip joint pain referred to knee•
List 3 signs of
inflammatory arthritis?(4)
Limitation of range of motion is common to both inflammatory and
noninflammatory arthritis
•
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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
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
•
Tendons around
the shoulder
Can palpate supraspinatus by moving arm back•
Subscapularis: internal rotation•Supraspinatus: early part of abduction•
Teres minor and infraspinatorus •
rotator cuff pain
is felt at the shoulder!!!
•
Can test impingement at full abduction•
Palm down, hold down scapula and try to
bring rotator cuff tendon forcibly against acromioclavicular l igament; may produce pain if jhas impingement
a.
Thumb down, internally rotate bent armb.
Two other tests:•
Rotator cuff pain
is referred to the ___?
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Forced forward flexion•
tendonitis, bursitis and impingement
syndrome, often go together
•
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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 problems with
achilles tendon
•
Very common
List of differentials are important to keep in back pocket; these are
the commonest things that people come in with and if you havea l ist 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 - seminarSunday, February 24, 2008
12:59 PM
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Allopurinol is a ___
inhibitor which decreases uric acid synthesis?
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 the
preferred ___ lowering drug?
Gout chiefly affects middle-aged
and elderly (men or women)?
Gross urate crystal deposits are
also known as ____?
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The LEAST
common type of microcrystalline arthritis is ___?
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Go to smhrheumatology.com and see presentations
Then go to lab presentations; l ittle 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 l ikely that you don't have lupus
•
Extractable nuclear antigens: everything that DNA isn't•
Website gives expalantion of every test○
Eg. Staff doctor says work patient up for VASCULITIS•
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
•
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!
•
What is the main
way in which RA and SLE are screened for?
T/F: There are
conditions, such as in some infections, in which rheumatoid factor levels decrease
markedly?
11 THURS Special Tests in Rheumatology Seminar NotesFriday, February 22, 2008
5:40 PM
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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 myelomaSo anythign that makes it go faster is a cuase of inflammation•
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 (l iver 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=applyStylesheet([email protected],dor@p/12656167.pub)&sword=12656269>
In polycythenmia vera get clumping of RBCs•
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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 fi ind 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•
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
•
Endeocarditis, Hep
C
○
Certain types of infection
that are classically associate with rehumatoid factor
•
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
•
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complement control
protein, (CCP) any of a superfamily of proteins involved in complement regulation, encoded in a
closely l inked 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 (SS-B) 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?
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 __________?
Which test
VIRTUALLY RULES OUT SLE if negative?
The major target protein
of cANCA is ___?The major target protein
of pANCA is ___?
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Is a positive ANCA
diagnostic of vasculitis?What is the
approximate sensitivity of HLA-B27 in patients with ankylosing
spondylytis?
In a usual patient with
lower back pain, would you test HLA-B27?
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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Diagnoses of
exclusion
In terms of how they are
DIAGNOSED, fibromyalgia syndrome and major depressive disorder are similar in that they are
both …?
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What does PMR
stand for?What does GCA
stand for?
What value of ESR
must be present (mm/hr) to suggest PMR (Polymyalgia Rheumatica)?
Myositis/Myopathies
are characterized by (proximal/distal) muscle weakness?Bloodwork of a
patient with myositis/myopathies would reveal high levels of which
enzyme?
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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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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 ?•
Case 1
Tender swollen wrists all mcps pip and right knee•Small subcutaneous nodule, extensor right ulna•Weak grip•Normal back, neck, skin, mucous membranes, neurological•
PhysicalNormal general physical exam
Which pattern characteristic this patient's illness in terms of anatomic distribution and historic evolution1.Acute inflammatory monoarticular arthritisa.Subacute symmetrical inflammatory oligoarthritisb.Chronic symmetrical inflammatoryc.?d.?e.
Answer c): Chronic symmetrical inflammatory
Clinical evaluation of arthritis
Which most likely process causing this patient's illness2.Hla b27 associated seronegative arthritisa.Crystal induced inflammationb.Infectionc.Immune mediated connective tissue diseased.Trauma e.
Answer d): Immune mediated connective tissue disease
Which of the following blood test most likely to clinically dx3.Rheumatoid factor a.Hlab27 antigenb.Sedimentation ratec.Uric acidd.Blood sugare.
Answer: a) rheumatoid factor
Which additional test would be necessary to establish a dx?4.Lab resultsHb. 100 gm/LWBC 8x109/LPlatelets 580x109/l Complete normalUrinalysis, uric acid, calcium phosphate, kidney, CK
Which additional test would be necessary to establish a dx?
What Did You Learn This Week? Lecture by Dr. Bookman, MD FRCPCFriday, February 29, 2008
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Biopsy of elbow nodulea.Synovial fluid analysisb.Chest x-rayc.All the aboved.None the abovee.
Answer e): None of the above
What treatment would be most appropriate at this stage of her disease?5.Naproxen 500 mg bid and prednisone 10 mg every morninga.Naproxen 375 mg twice a day and observeb.Cyclophosphamide, 2mg/kg intravenousc.Naproxen 500 mg b.i.d. and methotrexate 15 mg weeklyd.Etanercept 25 mg sc twice weekly and naproxen 500 mg bide.
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 270 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
What disease?1.Local non-articular rheumatisma.Crystal induced arthritisb.Degenerationc.General non-articulard.Seronegative arthritis, B27 positivee.
Answer: d): General non-articular
Which investigation would be least helpful2.Muscle nexumes (???)a.An electromyogramb.Serum uric acidc.X-ray of chest d.Sedimentation ratee.
Answer: C) uric acid
Lab test resultsESR 120, Hb low, white count normal, platelets elevated, normal urine creatinine, alt 25, alp increased somewhat, TSH normal,ANA negative, chest X-ray normal
What' most worrisome possible complication in this patient3.Pneumonitisa.Peripheral neuropathyb.septic arthritisc.Blindnessd.Myocarditise.
Answer: d) blindness
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Answer: d) blindnessBecause 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 334 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:
What problem most likely:1.An acute inflammatory polyarthritis.a.A degenerative monoarthritisb.A localized non-articular rheumatismc.An acute inflammatory monoarthritisd.A generalized non-articular rheumatisme.
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
Which best diagnostic test to order2.x-ray of knee a.Uric aidb.Culture elbow abrasionc.Arthrocentesisd.X-ray SI (sacro-iliac) jointse.
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•
What's the best diagnosis?3.Diabetic neuropathic jointsa.RAb.Septic arthritisc.Medial meniscus teard.Acute goute.
Answer: c) Septic arthritis AND acute gout most likely dx's
Which of the following lab results NOT expect in the synovial fluid sample?4.WBC…?a.WBC…?b.
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WBC…?b.WBC…?c.Negative birefringent needle shaped crystalsd.Positive birefringent …?e.
Answer: ?) WBC 500 x 106/L with 80% monocytes
Birefringence
A calcite crystal laid upon a paper with some letters showing the double refractionBirefringence, or double refraction, is the decomposition of a ray of l ight 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 birefringenceIt is also util ized 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 450 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
What was the probable course of evolution of her arthritis1.Chronic slowly progressivea.Axax. (?) And remiss. With accumulation of deformityb.Acute with rapid progression to deformityc.Evolution of Crohn's disease?d.Repeated acute exacerbations …?e.
Answer: a) Chronic slow progressive course, because diagnosis was RA
Gradual accumulations
Which 2 tests most helpful2.EMG quads bilaterallya.Weight bearing x-ray both kneesb.Bone scanc.Serum uric acidd.Arthrocentesis of right kneee.
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 ofE 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.
What least significant risk factor in the patient3.She walks 3 miles a daya.She has genu varusb.She is overweightc.She is femaled.She is 72 years olde.
Answer: a) point being least sign risk factor
Case 556 year old lady abrupt onset thoracolumbar junction back pain•Bed confined for 3 days•Muscle spasms on physical •
Which of these risk factors is least significant?1.She weights 90 pointsa.She smokesb.Her mother had kyphosisc.She is sedentaryd.She golfse.
Answer: e) she golfsSmoking 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(?)
•
T-score -2.5; which best improve:2.Estrogen supplementationa.Calcium carbonate talest (?)b.Vitamin dc.Risedronated.Calcitonin spraye.
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 - TreatmentCalcitoninCalcitonin is a hormone secreted by the thyroid gland. It binds to receptors on the osteoclasts and decreasing their ability
to break down bone.
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:
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).
local irritation, dryness or inflammation in the nose
Possible side effects of the nasal spray include:
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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 InjectionCalcitonin 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.
local pain or irritation at the site of the injection•
facial flushing, nausea and chills•
rarely, skin and allergic reactions•
Possible side effects of the injection include:
These side effects are temporary and may decrease with a lower dose.Pasted from <http://www.womenshealthmatters.com/centres/osteo/treatment/calcitonin.html>
What's her prognosis?3.Her relative risk of subsequent fractures increased 25 folda.A hip fracture as she ages and a 20% mortality followingb.She has only 25% …?c.
Answer: All above are true
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Dr. Bookman: What did you learn this week?
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FMP 2007-2008 REVIEW QUESTIONS - WEEK 10 – RHEUMATOLOGY
What are major categories of rheumatic disease?1.
What are the seropositive diseases?2.
What are the seronegative diseases?3.
What is meant by symmetrical versus asymmetrical?4.
What joints are affected by osteoarthritis?5.
What are non-articular causes of rheumatism?6.
What are features of degenerative versus inflammatory arthritis?7.
What is a useful fourfold classification of functional capacity?8.
What does “avocational activities” mean?9.
Approach to arthritis
What are the major causes of mono-arthritis?10.
What tests should joint fluid be sent for in the investigation of a patient with monoarthritis?11.
What tests are available for viscosity?12.
What are the characteristic patterns of findings in the joint fluid for each major category of monoarthritis?13.
What is birefringence?14.
What is chodrocalcinosis?15.
What infectious cause of monoarthritis is most threatening for the joint?16.
What are the features of gonococcal arthritis?17.
What crystals cause arthritis?18.
Acute phase (list four possible treatments)a.
Prevention phaseb.
How is gout treated in the:19.
Monoarthritis
What is the immunopatogenesis of SLE?20.
What are the 11 criteria for the diagnosis of SLE?21.
What is responsible for deaths in patients with SLE early and late in the course of the disease?22.
What are the clinical features of dermatomyositis and polymyositis?23.
What is the most concerning underlying illness in patients with polymyositis?24.
How is the disease diagnosed?25.
What are the clinical features of scleroderma/CREST/PSS?26.
What is the pathology of scleroderma?27.
Connective tissue diseases
What is a classification of causes of shoulder pain?28.
What are the major causes of shoulder pain?29.
What is differential diagnosis of elbow pain?30.
What is the differential diagnosis of foot pain?31.
What is an enthesopathy?32.
Where does disease of the hip cause pain?33.
What are the differential diagnoses of hip pain?34.
Localized non-articular disorders
What is spondyloarthropathy?35.
What are the major diseases that are spondyloarthropathies?36.
What are typical extra-articular features of spondyloarhropathies?37.
What is HLA-B27?38.
What are clinical findings in a patient with ankylosing spondylitis?39.
What are radiographic findings in a patient with AS?40.
What is amyloidosis?41.
What are the two major categories of causes of chronic low back pain? Which is more common?42.
What are the key features of inflammatory back pain?43.
What are the New York criteria for diagnosis of AS?44.
What are the two major enteropathic arthritidites?45.
What are 5 patterns of psoriatic arthritis?46.
What is reactive arthritis? What is Reiter’s syndrome?47.
What are extra-articular manifestations of reactive arthritis?48.
What are the major elements of therapy of AS?49.
Spondyloarthropathy
Week 10 Review QuestionsThursday, March 06, 2008
6:00 PM
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What is the safe limit of dosing for acetaminophen?50.
What are the toxicities of acute acetaminophen excess?51.
What are the mechanism of action and effects of NSAIDs?52.
List four categories of side effects of NSAIDs.53.
What are risk factors for NSAID gastropathy?54.
What are cox-2 antagonists?55.
Are they safer? What specific concern is there about cox-2 antagonists?56.
What strategies can be used to reduce the risk of gastric complications in patients taking NSAIDs?57.
What is the value of colchicine in treatment of gout? Side effects?58.
What are the major side effects of allopurinol.59.
List 14 side effects of corticosteroids. 60.
What is avascular necrosis?61.
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?
62.
List 4 DMARDs, used most commonly for patients with RA? What are their side effects?63.
What is a treatment algorithm for mild RA? For severe RA?64.
When should DMARDS be started?65.
What are three biological agents used for treatment of RA, and what are their major side effects?66.
What is the target of these biological agents?67.
What is the impact (in general terms) of these various agents on disease outcome in RA?68.
What is rituximab?69.
Pharmacologic issues
What are pathological features of a rheumatoid arthritic joint?70.
What joints are affected in a patient with rheumatoid arthritis? What joints are seldom affected?71.
What are the criteria used to make a diagnosis of RA?72.
What problems may a patient with RA develop related to the cervical spine?73.
What are typical abnormalities in the blood tests of patients with RA that reflect systemic inflammation?74.
What are the radiographic abnormalities seen in a patient with chronic RA?75.
What is the typical evolution of joint problems in a patient with RA?76.
Rheumatoid arthritis
What are three pathways that lead to autoimmune reactions?77.
What is meant by organ-specific autoimmune versus non-organ specific autoimmune diseases, and what are examples of each?
78.
Which organs tend to be affected by non-organ specific autoiimune reactions?79.
What is tolerance?80.
What is a rheumatoid factor?81.
Autoimmunity
What is the overall classification of vasculitides?82.
Skin (medium versus small vessel)a.
Kidneysb.
Nervous systemc.
Heart d.
Lungse.
ENTf.
Eyesg.
How does vasculitis affect each of the following:83.
What are the clinical features of giant cell arteritis?84.
What are the two major diagnostic tests for giant cell arteritis?85.
What is the treatment for GCA?86.
What are clinical features of PAN?87.
What underlying viral illness is associated with PAN?88.
What are three types of vasculitis associated with ANCA?89.
What are renal manifestations of ANCA-associated vasculitis?90.
What are the therapeutic strategies used for ANCA-associated vasculitis?91.
Vasculitis
What are “routine” blood tests that may be helpful in the diagnosis of rheumatic disease?92.
What is the main particular use of ESR?93.
What is CRP? How is it helpful?94.
When should rheumatoid factor be ordered?95.
What other than RA is associated with rheumatoid factor?96.
When should ANA be ordered?97.
What are the sensitivity and specificity of RF for RA, and of ANA for SLE?98.
Blood tests in diagnosis of rheumatic disease
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What are the sensitivity and specificity of RF for RA, and of ANA for SLE?98.
What else causes elevated levels of ANA?99.
What form of ANA is most useful for monitoring SLE disease activity?100.
What forms of ANA are associated with scleroderma and with Sjogren’s syndrome?101.
What is the utility of serum complements?102.
What are ANCA? What are their antigenic targets?103.
What is fibromyalgia?104.
What are associated complaints in a patient with fibromyalgia?105.
What is the basis for fibromyalgia (probably)?106.
What are elements of therapy for fibromyalgia?107.
What is PMR? How is it diagnosed and treated?108.
What are other causes of generalized pain?109.
Generalized pain syndromes
Which joints are most frequently affected by osteoarthritis?110.
What is the pathogenesis of OA?111.
What are clinical manifestations of OA?112.
What are risk factors for OA?113.
What are the elements of management of OA?114.
What medications are available for the management of nociceptive and neuropathic pain in OA?115.
What are red flags in a patient with low back pain?116.
What is appropriate workup of a patient with low back pain with no red flags?117.
What is appropriate treatment of a patient with acute low back pain?118.
Osteoarthritis and low back pain
What is osteoporosis?119.
What determines bone strength?120.
What are the frequency and consequences of hip fracture in women?121.
What about men?122.
What is a fragility fracture? Where do they occur?123.
What are consequences and physical findings of vertebral compression fracture?124.
What are major risk factors for fracture?125.
What are risk factors for low bone mass?126.
What are minor risk factors for osteoporosis?127.
List 4 pharmacological agents useful in the treatment of osteoporosis.128.
Osteoporosisa.
Osteopeniab.
With respect to osteoporosis, what is a “T-score” and what level of a T-score is diagnostice of:129.
What is appropriate intake of calcium at various ages (principles)?130.
What strategies are available in the management of osteoporosis?131.
What are anti-resorptive agents? What is an anabolic agent?132.
Osteoporosis
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_IntroFriday, February 29, 2008
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Here that we need to have some sort of rational
system to decide whether or not patient will benefit from surgery
•
Assessing benefits usually much easier and more
straightforward than asessing risks
•
Acute physiology and chronic health evaluation (APACHE) -
semi-quantitative way of assessing risk
•
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
○
APACHE II 3 factors:•
Most of patients we deal with have variety of i l lnesses
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
•
What does APACHE II stand
for? What is its util ity?Which 3 factors does the
APACHE II scoring system take into consideration?
In deciding whether or not you
should operate on a patient, what should you consider? (hint: _____ vs. _____?)
2_Pre-Op Eval and PrepFriday, February 29, 2008
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APACHE-acute physiology and chronic health evaluat...[Crit Care Med. 1981] - PubMed Resulthttp://www.ncbi.nlm.nih.gov/pubmed/7261642Screen clipping taken: 3/3/2008, 9:42 AM
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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 you do to prepare depends on urgency•
What kind of help do we have?
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
•
Apart from history and
physical, how would you
assess endocrineorgan
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 systemdysfunction?Apart from history and
physical, how would you
assess cardiovascular system dysfunction?
Apart from history and
physical, how would you
assess hepatobiliarydysfunction?
T/F: Patients who
are hypothyroid react poorly to general anesthesia and surgery but not
patients who are hyperthyroid?
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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
○
Use of anticlotting agents such sc heparin decrease sig.
chance of dying from pulmonary embolus
•
"An ounce of prevention is worth a pound of cure"
Been shown to decrease the length of time of i leus○
Stress GI bleeding one of complications of srugery or being
il l in general
○
Ulcer prophylaxis will eliminate stress bleeding or stress
ulceration
○
NOT feeding the patients is the WORST thing you can do to
patients!
•
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•
(Ie. How do we prevent post-operative infections?)
OR's are cold; even a degree or two of hypothermia will result
in poor outcomes
•
Patient who did NOT get blood transfusion during
surgery is more likely to survivie cancer surgery!
○
So can be used to one's adv., the fact that blood
transfusions cause immunosuppresion
Also in renal transplatn operation; patient who has
already had multiple transfusions are less l ikely to reject kidney s
○
Prophylactic antibiotics: endless studies: will decrease
rate of surgical site infection
○
Blood is l ike an immunosuppresant drug; if give blood
transfusion, the infection rate is higher
•
List 2
cardiovascular system conditions and their associated
treatments that you can prevent post-surgical cardiovascular
complications for?
Which drug class is used
for ulcer prophylaxis prior to surgery?
List 4
preventative actions that could be undertaken to prevent post-
surgical cardiovascular system complications?(6)
List 4 preventative
actions that could be undertaken to prevent post-operative infections?(4)
Week11 Page 8
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
•
List 2 preventative
actions that could be undertaken to prevent post-operative endocrine system
complications?
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Pain Assessment:
VAS - Visual analogue scale (impracticall at bedside)•
Studies correlating VAS and VRS; correlate extremely well○
Very important to ask for pain with movement! Not just at rest!○
VRS - Where is your pain 1/10 (10 worst)•
Grimace shown to be very accurate reflection of pain degree•
3_Pain MgmFriday, February 29, 2008
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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
•
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?
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?
Week11 Page 13
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 l ike
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, …)
Pasted from <http://www.alphachimp.com/clients/blog/pain-map.jpg>
PREVENT ACUTE PAIN TO PREVENT CHRONIC PAIN!
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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!
•
T/F: Coxib's DO NOT
affect platelet function?
T/F: Preventing acute
pain is a minor risk factor in the prevention of post-operative chronic pain?
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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 side-effects?
So if have someone on acetaminophen and
ibuprofen then additive effects
•
Name 6 drugs
and/or drug classes involved in multimodal analgesia?
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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•
In addition to
being an analgesic, Gabapentin is also a(n)
_______?The optimal dose
of gabapentin is ______mg?
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What effect does
Gabapentin have on opioid consumption?What effect does
Gabapentin have on opioid-related side-effects?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?
Speed recovery•
No adverse effects from single dose•
No adverse effects
from single dose of dexamethasone
•
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?
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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•
Major problem after colon surgery: get reflex i leus•
So ambulating and drinking and eating helps people get out of hospital; with epidural can start feeding and walking immediate ly○
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
•
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
○
Best way to give opioids: pain/sedation cycle•
Oxycodone: AbsorptionAbout 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.Pasted from
<http://www.rxlist.com/cgi/generic/
oxy contin_cp-page2.htm>
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?
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List 5 multimodal
analgesics that have additive effects?
Ketamine or Clonidine
consumption will decrease the consumption of which other class of
analgesics?What is a downside to
the use of ketamines?
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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!
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
•
What does PCEA
stand for?List 2 drugs that
reduce PCEA use?
Why is it
advantageous to give analgesics prophylactically rather than after
surgery has started?
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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
Ketamine has a higher side effect profile and
gabapentin does basically the same thing so best to use gabapentin if you can
•
If you could use Ketamine
OR Gabapentin, which would you use for intraoperative analgesia, if both were equally
indicated? Why?Pre-operatively, l ist 4
medications and one optional medication that you would give for pre-operative analgesia?
Intra-operatively, l ist 3
medications/techniques and one optional medication that you would give for intra-operative
analgesia?
List 5 multimodal
analgesia agents that improve outcomes?
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: TOTAL HIP ARTHROPLASTY
HAVE TO CONTINUE MULTIMODAL
ANALGESIA when patient goes home!
•
(usually takes 2 hours for peak effect of
these drugs when given orally)
Put spinal in to decrease
sensitization of the CNS
•
Post-operatively, l ist 5
medications/techniques that you would consider for post-operative
analgesia?(7)
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 pre-operatively (ie. 1000 mg)
and which one with the lowest dosage pre-operatively (ie. 8mg): celecoxib,
acetaminophen, gabapentin, dexamethasone?
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PCA: patient controlled
analgesia: eliminating for most surgeries now for total hip; basically eliminated because if can
manage pre-operatively then don't need post-operative PCA
•
Give an example of
dosages and medications for 3 drugs one would use for post-operative (2hr) total hip arthroplasty?(5)
Intra-operatively,
which mediation would a surgeon administer via local infiltration?
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 pre-operatively (ie.
5-10mg): celecoxib, acetaminophen, gabapentin, oxycontin,
oxycodone?
Post-operatively, 1000mg
acetaminophen would be approximately every ___ hours?Post-operatively,
100-200mg gabapentin would be approximately every ___ hours?
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IL-1Monday, March 03, 200810:44 AM
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GabapentinMonday, March 03, 200810:43 AM
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Cox-2 InhibitorsMonday, March 03, 200810:45 AM
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Oxycodone / OxycontinMonday, March 03, 200810:50 AM
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KetamineMonday, March 03, 200810:56 AM
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PCAMonday, March 03, 200810:58 AM
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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?
5_Gallbladder & Biliary TreeFriday, February 29, 2008
Week11 Page 56
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
i leum lead to formation of gallstones - because terminal i leum 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?
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
•
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?
T/F: Prophylactic
cholecystectomy is indicated in 1% of asymptomatic patients over 20 years?
When is surgery
recommended for patients suffering from gallstones?
What are the 3 critical
phases in the formation of gallstones?
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?
Week11 Page 57
http://rezidentiat.3x.ro/eng/litbiliaraeng.files/image002.gifScreen clipping taken: 3/5/2008, 9:29 AM
found that you should not take gallbladder 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?
Week11 Page 58
Explainging what are the different type of symptom complexes
that patients can present with.
•
Biliary colic is CONSTANT pain!•
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
•
List 2 treatments that are
indicated for bil iary colic?
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?
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?
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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"
•
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?
Week11 Page 60
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
•
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?
Week11 Page 61
Gallbladder performation is RARE, except for severe diabetics; 95%
of time, even with severe cholecystitis, won't have perforation
•
AIR IN THE BILIARY TREE IS NOT NORMAL! Treatment is to take out
stone from gallbladder
•
Gallbladder carcinoma: a complication of chronic gallstones; almost never
get unless if have stones in gallbladder; stones irritate the gallbladder wall; gallbaldder CA is a terrible disease; 1% of the gallbladders that surgeons send to the pathologist contain gallbladder cancer
•
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?
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?
Week11 Page 62
Most common cause of pancreatitis: gallstones and alcohol•
Best treatment here is to get rid of the stones using endoscopic
means (ERCP)
•
How is alcohol
consumption related to gallstone formation?Why should
cholecystectomies be very carefully considered AGAINST in patients with cirrhosis?
Week11 Page 63
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 bil iary sepsis?
Within the context of
cholangitis, what is charcot's triad?
What is the
etiology of cholangitis?
Fever, Jaundice, and
RUQ pain together are known as ___?How common is
Charcot's triad in patients with cholangitis?What is Reynaud's
Pentad?
After which surgical
procedure is there an increased risk for cholangitis to develop?
Week11 Page 64
List 3 different methods of
bil iary 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 advantagesof 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?
List 3 steps in the
management of cholangitis?
Week11 Page 65
Inflamatory response not only kil ls 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 kil ls bactera?
Reticuloendothelial system
•
Some terminology...
6_Abdominal InfectionFriday, February 29, 2008
Week11 Page 66
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!•
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 i leus by the classic definition [3].
Pasted from <http://en.wikipedia.org/wiki/Ileus>
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 l ikely diagnosis for pain starting in
left lower quadrant rebound tenderness, generalized abdominal pain severe after 5 minutes, pain now radiating up to upper right
•
Eg. Leak from the gut to bladder or another site of the body○
Fistula: abnormal connection between two epithelial l ined
surfaces
•
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 l ife
•
Week11 Page 67
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 down; on high doses of steroids, immune suppresents; they don't send him home; on day 5 he gets short of breath; do chest xray and see gross free air;
•
Age is l ike an immunosuppressant; also don't feel/complain about as much pain•
Ischemic gut: common in older people; may thrombose to a vessel supplying
part of the gut
•
PEG: Percutaneous Endoscopic Gastrostomy •Common enough that in the ICU you'l l learn that when patient
going sour in the icu, abdominal infection is always on the differential dx
•
What is a PEG
tube?
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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 capil laries 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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Intramural causes of small bowel obstruction•
One common example of an intramural benign inflamatory cause of bowel obstruction○
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
Another one: radiation stricturs○
Crohn's disease can go on to cause stricturse•
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:•
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
○
Peirtoneal carcinomatosis: many cancers in the perineal cavity: thesecan grow up and twist off any portion of bowel
•
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
Intralumnial○
Number of posibilities
Intramural○
Large bowel•
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.
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?
What is anotehr name for
colonic i leus?
7_Bowel ObstructionFriday, February 29, 2008
Week11 Page 73
Ibd - particularly crohn's diseaseradiation strictursre (women radiated for carx of the cervix)
Benign□
Most common: ADENOCARCINOMA: commonly prsents with large bowel obstruction
MALX:□
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
•
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
•CLASSIC PX (PRESENTATION):•
(PASSAGE OF NOTHING PER RECTUM)
If wall tension in your colon does
incrase suddenly
•
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
○
Should NOT have periteonale signs
such as tenderness or guarding
•
List 2 common
signs/symptoms of gastric outlet obstruction?List 3 common
signs/symptoms of small bowel obstruction?
How does small bowel
obstruction typically present?What is the definition
of obstipation?
Week11 Page 74
(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
•
With respect to
laboratory findings, prolonged gastric outlet obstruction leads to ___?
The laboratory finding of
hypochloremic, hypokalemic metabolic alkalosis is pathognomic of ___?
What is the treatment for
a malignant obstruction?What is an incarcerated
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 l inelaterally. These hernias almost always develop at or below the l inea arcuata, probably because of the lack of posterior rectus sheath. These are generally interparietal hernias, meaning that they do not l ie 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 l ife). 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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If make a diagnosis of malx obstruction, then never going to get beter if you just lleave them alone; typically fixing done surgicallyNowadays, particularly, if in rctum, then can do stent placed in
•
Not often can do this though○
Occassionally perioteneal carcinosis due to carcinoma of the ovry, then can treat with radiation
•
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 obstructionTuesday, April 01, 20088:48 PM
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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
•
underlying serositis and ascites is common
complication; may result in abupt change in general condition; primary means there is no obvious perforation
○
Primary: •
CAPER: Community acquired peritonitisk
HOPER: HOSPITAL AQUIRD PERITONITIS: tend
to be due to mor drug resistanct or abx rseistant bacteia; may influence management
large number of bacteria normally present in bowel
at hat level infect peritoneal spaces
○
Secondary: •
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
•
What do CAPER and
HOPER stand for?
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 intra-
abdominal abscess (localized) can be categorized into which two categories?
8a_Abdominal InfectionsFriday, February 29, 2008
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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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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 bil iary tract, stomach/duodenum,
and small bowel include which two antibiotics?
Approximately how
long before surgery should prophylactic antibiotics be started (pre-
operatively)? Why may you need a second dose to be administered?
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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 NotesFriday, February 29, 2008
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9_Intro to AnesthesiologyFriday, February 29, 2008
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Propofol: makes people go to sleep; doesn't do anything for pain
control; not part of any major drug group
•
What are the 5 A's of
anesthesiology?
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Story of the wimpy football player :-)○
Most common benzo is midazolam: has prominent amnesia
effects
•
Rohipnol: what they call midazolam in the UK; most chemically
resembles midazolam
•
Koran patient diagnosed with pancreatic cancer; tried to kil l himself
stabbing with kitchen knife
•
ANY OPERATION IS CONTROLLED TRAUMA•
Job of anesthesiologist is to keep vital signs stable•
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
•
In the process of
preparing someone for surgery and during the surgery is itself,
when is sympathetic tone the highest?
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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 l ittle l idocaine around area of wound
•
If neve has name, then it's regional○
In this case would do an ankle block○
Distinction between a local and rgional 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
•
What is the
distinction between a regional and local never block?
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Another example of regional anesthetic
Local anesthetic options: specific nerve blocks around the cervix•Early in labor most of pain coming from cervical dilation•
General anesthesia is too much for labor•
Midline solution is the epidural (spinal)•
In this case, rathe rthan blocking
small neve, block at level of the spinal chord
•
Epidural: insert eedle
patient back, just outside the dura; princple ther is that if you inject l idocain, 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 l ittle bbies or anything in the lower body
○
Why not higher? C345
keeps the diaphragm alive..put patient in rsep failure
○
Can do an epidural
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
○
Diff between spinal and epidural:•
Sinal tap is L1 or L2: where the spinal chord ends□
What's the highest you can do this at?
Same procedure, through skin, l igaments, between spines, and then actually
through the dura; much smaller needle, then give a much lowr dose, and one shot (because don't have to worry about diffucison of meds); principle is the sam though, blocking nerve impulses
○
Spinal•
Ketamine causes TERRIBLE NIGHTMARES•
What is the difference
between an epidural and a spinal?What effect does
ketamine have on sleep?
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Skipped everything until here (from gen. anesth. Slide)
Ventricular fibrillation
Classic description of MALIGNANT HYPERTHERMIA!•
KNOW MALIGNANT HYPETHERMIA FOR EXAM!
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)•
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?
Malignant hyperthermia
typically occurs in response to administration of which anesthetics?
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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 l ike sand; very difficult to administer
•
NMS DOES NOT EQUAL MHS (MALIGNANT HYPERTHERMIA SYNDROME)
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?
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PropofolFriday, March 07, 200810:23 AM
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HalothaneFriday, March 07, 200810:24 AM
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MidazolamFriday, March 07, 200810:30 AM
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Digital Ring BlockFriday, March 07, 200810:42 AM
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Obstetric AnesthesiaFriday, March 07, 200810:50 AM
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Malignant HyperthermiaFriday, March 07, 200810:56 AM
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11_Pre-Op PrepFriday, 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
•
CT is not insignificant radiation○
Time ○
What are the downsides of doing a CT•
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
•
Once the appendix is out, we don't really need give more Abx's○
Because of risk of aspiration; general anesthetic with layngyscope then will vomit and aspirate
NPO before surgery○
Analgesia - morphine○
Antibiotics preoperative - against gram negatives, anaerobes, and gram postiives (on skin)
•
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
○
Wound infection: 5 to 10% of patients who have appendectomiesRisks of the general anesthesia: infection:○
INFORMED CONSENT! •
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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○
Appendix will perforate and get gram negative bacteria and develop intraabdominal abscess and then travel through portal vein and settle into liver abscesses
If it hasn't perforated, then will have risk of perforation○
No CT US instead○
10-11,000 normal WBC for woman○
What would you do differently if patient was a 12 week pregnant 19 year old 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 •
Ablation! Can do endoscopic ablation; or cryotherapy (don't have seame durative bneefit); so other options besdies abdominal curative resection
○
What if guy is 82, diabetic, leg amputation, dbtc, tumor in rectum•
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No good chemotherapy for gastric carcinoma•No survival benefit for stage IV gastric carcinoma•
palliation
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trusstruss (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 & ComplicationsFriday, 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)•
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
○
Irrigate really well then culture it! Want to know what this is!
Open wound and get foul smelly think darksih tissue fluid; ○
Examine the wound: pinkish erythema; sore on touch, crepitus•
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•
Bleeding
Third space loss
Cardiogenic (MI)□
Obstructive (PE)□
Sepsis
If Hb post-op was low□
Transfusion reaction
Post-op diff: ○
Maybe having PE: pulmonary embolism (can cause hypotension and oligouria))•
Says no chest pin, breathing fine, lightheaded□
Chest pain? SOB? When did this start? Any pain anywhere?
Had MI two years ago on aspirin since; got betablocker pre-operatively□
Maybe anemic
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!□
O/E: check JVP
3rd space: capilaries become leaky in surgery: absorb third space loss after leaked out of capillaries
Ask patient questions: ○
1st thing: bang in 2L of ringer's lactate to resuscitate•
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NPO, NG tube stays in!•Will have significatn gastric ileus•
(from Tuesday case)
DDx: PE, PE, PE!•H&P•
May go into R. ventricular failure ○
V/Q scan can make dx of (ventilation perfusion scan) nuclear med study; gas venilated to perfusion○
Angiography○
Time►
What lowers their clotting capacity more: TPA►
Want to make sure therefore that patient's clot burdern is significant enough ; then give TPA
►
Indications◊
Pregnant►
Just had surgery (unless acdcept risk that she'll bleed); with heparin, ►
Contraindications◊
Thrombolysis
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
So what do now? Normal cx, sinus tachycardia, bp 100, □
Of chest, in 2008 this is most senstiive way; will see pulm onary arteries and tributaires and will see an abrupt defect
CT/A (ct angiography)○
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
Chest Xray○
On cardiogram: have SINUS TACHYCARDIA (rhytm is normal bur rate is up)
in MI will have depressed segments□
Make sure has no electrophysiological abnormalities
Also want blood gas
MUST do cardigram and MSUT do chest xray
Cardiac enzymes and EKG on every patient short of breath!○
Priority: bring up O2 sats; low O2 causes lots of anxiety; make sure IV's are secure•
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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 TraumaFriday, March 14, 2008
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2_Mgm Airway BreathingFriday, March 14, 2008
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3_Hypotx in TraumaFriday, March 14, 2008
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4_Thracic and Abd TraumaFriday, March 14, 2008
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Can get lots of false positives and negatives•
Usual way assess abdomen in trauma room•
Injury to spleen often accumulates between spleen and kidney
•
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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
•
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
•
(and you have an indication that there's blood in the
abdomen)
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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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•
Increased pressure of abdomen following this called abdominal compartemtn syndrome○
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
•
Ful laparotomy; pack all 4 sponges and take out
one at a time to see if bleeding from any 4 quadrants; can get l iver bleeding stopped, etc.
•
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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In blunt trauma, the overall incidence of inuries to the c-spine 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
5_Cerv Spine and Spinal Cord TraumaFriday, March 14, 2008
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Incidence of patients worsening neurologically after reaching hospital is 2 to 10%
•
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
•Chin lift or jaw thrust DO cause movement of c-spine; 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
•
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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
l igamentous injury; SO NOT ENOUGH TO JUST DO A CT scan
•
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
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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Complete: spinal cord function below level of injury is TOTAL; the impulses from above are NOT getting past area of injury
•
Sacral nerves are spared (sacral sparing); may be indication of incomplete injury
•
Level of lesion;
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 Intercostals can helps you draw air in; if only have diaphragm; under normal
circumstance may be adequate but if have asthma attack
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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Don't have to know actual numbers; appreciate drastic nature of TBI
Google brain trauma foundation for great resources related to this lecture•
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
•
6_Neurotrauma - Brain InjuriesFriday, March 14, 2008
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SUBDURAL HEMATOMA
Look at diff: instead of being lens shaped, here dura is sti l l
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
•
CONTUSION; really hematomas in the brain
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 mill ions 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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Hospitals DON't accept spinal cord donations following death•
Donation can come from anyone who dies from any cause•
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?
List 3 conditions
associated with Neurological Death Donation?(4)In order for
Neurological Death to be diagnosed, which 3 conditions must absolutely be
met?
7_Organ_Tissue DonationFriday, March 14, 2008
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Clinical examination for
NDD requires that there be bilateral absence of …(4)?Clinical examination for
NDD requires that there be absence of …(3) (l ist 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?
Canadian medical
standard for the neurological determination of death (NDD) require that
which 6 factors be fulfi l led?If the 6 factors from
the minimum clinical criteria CANNOT be fulfi l led, then what types of ancillary tests
can be done?
What 2 types of
cerebral imaging studies could one do to investigate neurological death?
T/F: Ancil lary testing
is done IN CONJUNCTION WITH and NOT AS A SERIES OF STAND-
ALONE CONFIRMATORY TESTS for NDD?
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These patients sti l l 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)
•
"so what is your understanding of what just happened?"○
"We are very sorry that [John] has died"○
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
•
TGLN = Tril l ium
Gift of Life Network
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8_Tues SemFriday, March 14, 2008
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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)
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?
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The horizontal fissure is located on the right or left lung?
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<file://C:\Documents and Settings\Mr. Intensity\My Documents\1Medicine\2ndYearFiles\1FMP-2007\Week12\09
FMP 2008 THURS Trauma Radiology Seminar Notes.pdf>
09 FMP 2008 THURS Trauma Radiology Seminar Notes.pdf
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FMP 2008 Trauma Week Q & A - PART 1.pdfTuesday, April 01, 200810:20 PM
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FMP 2008 Trauma Week Q & A - PART 2.pdfTuesday, April 01, 200810:20 PM
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FMP 2008 Trauma Week Q & A - PART 3.pdfTuesday, April 01, 200810:20 PM
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Week 12 Review QuestionsSaturday, March 22, 20085:30 PM
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00 FMP 2008 Week 13 Intro Pages.pdf
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Pain Week Student Manual 2008Saturday, 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 non-cancer and cancer
related pains, most people usually have more than one type.
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