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

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

FMP 2008 week 09 review questions

Liver enzyme abnormalities


1. What are the different patterns of liver to injury?
2. What are the elements of “fibrotest”?
3. What are the tests that actually assess liver function?
4. How can liver fibrosis be diagnosed?
5. What liver enzymes can have their level elevated in the setting of hepatitis?
6. What are enzymes of cholestasis?
7. What causes “mild” hepatitis with ALT > AST? Of AST > ALT?
8. What are genetic causes of liver disease, what are the clinical features of each, and how can they be treated?
9. Which causes of viral hepatitis are vaccine-preventable?
10. Which causes of chronic viral hepatitis are treatable?
11. What is non-alcoholic fatty liver?
12. What are 36 drug causes of hepatitis? (just kidding)
13. What is autoimmune hepatitis?
14. What causes severe hepatitis? (What constitutes “severe” in this context?)
15. What causes cholestasis?
16. What is primary sclerosing cholangitis?
17. What is primary biliary cirrhosis?

Viral hepatitis
18. What are the 5 major types of viral hepatitis?
19. What are the clinical features and clinical course of hepatitis A?
20. How is hepatitis A transmitted?
21. How is hepatitis A managed?
22. Who should receive the hepatitis A vaccine?
23. How is hepatitis B transmitted?
24. What are clinical features of hepatitis B?
25. How is hepatitis B infection diagnosed? What is the relevance of tests for hepatitis B e antigen and antibody?
26. What are the serologic patterns of infection with hepatitis B that recovers, and that stays chronic?
27. Who should receive hepatitis B vaccine?
28. What are sequelae of chronic viral hepatitis?
29. What are the available treatments for chronic hepatitis B?
30. Who should receive treatment for chronic hepatitis B?
31. How is hepatitis C transmitted?
32. What is natural history of hepatitis C infection?
33. What is treatment of chronic hepatitis C?
34. What is hepatitis D?
35. What is hepatitis E?
36. What is hepatitis G?

Esophageal disorders
37. What is dysphagia?
38. What are the major causes of dysphagia?
39. What is a reasonable algorithm for the diagnosis of dysphagia?
40. What is odynophagia?
41. List three treatments for achalasia.
42. What is the mechanism of GE reflux in most cases?
43. How can the diagnosis of reflux be confirmed?
44. What are the major complications of GE reflux?
45. What is esophagitis?
46. What is Barrett’s esophagus?
47. What is the key element of treatment of GE reflux?
48. What is the mechanism of parietal cell acid secretion?
49. List 5 proton pump inhibitors.

Dyspepsia and peptic ulcer


50. What is dyspepsia?
51. What is the commonest cause of dyspepsia:

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51. What is the commonest cause of dyspepsia:
a. Overall
b. That has an organic basis
52. What are other important causes of dyspepsia?
53. What laboratory tests are appropriate for work-up of patients with dyspepsia?
54. What are the two major underlying causes of peptic ulcer disease?
55. What is Zollinger-Ellison syndrome?
56. What are complications of peptic ulcer disease?
57. What is H. Pylori?
58. What are complications of H. pylori?
59. How is H pylori treated?
60. What are the potential effects of NSAIDs on the GI tract?
61. Why do NSAIDs lead to peptic ulcer?
62. What is the best way to diagnose peptic ulcer disease?
63. List four categories of drugs that can heal a peptic ulcer without the use of antibiotics. What is the chief benefit of adding
antibiotics to this regimen?

Gastrointestinal bleeding
64. What are the major causes of upper GI bleeding?
65. What are three high risk unusual causes of upper GI bleeding?
66. What do the following terms mean?
a. Hematemesis
b. Melena
c. Hematochezia
67. What is the natural history of bleeding due to peptic ulcer disease?
68. What are the prognostic factors related to overall outcome in patients with upper GI bleeding?
69. What is the general mortality rate in patients with upper GI bleeding due to peptic ulcer?
70. What are endoscopic findings that predict an adverse outcome in patients with upper GI bleeding due to peptic ulcer?
71. What are general supportive measures related to management of patients with upper GI bleeding?
72. What are specific therapeutic measures for patients with upper GI bleed due to peptic ulcer?
73. What are indications for surgery in patients with upper GI bleeding?
74. What leads to esophageal varices?
75. What are risk factors for bleeding among patients with esophageal varices?
76. What are adverse prognostic factors for bleeding esophageal varices?
77. What specific therapeutic modalities are available for bleeding varices?
78. What is octreotide?
79. What is TIPS?
80. What are major causes of lower GI bleeding?
81. What are the major investigative modalities available for lower GI bleeding?
82. What is a Meckel’s diverticulum?

Acute pancreatitis
83. What are the two major causes of acute pancreatitis?
84. What are the additional important causes of acute pancreatitis?
85. What do patients with acute pancreatitis complain of?
86. What are the major physical findings in a patient with pancreatitis?
87. What laboratory tests are most helpful in the diagnosis of acute pancreatitis?
88. What are other causes of hyperamylasemia?
89. What imaging tests are helpful in diagnosis of acute pancreatitis and its complications?
90. What are the local complications of acute pancreatitis?
91. What are the major elements of treatment?
92. What is the role of endoscopy in the therapy of acute pancreatitis?

Diarrhea
93. What causes acute diarrhea?
94. What causes chronic diarrhea?
95. What are major causes of bloody diarrhea?
96. What tests are appropriate in a patient with chronic diarrhea?

Inflammatory bowel disease


97. What are the major differences in the histopathology of Crohn’s disease versus ulcerative colitis?
98. What are the locations of Crohn’s disease in the GI tract?
99. How does IBD present?
100. What are intestinal complications of IBD?
101. What are the extraintestinal manifestations of IBD?
102. What items are appropriate to consider in the differential diagnosis of the patient with suspected IBD?
103.

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103. What factors on history, physical exam and lab testing contribute to the assessment of disease severity in a patient with IBD?
104. What are the major treatment options for patients with Crohn’s and those with UC?
105. What is infliximab?
106. What is azathioprine?
107. What is 5-ASA?
108. What are adverse effects of corticosteroids?
109. What is cyclosporine?
110. What is budesonide?
111. What is methotrexate?
112. What are indications for surgery in patients with IBD?
113.
Liver failure
114. What are the pathologic features of cirrhosis?
115. What are the causes of cirrhosis?
116. What are the physical findings of cirrhosis?
117. What are the laboratory test abnormalities seen in patients with cirrhosis?
118. What are the elements of the Child-Pugh-Turcotte prognostic scale?
119. What are the major complications of cirrhosis?
120. What is the pathogenesis of cirrhotic ascites?
121. What are the elements of management of cirrhotic ascites?
122. What is a paracentesis?
123. What are the major indications for liver transplantation?
124. What is fulminant hepatic failure?
125. What are symptoms associated with jaundice, and how do they help to differentiate the causes?
126. What are major differences between Crohn’s disease and ulcerative colitis:
a. Pathologically
b. Clinically
c. In terms of treatment
127. What are the major complications of portal hypertension?
128. How is spontaneous bacterial peritonitis:
a. Diagnosed
b. Treated
129. What are the indications for liver transplantation?
130. What are the clinical features of sclerosing cholangitis?
131. What is the pathogenesis of cirrhotic ascites?
132. What is a TIPS procedure?

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

Pasted from <https://portal.utoronto.ca/courses/1/Fall-2007-FMP211Y1-Y-LEC0101/content/_913894_1/FMP%202008%20week%2009%20review%20questions.doc?


bsession=11327372&amp;bsession_str=session_id=11327372,user_id_pk1=501825,user_id_sos_id_pk2=1,one_time_token=>

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

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

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Give an example of a
non-inflammatory,
non-immune
rheumatoid disorder?
Give an example of an
inflammatory, 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?

Autoimmunity results from


failure or breakdown of
tolerance in ___, ___ or both?

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

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List the 3 main
categories of
autoimmune
reactions?

List 3 different types of


autoimmune reactions?

Autoimmune
diseases may be
either ___ or ___?

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

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

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

• Polyclonal Gammopathy: A gammopathy in which there is a


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

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

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

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List 3
inflammatory
mediators
involved in RA?

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

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List 2 Anti-TNF
antibodies that are used
in Arthritis
management?
Etanercept is a solube
___ used in Arthritis
management?
Anakinra is a popular
___ used in the
management of
Arthritis?
In the management of
Arthritis, drugs such as
methotrexate and
lefluonmide
counteract the actions
of which cell in the
pathogenetic
progression of Arthritis?
In the management of
Arthritis, cytokine
neturalization drugs
counteract the actions
of which cytokines in the
pathogenetic
progression of Arthritis?
In the management of
Arthritis, Rutizimab
counteracts the actions
of which cells in the
pathogenetic
progression of Arthritis?
While both Etanercept
and Infliximab are both
exert their effect
through cytokine
neutralization, one is a
soluble TNF receptor
while the other one is an
Anti-TNF alpha
antibody; which is
which?
Is Adulimumab a soluble
TNF receptor or an anti-
TNF antibody?
Apart from using a
soluble TNF receptor or
an anti-TNF antibody,
which other drug
mechanism is used for
cytokine neutralization
in the treatment of RA?
IL-1 receptor
blocker

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

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

What is
seropositivity?
Into which
categories may
inflammatory
Arthritis be classified
into?
Into which
categories may
degenerative
Arthritis be classified
into?
Into which
categories may non-
articular Arthritis be
classified into?

Seropositivity is the presence of a


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

Polymyositis is a type of inflammatory myopathy, related to Scleroderma is a chronic disease characterized by


dermatomyositis and inclusion body myositis. Polymyositis means excessive deposits of collagen in the skin or other organs.
'many muscle inflammation'. The localized type of the disease, while disabling, tends not
Polymyositis tends to become evident in adulthood, presenting to be fatal. Diffuse scleroderma or systemic sclerosis, the
with bilateral proximal muscle weakness, often noted in the upper generalized type of the disease, can be fatal as a result of
legs due to early fatigue while walking. Sometimes the weakness heart, kidney, lung or intestinal damage.[1]
Pasted from <http://en.wikipedia.org/wiki/Scleroderma>
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

Week10 Page 24
be infectious, associated with the pathogens that cause Lyme
disease, toxoplasmosis, and others.
Polymyositis, like dermatomyositis, strikes females with greater
frequency than males. The skin involvement of dermatomyositis is
absent in polymyositis.
Pasted from <http://en.wikipedia.org/wiki/Polymyositis>

List 4 different
classifications for
seropositive
Arthritis?

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

Which of the following


has asymmetric spine
involvement:
Ankylosing spondylitis,
• Spondylitis: inflammation of the or psoriatic arthritis?
vertebrae; called also rachitis.

What is podagra?

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Infectious
arthritis may be
classified into
which two types?

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

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

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

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

What are tophi?

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

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

calcium pyrophosphate deposition disease,


(CPDD) an acute or chronic inflammatory
arthropathy caused by deposition of calcium
pyrophosphate dihydrate (CPPD) crystals in the
joints and characterized by chondrocalcinosis and
the presence of the crystals in synovial fluid.
Clinically, it may resemble numerous connective
tissue diseases, including osteoarthritis,
rheumatoid arthritis, and gout, or it may be
asymptomatic. While most commonly idiopathic,
CPDD can also be hereditary or associated with a
variety of metabolic diseases. Acute attacks are
sometimes called pseudogout. Called also CPPD d. Figure 123-20 Calcium pyrophosphate deposition disease
Pasted from <http://127.0.0.1:8080/rami?
COMMAND=applyStylesheet(dor@doc.xsl,dor@d/12300762.pub)&sw (CPDD).Chondrocalcinosis of menisci, best shown anteriorly (black arrow),
ord=12301439> and characteristic distal femoral cortical notching (open arrow).
P asted from <http://w iserw iki.com/D iagnostic_Imaging_of_Rheumatologic_D isorders>

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

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

Pasted from <http://en.wikipedia.org/wiki/Tophus>

How is class I
functional status
different from class III
functional status in
the clinical evaluation
of Arthritis?
What is the
distinguishing feature
between class I and
class II functional
capacity, as it relates
to the clinical
evaluation of
arthritis?
What is the
distinguishing feature
between class Ii and
class III functional
capacity, as it relates
to the clinical
evaluation of
arthritis?

For the clinical evaluation


of arthritis, Lab tests done
for ___ blood include
CBC, Urinalysis, ___, and
___?(2)
For the clinical evaluation
of arthritis, Lab tests done
for ___ blood include
___?(1)
For the clinical evaluation
of arthritis, lab tests done
Eburnation: e"b6r-na1sh6n) [L. ebur ivory] 1. to explore degenerative
the conversion of a bone into an ivory-like and non-articular
mass. rheumatism include
○ In osteoarthritis, the thinning and loss of the ___?(1)
articular cartilage resulting in exposure of the For the clinical evaluation
subchondral bone, which becomes denser of arthritis, lab tests
and the surface of which becomes worn and performed include ___
polished. 2. e. of dentin. and ___?(2)
For the clinical evaluation
of arthritis, lab tests
performed to investigate
an infectious cause
include ___ and ___?

How are the xray


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

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

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

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

List 9 criteria
included in the
1997 Revised
Criteria for the
(mea ning a ra sh with a round or oval shape) Classification of
SLE?(11)

Serositis: Inflammation of the serous tissues of the body. The


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

What is serositis?

A mnemonic for SLE diagnostic criteria


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

A RASH POINts MD
Arthritis

Renal disease (proteinuria, cellular casts)


ANA (positive antinuclear antibody)
Serositis (pleurisy or pericarditis)
H aematological disorders (haemolytic anaemia or leucopenia or lymphopenia or thrombocytopenia)

Photosensitivity
Oral ulcers
I mmunological disorder (positive LE cell, anti-DNA, anti-Sm, false positive serological test for syphilis)
N eurological disorders (seizures or psychosis, in the absence of other causes)

Malar rash
Discoid rash

Because the malar rash is the most easily recalled finding, this mnemonic uses that word and an
accompanying message that it "points an MD to a possible diagnosis."

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

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

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

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

• Anti -Sm is an immunoglobulin


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

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

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

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

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

An illness in which there's inflammation in only


two organs; happens in children and adults

Dermato/Polymyositis
is a disease in which
inflammation may be
present in which 2
organs?

• Dermato/polymyositis is in mucle only or in skin • Also a red, scaly flaky rash; different from luypus in
only; separate illness that the nasolabial foold is NOT spared
• Usually associated with an underlying illness

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Upper eyelid in patients with dermatox/myox often has a
Nonspecific rash purple discoloration; VERY PATHOGNOMONIC (THESE
HELIOTROPE RASHES) of dermato/polx (dpx)
Purple
discoloration, or
a purple
heliotrope rash,
on the upper
eyelids of
patients is very
pathognomonic
of which disease?
T/F: Patients with
dermato/polymy
ositis have a
typical malar
rash?

Gottren's papules: red rash over


the knuckles themselves 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
• Also, shoulders and hips tend to be weak; when you do some characteristically weak are
blood tests, these inflamed muscles tkleak out their enzymes; the hands and feet?
• So characteristic rashes were: one enzyme, CPK (creatine phosphokinase) leaks out of these
muslce snad you have a high level CK in the blood; probably
purple heliotrope rash over eyelid inflamed; if do EMG, find signs of irritability; inflamed; finally, if
and gottren's nodules on knuckles want to be absolutely sure, you do muscle biopsy and as in next With respect to the
slide, see inflammatory scells between muscle fibers 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.
• So what causes this?
○ Dermatomyositis or the myositis by iteself may Dermato/polymyositis
is more common in
have 2 dfft mechs
males or females?
 Dermx - may be due to immune comlex's Dermato/polymyositis
 Polymositis wihtout the skin,k seems imp is more common in
Inflammation in muscles mech is lymphocytes tat are cytotoxic patients over the age
agains the muscle of ___?

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Major issues here:

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?
Scleroderma = progressive systemic sclerosis
• Malignancies that occur are the common malignancies: man: • Everything we've talked about today is about the tissue getting
lung, pancreas, stomach inflamed; in this condition, there's virtually NO
• Women: ovary, etc. inflmmation; there's progressive sclerosis; tighening,
• This underlying malignancy is more common in men, with thickening, fibrotic reactions in the tissues; these patients do
dermato, and over 50 have autoantibodies but they don't lead to inflammation; they
• So a man, over 50, with dermatocytis, will receive an intensive somehow lead to progressive inflammation through the tissues
workup for an underlying malignancy

The mnemonic
CREST, relating to
the symptoms of
scleroderma,
stands for…?

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

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

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X-ray of calcinonsis

As tissue is being choked, there's a tendency to lay down C=


calcinosis (laying down of calcium under the fingers

Weakened Intima

E= esophagus: when you eat food, get peristalsis; patients with


scleroderma and those with reynaud's henomenon in general • Here's an example of why this occurs: intima
tend to lose peristalsis so esophagus tends to become like a solid of the blood vessel is proliferating and intima
tube; you're pushing it down with gulping but the normal wave is weakened; again coming back to the
that you get in isn't pushing it down
vascular story; blood vessel who's lumen is
being obliterated
T/F: patients with
scleroderma and
those with
reynaud's
henomenon in
general tend to
lose peristalsis in
the esophagus?

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

So heard now 3 different disease


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

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

In the clinical evaluation


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

Spectrum of Seronegative Diseases List 4 subsets of the


spondylarthropathies?
There is an overlap
between AS and
which 3 other
spondylarthropaties?
Enteropathic Arthritis

Psoriatic Arthritis
Ankylosing spondylitis

List 2 different types


of enteropathic
Reactive Arthritis arthritis's?

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

Where is the
entheses
located?
What is
enthesitis?

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

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

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

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What is a
syndesmophyte?

Schober's Test
1. Indication: Evaluation of Lumbar Spine Range of Motion
1. Ankylosing Spondylitis
2. Technique
1. Patient stands erect with normal posture
2. Identify level of posterosuperior iliac spine
1. Mark midline at 5 cm below iliac spine
2. Mark midline at 10 cm above iliac spine
3. Patient bends at waist to full forward flexion
4. Measure distance between 2 lines (started 15 cm apart)
3. Interpretation
1. Normal: distance between 2 lines increases to >20 cm
2. Abnormal: distance does not increase to >20 cm
1. Suggests decreased Lumbar spine range of motion
2. May suggest Ankylosing Spondylitis

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

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

FABER stands for Flexion,


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

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

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

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(7)

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

Approximately
what percentage
of patients who
have ankylosing
spondylitis are
positive for HLA-
B27?

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?

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The KEY clinical
symptom of
ankylosing
spondylitis is
___?

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

List the 4 New York


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

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

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

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

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

List 4 common patterns of


psoriatic arthritis?

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

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

• Balanitis is a term used to include all inflammation of the


skin covering the head (glans) of the penis.

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

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List 3 possible
treatments for
Psoriatic
arthritis?(5)

(ie. AS NOT responding to treatment using NSAIDs)

What do the CRA


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

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

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

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

List 3 pharmacologic
interventions for RA?

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

List 4 drugs that


are in current use
for the treatment
of RA?
The goal of
disease
modifying 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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06 CARETTE 2008 Vasculitis
Friday, February 22, 2008
5:26 PM

1. Skin
2. Joints/muscles
3. Kidneys
4. Nervous system
5. Heart/Lungs
6. Gastro-Intestinal
7. ENT/EYES
8. Other

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

List 3 signs of small


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

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Giant cell arteritis
is more common
in females or
males?

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

• Distal and proximal IP joints most common (rarely


involvement of MCP joints)
• Knees are by far most common join involved in OA

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• NOT just a cartilage problem!

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

• Decreased bone mass and proteoglycans


lead to fissuring, leading to exposed bone

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

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

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

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

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Fra cture of the
di s tal ra dius bone

List 4 common
locations for
fragility fractures?

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

• At highest risk of
getting in trouble

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

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• Many people take more than one product with acetaminophen

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Aspirin also is an 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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• Celecoxib, robacoxib (Vioxx): became
Misoprostol: at doeses of even 600mg, blockbuster drugs; several large clinical trials
caused diarrhea; people couldn't tolerate more than 10,000 patients; clear that they
it; remember this is the same were safer but they got used in people who
Misoprostol we learned in FMP1, which were never even considered for traditional
is a teratogen NSAIDS in the first place

• How sticky your platelets are


(sticky = thromboxane; non-sticky
= prostacyclin)

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• At least now 10,000 lawsuits re: Vioxx

It appears that all NSAIDs


(selective AND 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?

Podagra: gouty pain in the great toe.

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Podagra refers to …? ASA is NOT used in the
The end product of purine treatment of gout
breakdown is ___? because …?
In the treatment of
acute gout, NSAIDs are
genereally the
preferred treatment
unless the risk of
adverse effects is
deemed too high, such
as (list 2)?

Indomethacin: [USP] a nonsteroidal antiinflammatory drug; used in the


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

What is the mechanism of


action of colchicine?

2 important side effects of


colchicine are ___ and ___?

Really is very dangerous in large amounts; interferes with


metaphase not just in neutrophils

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

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T/F: In the prevention of
KNOW THIS LIST FOR EXAM! gout attacks, ___
decreases the frequency
of gout episodes by about
75%?

T/F: dietary modifications are


generally effective for the
prevention of gout?
List 3 drugs that should be
avoided in persons with gout
because they increase uric
acid levels?(6)

A common drug used


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

Does allopurinol
stimulate or block
xanthine oxidase?

List 2 adverse effects of


allopurinol?(4)

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

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The KEY drug
interactions with
allopurinol are ___
and ___?

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

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

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

If patients are taking


prednisone >5mg/d for 3
or more months, then 3
other medications
should be given to
prevent steroid-
associated osteoporosis,
namely…?

In avascular necrosis,
there is death of ___
and progressive ___?
(ni trogen narcosis) 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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Which group of
patients have the
highest risk for
developing steroid
avascular necrosis?

Lots of sclerotic
bone with
radiolucency

Treatment for Addisonian


Crisis secondary to abrupt
cessation of steroid
administration is to …?
Symptoms of acute
Addisonian Crisis include
(list 3)?(6)

• If you stop the steroid purposefully or not, person goes


into period of abrupt or severe period of steroid
withdrawal called Addisonian Crisis (complain of
HPA axis suppression
nausea, vomiting, hypotensive, potassium a little high);
similar to an autoimmune adrenalitis (Addisonian Crisis)
• Treatment for Addisonian Crisis is giving more steroids commonly occurs during
EXAM QUESTIONS! which 2 common
conditions?

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

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

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Name 3 synovial
lined spaces?

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What is the best
way to treat
acute
monoarthritis?

Does
inflammatory
synovial fluid
have high or low
viscosity?
What is the 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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List 3 systemic
therapy options
for acute gouty
arthritis?
In which 2
categories of
patients should
colchicine be
avoided?
In which 3
cateogires of
patients should
you avoid NSAID
treatment of
acute gouty
arthritis?

What are the 2


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

• Gonococcal responds great to 3rd generation ceph


• Non-gonococcal- need treat with IV Abx

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

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

• The sooner you treat the better but don't treat until you have that culture
• Not every joint problem is arthritis;
sometimes may have periarticular

• When thinking
about mono or
polyarthiritis,
always think
about
inflammatory vs.
noninflammatory
• Criitical cell
count: 2000 x
10x6 per liter

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

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

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

• Joint problems can arise in the acromioclavicular or glenohumeral joints

How recognize non articular problems?


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

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List 3 signs of
inflammatory
arthritis?(4)

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


noninflammatory arthritis

• If patients have bursitis, 3 important things to recognize


• Pain arising in one joint area, eg. Hip joint pain referred to knee

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• If do experiemnt and stimulate diff cervical levels can se pain in the • Persistent knawing pain, for example, subphrenic abscess causing
for example peri-scapular area originating in the lower cervical shoulder pain, may not be MSK pain anyway
elements

Now, in this paritcular patient, not worriesd about arthiritis or referred


pain, but focusing on rotataor cuff tenditinitsis

Tendons around
the shoulder

• rotator cuff pain


is felt at the
shoulder!!!

• Even if you forget what a particular tendon's name is , just • Can palpate supraspinatus by moving arm back Rotator cuff pain
rmember you're looking for tenderness along lentght of tendon by • Subscapularis: internal rotation
palpating or put tendon under stretch or stress is referred to the
• Supraspinatus: early part of abduction ___?
• So locla tenderness on plapation, stretch or stress then • Teres minor and infraspinatorus
• If palpate along head of humerus by arm going back then can feel
insertion on humerus; is hard however to stretch the tendons;
most often therefore stress
• Can test impingement at full abduction
• Two other tests:
a. Palm down, hold down scapula and try to
bring rotator cuff tendon forcibly against
acromioclavicular ligament; may produce
pain if jhas impingement
b. Thumb down, internally rotate bent arm

Week10 Page 141


• tendonitis, bursitis and impingement
syndrome, often go together

• Forced forward flexion

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Common extensor tendon: lateral epidcondyle We're going to focus on tennis elbow

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

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• Articular
• Nonarticular
• Referred
• Non-MSK

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

List of differentials are important to keep in back pocket; these are


the commonest things that people come in with and if you havea list
of ddx, then it reminds you of the other things to check for

Week10 Page 144


• Commonly caused by flat feet or bad footwear

• Anteromedial portion of the calcaneus Hip pain means difft things to difft people; if at the side, then from the spine;
• DORSIFLEX TOES CAN STRESS PLANTAR FASCIA TRUE HIP PAIN IS FELT IN THE GROIN REGION!

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• Sometimes osteoporotic patients can come in with pubic ramus fracture

• Abducting or adducting leg puts pressure on trochanteric


bursae

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

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

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The most frequent crystal
induced arthritis is ___?

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

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

Gross urate crystal deposits are


also known as ____?

Allopurinol is a xanthine oxidase


inhibitor which decreases ___
synthesis?

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

Allopurinol is a ___
inhibitor which
decreases uric acid
synthesis?

Allopurinol is the
preferred ___
lowering drug?

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The LEAST
common type of
microcrystalline
arthritis is ___?

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

Go to smhrheumatology.com and see presentations


• Then go to lab presentations; little panel, orange card that you carry • Extractable nuclear antigens: everything that DNA isn't
around in pocket • Eg. Staff doctor says work patient up for VASCULITIS
• In screening looking for sensitivity not specificity; since the tests are ○ Website gives expalantion of every test
not diagnostic; merely support our clinical impression; so if you have a
postiive ana and you feel perfectly okay then likely that you don't have
lupus

• 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
• CRP, ESR
MARKERS OF THE
• Screening test is rheumatoid factor so doesn't matter if goes up
ACTIVITY OF DISEASE;
• HOW DO WE KNOW RHEUMATOID FACTOR DOESN'T or down; value of rheumatoid factor is whether or not it's
ONCE YOU HAVE THE
CORRELATE WITH CLINICAL FINDINGS OF ACTIVITY? Not all positive; if treat, their rhumatoid factor may or may not go
DISEASE THEN
patients with RA have rheumatoid factor; tells you that it's away; it doesn’t' really matter because once positive then it's
UNFORTUNATELY YOU
a marker of disease of how active it is, not of RA itself positive
HAVE THE DISEASE; BUT
• So pick the tests that ARE GOING TO HELP YOU TO MAKE
IF YOU HAVE MESAURES
DECISION S ABOUT TREAMTNET, NOT ABOUT DIAGNOSIS; THAT TELL YOU HOW
YOU'VE ALREADY MADE THAT!
ACTIVE THIS IS THEN
YOU CAN FOLLOW THE
DISEASE
APPROPRIATELY

T/F: There are


conditions, such as in
some infections, in
which rheumatoid
factor levels decrease
markedly?

What is the main


way in which RA
and SLE are
screened for?

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

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

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

• IN RHEUMATIC DISEASES, CRP is a marker for inflammation


• In RA, crp is an indicator of more aggressive jiont damage over
time

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• Note that it's binding to
the common structural
element so it can do so
non-spcifically; only
lookking for that portion
of the IgG
• Certain types of infection
that are classically
associate with
rehumatoid factor
○ Endeocarditis, Hep
C
• If take rheumatoid factor
and inject it into a normal
individaul, LIKELIHOOD IS
THAT THEY DO NOT GET
RA, OR LUPUS
• Rheumatoid factor can also be IgG • Antibodies are a mesareu
• IgG is a measure of chronicity fo the disease being
• Whatever was the stimulus, IgG is the body's reaction to it 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 linked gene
cluster, and having one
or more stretches of a
common short
consensus repeat
encoding a 60 amino
acid domain. Included
are factor H, C4 binding
protein, decay
accelerating factor,
membrane cofactor
protein, and several
complement receptors .
Called also regulator of
complement activation.

• Citrulline: alpha-amino
delta-carbamido normal
valeric acid; it is formed
from ornithine and is
itself converted into
arginine in the urea
cycle.

• Citrullinated = arginine
been replaced with
serine

• Problem with these tests: great in the investigation of disease


• So when no clinical features, no point to ordering tests

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

Almost all patients with


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

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

When should you


order an ANA?

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Anti-Ro (SS-A)
and Anti-La (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?

Which test
VIRTUALLY RULES
OUT SLE if
negative?

What are ANCAs?


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

The major target protein


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

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

Is a positive ANCA
diagnostic of
vasculitis?
What is the
approximate
sensitivity of HLA-
B27 in patients with
ankylosing
spondylytis?

When is HLA-B27
testing useful?

Week10 Page 180


What is
fibromyalgia
syndrome?

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Is fibromyalgia
syndrome more
common in males
or females?

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

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

What value of ESR


must be present
(mm/hr) to suggest
PMR (Polymyalgia
Rheumatica)?

What does PMR


stand for?
What does GCA
stand for?

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

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

Case 1
• History
• 32 year old female
• Pain/swelling hands wrists x 6 mo
• Morning stiffness x 2hrs
• Right knee both wrists tender warm swollen, red
• Weaker by mid morning
• Exhausted painful feet by 3:30 pm
• Ibuprofen 8 tablets per day helped
• 5lb weight insomnia down in the ?

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

1. Which pattern characteristic this patient's illness in terms of anatomic distribution and historic evolution
a. Acute inflammatory monoarticular arthritis
b. Subacute symmetrical inflammatory oligoarthritis
c. Chronic symmetrical inflammatory
d. ?
e. ?

Answer c): Chronic symmetrical inflammatory

Clinical evaluation of arthritis

2. Which most likely process causing this patient's illness


a. Hla b27 associated seronegative arthritis
b. Crystal induced inflammation
c. Infection
d. Immune mediated connective tissue disease
e. Trauma

Answer d): Immune mediated connective tissue disease

3. Which of the following blood test most likely to clinically dx


a. Rheumatoid factor
b. Hlab27 antigen
c. Sedimentation rate
d. Uric acid
e. Blood sugar

Answer: a) rheumatoid factor

4. Which additional test would be necessary to establish a dx?


Lab results
Hb. 100 gm/L
WBC 8x109/L
Platelets 580x109/l
Complete normal
Urinalysis, uric acid, calcium phosphate, kidney, CK

Which additional test would be necessary to establish a dx?

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a. Biopsy of elbow nodule
b. Synovial fluid analysis
c. Chest x-ray
d. All the above
e. None the above

Answer e): None of the above

5. What treatment would be most appropriate at this stage of her disease?


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

Answer: d): Naproxen 500 mg b.i.d. and methotrexate 15 mg weekly

• Naproxen twice a day wouldn't be sufficient to treat her and cyclophosphamide would be overkill; methotrexate is the gold
standard now for management
• Etanercept use if your more modest treatments failed
• No prednisone because no DMARD added

Radiographic profusion of joint erosion and deformity in RA patients


• Most DMARDS we use today actually retard development of erosions of join

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

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

1. What disease?
a. Local non-articular rheumatism
b. Crystal induced arthritis
c. Degeneration
d. General non-articular
e. Seronegative arthritis, B27 positive

Answer: d): General non-articular

2. Which investigation would be least helpful


a. Muscle nexumes (???)
b. An electromyogram
c. Serum uric acid
d. X-ray of chest
e. Sedimentation rate

Answer: C) uric acid

Lab test results


ESR 120, Hb low, white count normal, platelets elevated, normal urine creatinine, alt 25, alp increased somewhat, TSH normal,
ANA negative, chest X-ray normal

3. What' most worrisome possible complication in this patient


a. Pneumonitis
b. Peripheral neuropathy
c. septic arthritis
d. Blindness
e. Myocarditis

Answer: d) blindness

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

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

Case 3
34 man, sever knee pain 24 hours, twisted knee and scraped elbow; pain severe at night; bad with movement, hx of diabetes
juvenile onset 15 year insulin dependent

On exam

Distress, painful immovable knee because of pain, tense warm, has effusion, mild left inguinal lymphadenopathy, and he has
normal general physical exam, and abrasion on left elbow
• Lost dimple in knee medially

Questions:

1. What problem most likely:


a. An acute inflammatory polyarthritis.
b. A degenerative monoarthritis
c. A localized non-articular rheumatism
d. An acute inflammatory monoarthritis
e. A generalized non-articular rheumatism

Answer: d) an acute inflammatory mono

Yes, monoarthritis

Lab results: Hb good, WBC 20, poly: 70% platelets elevated, Glucose 18, not well controlled, creatinine Somewhat
elevated; no cells, protein, ketones

2. Which best diagnostic test to order


a. x-ray of knee
b. Uric aid
c. Culture elbow abrasion
d. Arthrocentesis
e. X-ray SI (sacro-iliac) joints

Answer: d) Arthrocentesis

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

3. What's the best diagnosis?


a. Diabetic neuropathic joints
b. RA
c. Septic arthritis
d. Medial meniscus tear
e. Acute gout

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

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

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b. WBC…?
c. WBC…?
d. Negative birefringent needle shaped crystals
e. Positive birefringent …?

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

Birefringence

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

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

Case 4
50 y.o. female painful right knee, worse on golf course, good health, normal general exam; antalgic gait, favoring right, cool
effusion in right knee, stress pain in right knee

Physical: atrophy of right quads; varus alignment soft knees, means bowlegged

Hard bumps of DIPS in both hands

QUESTIONS

1. What was the probable course of evolution of her arthritis


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

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

Gradual accumulations

2. Which 2 tests most helpful


a. EMG quads bilaterally
b. Weight bearing x-ray both knees
c. Bone scan
d. Serum uric acid
e. Arthrocentesis of right knee

Answer: B, E (I'm almost positive this is what was written but a little less sure of this)
B would say joint space, loss degree of
E would tell you that there's bland fluid

(showed x-ray of knees, on right side medial compartment narrowed)

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

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

3. What least significant risk factor in the patient


a. She walks 3 miles a day
b. She has genu varus
c. She is overweight
d. She is female
e. She is 72 years old

Answer: a) point being least sign risk factor

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

1. Which of these risk factors is least significant?


a. She weights 90 points
b. She smokes
c. Her mother had kyphosis
d. She is sedentary
e. She golfs

Answer: e) she golfs


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

2. T-score -2.5; which best improve:


a. Estrogen supplementation
b. Calcium carbonate talest (?)
c. Vitamin d
d. Risedronate
e. Calcitonin spray

Answer: d) risedronate bisphosphonate

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

Osteoporosis Health Centre - Treatment


Calcitonin
Calcitonin is a hormone secreted by the thyroid gland. It binds to receptors on the osteoclasts and decreasing their ability
to break down bone.
Calcitonin:
• may prevent bone loss in the hip
• may maintain or increase bone mass in the spine
• can decrease the risk of fractures to the spine
• can provide some pain relief from bone pain, especially if related to a spinal fracture
Calcitonin is derived from salmon. It is available in Canada as both a drug that is injected under the skin
(subcutaneously) and as a nasal spray.
Calcitonin Nasal Spray
Calcitonin nasal spray is now available in Canada as Miacalcin® nasal spray. It is currently approved for the treatment of
osteoporosis in women who have been postmenopausal for AT LEAST five years. The nasal spray has also been shown to
reduce pain related to spinal fractures.
The dose of Miacalcin® Nasal Spray is ONE spray (200iu) into one nostril per day. Women are advised to alternate
nostrils from one day to the next (eg. LEFT nostril on EVEN days of the month, RIGHT nostril on ODD days).
Possible side effects of the nasal spray include:
local irritation, dryness or inflammation in the nose

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• local irritation, dryness or inflammation in the nose
• nose bleeds
Other side effects similar to the injection such as facial flushing nausea, chills or skin and allergic reactions may occur,
but RARELY do with the nasal spray.
Bottles of calcitonin nasal spray should be stored in the fridge before use. Women should 'prime' the pump before the
first squirt is used. Each bottle contains 14 full doses. It can be kept at room temperature for one month.
The cost of Miacalcin® Nasal Spray is approximately $600 per year. Miacalcin® Nasal Spray is covered by most extended
(private) health care plans. It is currently NOT covered by the Ontario* Government plan for seniors.
*note: Coverage of Miacalcin® varies for each province
Calcitonin Injection
Calcitonin injection is currently not approved for the treatment of osteoporosis but is prescribed for people who have
fractures of the vertebrae, mainly to relieve pain.
When the subcutaneous injection is used, it is first given as a test dose to check for an allergic reaction to the medication.
Usual treatment is for three to five days in a row, initially, followed by maintenance therapy three times a week. It is
used for up to about six months. Long-term use may decrease its effectiveness.
Possible side effects of the injection include:
• local pain or irritation at the site of the injection
• facial flushing, nausea and chills
• rarely, skin and allergic reactions
These side effects are temporary and may decrease with a lower dose.
Pasted from <http://www.womenshealthmatters.com/centres/osteo/treatment/calcitonin.html>

3. What's her prognosis?


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

Answer: All above are true

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Dr. Bookman: What did you learn this week?

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

FMP 2007-2008 REVIEW QUESTIONS - WEEK 10 – RHEUMATOLOGY

Approach to arthritis
1. What are major categories of rheumatic disease?
2. What are the seropositive diseases?
3. What are the seronegative diseases?
4. What is meant by symmetrical versus asymmetrical?
5. What joints are affected by osteoarthritis?
6. What are non-articular causes of rheumatism?
7. What are features of degenerative versus inflammatory arthritis?
8. What is a useful fourfold classification of functional capacity?
9. What does “avocational activities” mean?

Monoarthritis
10. What are the major causes of mono-arthritis?
11. What tests should joint fluid be sent for in the investigation of a patient with monoarthritis?
12. What tests are available for viscosity?
13. What are the characteristic patterns of findings in the joint fluid for each major category of monoarthritis?
14. What is birefringence?
15. What is chodrocalcinosis?
16. What infectious cause of monoarthritis is most threatening for the joint?
17. What are the features of gonococcal arthritis?
18. What crystals cause arthritis?
19. How is gout treated in the:
a. Acute phase (list four possible treatments)
b. Prevention phase

Connective tissue diseases


20. What is the immunopatogenesis of SLE?
21. What are the 11 criteria for the diagnosis of SLE?
22. What is responsible for deaths in patients with SLE early and late in the course of the disease?
23. What are the clinical features of dermatomyositis and polymyositis?
24. What is the most concerning underlying illness in patients with polymyositis?
25. How is the disease diagnosed?
26. What are the clinical features of scleroderma/CREST/PSS?
27. What is the pathology of scleroderma?

Localized non-articular disorders


28. What is a classification of causes of shoulder pain?
29. What are the major causes of shoulder pain?
30. What is differential diagnosis of elbow pain?
31. What is the differential diagnosis of foot pain?
32. What is an enthesopathy?
33. Where does disease of the hip cause pain?
34. What are the differential diagnoses of hip pain?

Spondyloarthropathy
35. What is spondyloarthropathy?
36. What are the major diseases that are spondyloarthropathies?
37. What are typical extra-articular features of spondyloarhropathies?
38. What is HLA-B27?
39. What are clinical findings in a patient with ankylosing spondylitis?
40. What are radiographic findings in a patient with AS?
41. What is amyloidosis?
42. What are the two major categories of causes of chronic low back pain? Which is more common?
43. What are the key features of inflammatory back pain?
44. What are the New York criteria for diagnosis of AS?
45. What are the two major enteropathic arthritidites?
46. What are 5 patterns of psoriatic arthritis?
47. What is reactive arthritis? What is Reiter’s syndrome?
48. What are extra-articular manifestations of reactive arthritis?
49. What are the major elements of therapy of AS?

Week10 Page 229


Pharmacologic issues
50. What is the safe limit of dosing for acetaminophen?
51. What are the toxicities of acute acetaminophen excess?
52. What are the mechanism of action and effects of NSAIDs?
53. List four categories of side effects of NSAIDs.
54. What are risk factors for NSAID gastropathy?
55. What are cox-2 antagonists?
56. Are they safer? What specific concern is there about cox-2 antagonists?
57. What strategies can be used to reduce the risk of gastric complications in patients taking NSAIDs?
58. What is the value of colchicine in treatment of gout? Side effects?
59. What are the major side effects of allopurinol.
60. List 14 side effects of corticosteroids.
61. What is avascular necrosis?
62. When does acute adrenal insufficiency occur in the context of glucocorticoid therapy, how can it be avoided, and how
should it be treated when it occurs?
63. List 4 DMARDs, used most commonly for patients with RA? What are their side effects?
64. What is a treatment algorithm for mild RA? For severe RA?
65. When should DMARDS be started?
66. What are three biological agents used for treatment of RA, and what are their major side effects?
67. What is the target of these biological agents?
68. What is the impact (in general terms) of these various agents on disease outcome in RA?
69. What is rituximab?

Rheumatoid arthritis
70. What are pathological features of a rheumatoid arthritic joint?
71. What joints are affected in a patient with rheumatoid arthritis? What joints are seldom affected?
72. What are the criteria used to make a diagnosis of RA?
73. What problems may a patient with RA develop related to the cervical spine?
74. What are typical abnormalities in the blood tests of patients with RA that reflect systemic inflammation?
75. What are the radiographic abnormalities seen in a patient with chronic RA?
76. What is the typical evolution of joint problems in a patient with RA?

Autoimmunity
77. What are three pathways that lead to autoimmune reactions?
78. What is meant by organ-specific autoimmune versus non-organ specific autoimmune diseases, and what are examples
of each?
79. Which organs tend to be affected by non-organ specific autoiimune reactions?
80. What is tolerance?
81. What is a rheumatoid factor?

Vasculitis
82. What is the overall classification of vasculitides?
83. How does vasculitis affect each of the following:
a. Skin (medium versus small vessel)
b. Kidneys
c. Nervous system
d. Heart
e. Lungs
f. ENT
g. Eyes
84. What are the clinical features of giant cell arteritis?
85. What are the two major diagnostic tests for giant cell arteritis?
86. What is the treatment for GCA?
87. What are clinical features of PAN?
88. What underlying viral illness is associated with PAN?
89. What are three types of vasculitis associated with ANCA?
90. What are renal manifestations of ANCA-associated vasculitis?
91. What are the therapeutic strategies used for ANCA-associated vasculitis?

Blood tests in diagnosis of rheumatic disease


92. What are “routine” blood tests that may be helpful in the diagnosis of rheumatic disease?
93. What is the main particular use of ESR?
94. What is CRP? How is it helpful?
95. When should rheumatoid factor be ordered?
96. What other than RA is associated with rheumatoid factor?
97. When should ANA be ordered?
98. What are the sensitivity and specificity of RF for RA, and of ANA for SLE?

Week10 Page 230


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

Generalized pain syndromes


104.What is fibromyalgia?
105.What are associated complaints in a patient with fibromyalgia?
106.What is the basis for fibromyalgia (probably)?
107.What are elements of therapy for fibromyalgia?
108.What is PMR? How is it diagnosed and treated?
109.What are other causes of generalized pain?

Osteoarthritis and low back pain


110.Which joints are most frequently affected by osteoarthritis?
111.What is the pathogenesis of OA?
112.What are clinical manifestations of OA?
113.What are risk factors for OA?
114.What are the elements of management of OA?
115.What medications are available for the management of nociceptive and neuropathic pain in OA?
116.What are red flags in a patient with low back pain?
117.What is appropriate workup of a patient with low back pain with no red flags?
118.What is appropriate treatment of a patient with acute low back pain?

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

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&amp;bsession_str=session_id=11327372,user_id_pk1=501825,user_id_sos_id_pk2=1,one_time_token=>

Week10 Page 231


0_Intro
Friday, February 29, 2008

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

In deciding whether or not you


should operate on a patient, what
should you consider? (hint: _____ vs.
_____?)

• Here that we need to have some sort of rational


system to decide whether or not patient will benefit
from surgery

What does APACHE II stand


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

• Assessing benefits usually much easier and more


straightforward than asessing risks • Most of patients we deal with have variety of illnesses
• Acute physiology and chronic health evaluation (APACHE) - that don't fit into these easy schemes (APACHE II)
semi-quantitative way of assessing risk • Instead, see how many organ systemsdysfunctional ;
• APACHE II 3 factors: assess each one to determine whether or not
○ How sick patient is when comes in workinga nd the number not working properly giv
○ Patient's chronic health status eyou guesstimate fo risk
○ 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

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

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Apart from history and
physical, how would you
assess endocrine organ
dysfunction?
Apart from history and
physical, how would you
assess coagulation status?
Apart from history and
physical, how would you
assess renal dysfunction?
Apart from history and
physical, how would you
assess respiratory system
dysfunction?
• Renal: use serum creatinine to tell you Apart from history and
whether or not kidneys working physical, how would you
• Toronto historically lead centre in world assess cardiovascular
for assessment of nutritional readiness of system dysfunction?
patients for surgery Apart from history and
• Endocrine: history: are you a diabetic, do physical, how would you
you take insulin, etc. assess hepatobiliary
dysfunction?

What kind of help do we have?

• What you do to prepare depends on urgency

T/F: Patients who


are hypothyroid
react poorly to
general anesthesia
and surgery but not
patients who are
hyperthyroid?

• Amazing how many patients suffer from pulmonary • Patients who are hypo or hyper thyroid react very poorly to
emboli and DVT's after surgery (now that we have CT's general anesthesia and surgery
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

Week11 Page 7
List 2
cardiovascular
system conditions
and their
associated
treatments that
you can prevent
post-surgical
cardiovascular
complications for?

• Use of anticlotting agents such sc heparin decrease sig.


chance of dying from pulmonary embolus
○ If look in journal CHEST every couple of years send
out special supplement describing how do DVT
prophylaxis in which patients
○ Similary neurosurgical patients with tumors;
hypercoagulable and more prone to get DVT and
pulmonary embolus but thing you have to prevent
after neurosurgery is prevent bleeding! So trickly
to prevent this

Which drug class is used


for ulcer prophylaxis
prior to surgery?

• NOT feeding the patients is the WORST thing you can do to


List 4
patients!
"An ounce of prevention is ○ Been shown to decrease the length of time of ileus
preventative
actions that could
worth a pound of cure" ○ Stress GI bleeding one of complications of srugery or being
be undertaken to
ill in general prevent post-
○ Ulcer prophylaxis will eliminate stress bleeding or stress
surgical
ulceration cardiovascular
system
complications?(6)

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

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

Week11 Page 8
List 2 preventative
actions that could be
• Some very influential papers in NEJM from western undertaken to prevent
europe showing in ICU pop. Tight control of blood post-operative
glucose greatly decreased morbitidy and mortality rates endocrine system
• Reasonable blood glucose control therefore improves complications?
outcomes
• Problem with oriignal papers: in reality, too many
episodes of hypoglycemia

Week11 Page 9
3_Pain Mgm
Friday, February 29, 2008

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

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What is multimodal
analgesia?

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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
• Pain pathway is complex but even this is an oversimplification of the pathway the transmission of pain
at which site of the pain
pathway?

Which nociceptive
factors does
dexamethasone
prevent the release of?
Which is the primary
nociceptive factor that
is blocked through the
use of celecoxib?
• When we have tissue damage, inflammation occurs; interleukins and cytokines Local anesthetic blocks
released; cyclooxygenase 2 is induced; makes prostaglandin E, which is necessary the transmission of pain
to activate nervous system via lowered threshold of nocicceptors and allows to fire along which arm of the
via stimulation by substances such as bradykinin pathway 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 like
gabapentin and Ketamine:
prevents sensitization of
the nervous sytem; thus,
prevents amplification of
the pain signal
• Finally, opioids, prevent
transmission from spinal
cord to the brain

• Therefore multiple drugs,


preventing pain
transmission

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

PREVENT ACUTE PAIN TO PREVENT CHRONIC PAIN!

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

Week11 Page 14
T/F: Preventing acute
pain is a minor risk
factor in the prevention
of post-operative
chronic pain?

• Calculated chronic pain rates correlating with surgeries


• Preventing acute pain will not necessairly prevent chronic pain; not ONLY risk
factor but certainly MAJOR RISK FACTOR!

ALSO important to treat pain before come to hospital

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

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

• So if have someone on acetaminophen and


ibuprofen then additive effects

What effect does


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

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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

In addition to
being an
analgesic,
Gabapentin is
also a(n)
_______?
The optimal dose
• Improves movement associated pain of gabapentin is
• If go up to 1200, 1400 mg. then have to consider greater side effects ______mg?

Week11 Page 17
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?

• No adverse effects
from single dose of
dexamethasone

• Speed recovery In using


• No adverse effects from single dose dexamethasone
as an analgesic,
which other
analgesic does it
reduce the
consumption of?
T/F:
Dexamethasone
and pregabalin
are in the same
drug class?

Week11 Page 18
Which analgesic
method gives the best
movement associated
pain relief?
Does oxycontin have a
biphasic or monophasic
release?
• The technique that gives best movement associated pain relief
The duration of
• Eg. Continuous femoral nerve blocks also good after knee arthroplasty
oxycontin release is ___
• Goal of nerve blocks: JUST enough nerve blocks to eliminate pain; want to keep sensory and nerve pathways
hours?
• Remember pain carried by C fibers, very small, unmyelinated; bigger ones responsible for motor and sensory

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

• Major problem after colon surgery: get reflex ileus


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

Week11 Page 19
Ketamine or Clonidine
consumption will
decrease the
consumption of which
other class of
analgesics?
What is a downside to
the use of ketamines?

List 5 multimodal
analgesics that
have additive
effects?

Week11 Page 20
What does PCEA
stand for?
List 2 drugs that
reduce PCEA use?

• PCEA: Patient controlled epidural analgesia


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

If use
multimodal
analgesia,
can
elminate
opioids
completely!

Why is it
advantageous to
give analgesics
prophylactically
rather than after
surgery has
started?

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

Week11 Page 21
List 5 multimodal
analgesia agents
that improve
outcomes?
• Gabapentin: with ACL
patients had better
knee flexion and less
anxiety: with breast
surgery: lower incidence
chronic pain at 6
months
• Dexamethasone:
laproscopic
cholecystecomies;
better outcomes, better
return to function
• Epidurals: less length
of stay after colon
surgery
• Use of long acting
opioids: less length of
stay after knee surgery
LES = lower extremity
surgery

If you could use Ketamine


OR Gabapentin, which
would you use for
What prof would do for most surgeries intraoperative analgesia, if
both were equally
indicated? Why?
Pre-operatively, list 4
medications and one
optional medication that
you would give for pre-
operative analgesia?
Intra-operatively, list 3
medications/techniques
and one optional
medication that you would
give for intra-operative
analgesia?

• Ketamine has a higher side effect profile and


gabapentin does basically the same thing so
best to use gabapentin if you can

Week11 Page 22
• HAVE TO CONTINUE MULTIMODAL
ANALGESIA when patient goes home!

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

: TOTAL HIP ARTHROPLASTY


(usually takes 2 hours for peak effect of
these drugs when given orally)

Give an example of
• Put spinal in to decrease dosages and medications
sensitization of the CNS 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?

Week11 Page 23
Intra-operatively,
which mediation
would a surgeon
administer via local
infiltration?

• PCA: patient controlled


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

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

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

Out of the following 4


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

Week11 Page 24
IL-1
Monday, March 03, 2008
10:44 AM

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Gabapentin
Monday, March 03, 2008
10:43 AM

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

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

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Ketamine
Monday, March 03, 2008
10:56 AM

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PCA
Monday, March 03, 2008
10:58 AM

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5_Gallbladder & Biliary Tree
Friday, February 29, 2008

List 4 factors that


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

Week11 Page 56
List 2 populations
in which there is a
clear correlation
between
increased
gallstone risk and
family history?
Why is there an
increased risk of
gallstones in
patients who are
morbidly obese?

List 5 diseases
which are risk
factors for
gallstone
formation?

• These risk factors are


key to know
• Long TPN: see in the ICU: patients
who are starved are on TPN; not
eating or drinking anything
• Why does resecting the terminal
ileum lead to formation of
gallstones - because terminal
ileum is area of small bowel that
bile acids are absorbed from; if
you don't have absorption of bile
acids, then the the enterohepatic
circ of bile depends on
reabstorption of bile from this
circulation but if don't have it
then liver keeps pumpting out bile
HOW DO GALLSTONES FORM?
What are the 3 critical
phases in the formation of
gallstones?

T/F: Prophylactic
cholecystectomy is
indicated in 1% of
asymptomatic patients
over 20 years?
When is surgery
recommended for
patients suffering from
gallstones?
List 4 symptom
complexes that
patients with gallstones
• US very common now; almost always find commonly present
gallstones; before, tradition was to take with?
gallbladder out but after landmark study,
Acute cholecystitis is
found that you should not take gallbladder
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
Acute cholecystitis is
found that you should not take gallbladder
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?

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

Week11 Page 58
List 2 treatments that are
indicated for biliary colic?

• Explainging what are the different type of symptom complexes


that patients can present with.

What is bilary colic?


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

• Biliary colic is CONSTANT pain!

How can cholecystitis be


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

• In biliary colic, the stone obstructs the cystic duct, • Positive murphy's: patient takes in big breath, and
but here, the stone stays stuck (in acute you palpate the right upper quadrant, then as the
cholecystitis), then get secondary infection; MUST patient breathes IN, you may feel the gallbladder
TREAT WITH ANTIBIOTICS coming down

Week11 Page 59
Treatment of acute
cholecystitis involves the
administration of ___, ___,
and ___?
Approximately which
percentage of patients with
acute cholecystitis improve
without surgery?
When is early laparoscopic
cholecystectomy indicated
for patients with acute
cholecystitis?

• Sympx: acute attacks of acute cholecystitis

• Means a patient will complain of vague abdominal


pain that is very hard to pin down! Will say "doctor, I
feel very bloated"

Week11 Page 60
• Gallbladder wall is very thin; 1mm in diameter

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?
• 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

Week11 Page 61
If in the presence of gallstones,
LFTs are abnormal, then one must
determine whether they are …(3)?

What is the incidence of acute


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

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

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

• Most common cause of pancreatitis: gallstones and alcohol


• Best treatment here is to get rid of the stones using endoscopic
means (ERCP)

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 biliary
sepsis?

What is the
etiology of
cholangitis?

Within the context of


cholangitis, what is
charcot's triad?

After which surgical


procedure is there an
increased risk for
cholangitis to develop?

Fever, Jaundice, and


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

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List 3 steps in the
management of
cholangitis?

List 3 different methods of


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

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6_Abdominal Infection
Friday, February 29, 2008

Some terminology...

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

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

• Barium + stoll is LETHAL!


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

• Perforated diverticulitis: most likely diagnosis for pain starting in


left lower quadrant rebound tenderness, generalized abdominal
pain severe after 5 minutes, pain now radiating up to upper right
• Fistula: abnormal connection between two epithelial lined
surfaces
○ Eg. Leak from the gut to bladder or another site of the body
• Renal failure one of multiple organ failures that can occur; if
sustain this and survive, then will be on dialysis for the rest of your
life

Ileus is a disruption of the normal propulsive gastrointestinal motor activity from non-mechanical mechanisms [1][2].
Motility disorders that result from structural abnormalities are termed mechanical bowel obstruction. Some
mechanical obstructions are misnomers, such as gallstone ileus and meconium ileus , and are not true examples of
ileus by the classic definition [3].

Pasted from <http://en.wikipedia.org/wiki/Ileus>

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

What is a PEG
tube?

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

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

• Need LOTS OF FLUID - UP TO 20L - because capillaries leak


• 7 day rule: if the patient will not get meaningful nutrition for a
week, needs TPN or some other kind of supplementation or
else will get immunosuppressed

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7_Bowel Obstruction
Friday, February 29, 2008

What is anotehr name for


colonic ileus?

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

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
• Intramural causes of small bowel obstruction extraluminal cause of
large bowel obstruction?
• Crohn's disease can go on to cause stricturse Give 2 examples of
○ One common example of an intramural benign inflamatory cause of bowel obstruction intraluminal causes of
○ Another one: radiation stricturs small bowel obstruction?
 Thrownthis in because a number of benign inflamatory problems that can cause this; mentioned Give an example of an
intraluminal cause of
ulcers; typically in women who have been treated with a combination of external beam radiation and
stomach and duodenal
internal seed radiation with carcinoma of the cevix; get rctal stricturse because of proxilmity and obstruction?
terminal ileum also sitting behind it so get radiation enteritis Give 3 examples of
 So ther are multiple benign lesions that can affect the bowel intramural causes of small
• Extramural causes of small bowel obstruction: dhesions: usually the result of a surey; wheneer operate on the bowel obstruction?
Give 3 examples of
stomach, in the process of healing, patients often left with fibrous bands from one arae of the body to the
extramural causes of
other; this allows a fixed point of the small bowel to kink or herniate small bowel obstruction?
• Basic idea is always the asme: adhesions sually from surgery; maybe also had appendicitis Give an example of an
• Adhesive bowel obstruction therefor quite common in ER extramural cause of
• 2nd to that and worldwide same order of magnitude: incarcerated hernias: can have a femoral aor groin stomach and duodenal
obstruction?
hernias: cough vigorously and the neck of the henia would be pinched by the contours of the hernia: px: painful
groin mass and signs and syplmtomsp of bowel obsturcution
• Incarceration:
• Peirtoneal carcinomatosis: many cancers in the perineal cavity: thesecan grow up and twist off any portion of
bowel
○ Usually metastases: caells on the serosal aspect of the stomach will go off and break off; most common
with overian cancer; usulally very diff. to treat, esp. if tumor dsn' respond to chemox
• Large bowel
○ Intralumnial
 Very uncommon; since bowel is so large;
 Typically see what appears to be large bowel obstruction due to constipation; usually hard stool in
distal ends of the rctum
○ Intramural
 Number of posibilities

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□ Benign
 Ibd - particularly crohn's diseaseradiation strictursre (women radiated for carx of the
cervix)
□ MALX:
 Most common: ADENOCARCINOMA: commonly prsents with large bowel obstruction
○ Sigmoid volvulus:

• So if you get bowel obstruction, what happens to you?


• Clinical presenation varies somewhat as to level of
obstruction and cause of obsutciton

List 2 common
signs/symptoms of gastric
outlet obstruction?
List 3 common
• Early satiety: Eat breakfast okay but not much lunch or dinner; signs/symptoms of small
don't get hunger pangs; sometimes may compalin of vomiting bowel obstruction?

• Typcially presnts very acutely ; typically come to


emerg within a few hours of theonset of obstruction;
ason is that most of the cuases of smal bowel
obstruction present suddenly: get incarcrated in a
chernia , for example; raction of bowle is to
peristalse with an even stronger magnitude of
• CLASSIC PX (PRESENTATION): • 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

• If wall tension in your colon does


incrase suddenly
(PASSAGE OF NOTHING PER RECTUM)
• Should NOT have periteonale signs
such as tenderness or guarding
○ Should laso not have fever or
white count
○ If do see patient in emerg with
bowel obstruction, want to lok
for signs fo groin hernias: often
miss dx of incarcerated henia

How does small bowel


obstruction typically
present?
What is the definition
of obstipation?

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With respect to
laboratory findings,
prolonged gastric
outlet obstruction
leads to ___?

(in bowel obstruction)

• One exception to what mentioned: gastric


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

• Nowadays, don't even really do 3


views of abdomen; do CT scan; if
suspecting obwel obstuction
because of clnical presentation,
etc. then just go straight to ct scan
• CT very good at showing rare
obturator hernia
• Strange abdominal wall hernia:
spigelian hernia

A Spigelian hernia (or lateral ventral hernia) is a hernia through the spigelian fascia, which is the aponeurotic layer
between the rectus abdominis musclemedially, and the semilunar linelaterally. These hernias almost always
develop at or below the linea arcuata, probably because of the lack of posterior rectus sheath. These are generally
interparietal hernias, meaning that they do not lie below the subcutaneous fat but penetrate between the muscles The laboratory finding of
of the abdominal wall; therefore, there is often no notable swelling. hypochloremic,
Most of these hernias are small, and, as such, there is a high risk of strangulation. Most of them develop around hypokalemic metabolic
age 50 (4th-7th decade of life). As an entity, they are rare,[1] when compared other types of hernias. alkalosis is pathognomic of
___?
Pasted from <http://en.wikipedia.org/wiki/Spigelian_hernia> What is the treatment for
a malignant obstruction?
What is an incarcerated
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
surgically
• Nowadays, particularly, if in rctum, then
can do stent placed in
• Occassionally perioteneal carcinosis due
to carcinoma of the ovry, then can treat
with radiation
○ Not often can do this though

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

• Don't operate on adhesive bowel


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

Closed loop bowel obstruction

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

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

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8a_Abdominal Infections
Friday, February 29, 2008

• Ulcer, appendix, diverticulum, inschemic bowel, all can perforate


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

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
• Primary: • From the microbiological point of view, it's logical that the
two categories?
○ underlying serositis and ascites is common cause of the inffection is not going to be homogeneous
complication; may result in abupt change in general • Because the gut has large numbers of different organisms, then
condition; primary means there is no obvious these infections are suuslaly polymicrobial; very commonly and
perforation typically will have mixture of anaerobic organisms
• Secondary:
○ large number of bacteria normally present in bowel
at hat level infect peritoneal spaces
 CAPER: Community acquired peritonitisk
 HOPER: HOSPITAL AQUIRD PERITONITIS: tend
to be due to mor drug resistanct or abx
rseistant bacteia; may influence management

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

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

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

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8b Abdominal Infections Notes
Friday, February 29, 2008

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9_Intro to Anesthesiology
Friday, February 29, 2008

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What are the 5 A's of
anesthesiology?

• Propofol: makes people go to sleep; doesn't do anything for pain


control; not part of any major drug group

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• Most common benzo is midazolam: has prominent amnesia • Koran patient diagnosed with pancreatic cancer; tried to kill himself
effects stabbing with kitchen knife
○ Story of the wimpy football player :-) • ANY OPERATION IS CONTROLLED TRAUMA
• Rohipnol: what they call midazolam in the UK; most chemically • Job of anesthesiologist is to keep vital signs stable
resembles midazolam

In the process of
preparing
someone for
surgery and during
the surgery is itself,
• Stres axis is euphamism for sympathetic tone (body's when is
esponse to stress or pain) sympathetic tone
• Opiates, muscle relaxants, propofol, have to give to the highest?
counteract stress rseponse

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• NOT GOOD TO DO ANESTHESIA IN THIS PATIENT BECAUSE WILL VOMIT IN RESPONSE
TO ANESTHESIA ADMINISTRATION • Here do a ring block
• Jaundice: suspicious: perhaps prolems with absorption and elminiation of anesthetics • If on area of the body you can't do a ring
• Chest pain: remember have stress rseponse with surgical sitmulus block, then just put a little lidocaine
• Best therefore get all these issues rsolved before operation or at least bette managed around area of wound

What is the
distinction between a
regional and local
never block?

• Distinction between a local and rgional block • Takes five needle punctures around area of the foot
○ If neve has name, then it's regional • All the complications of a general anesthetic can be avoided by doing
○ In this case would do an ankle block spot neve blocks

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

What is the difference


between an epidural and
a spinal?
What effect does
ketamine have on sleep?

• Ketamine causes TERRIBLE NIGHTMARES

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

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

Is malignant hyperthermia
autosomal dominant or
recessive?
T/F: The penetrance of
KNOW MALIGNANT HYPETHERMIA FOR EXAM! malignant hyperthermia IS
NOT variable?
What is the approximate
incidence of malignant
hyperthermia?
Ventricular fibrillation What is the incidence of
malignant hyperthermia
caused secondary to
nitrous oxide
administration?

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

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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
• Dantrolene blocks the ryanodine receptor • Should differentiate this from malignant hyperthermia hyperthermia, what was
the mortality rate from
malignant hyperthermia?
T/F: Malignant
Hyperthermia is the
modern name of
Neuroleptic Malignant
Syndrome?

• 2.5mg/kg is usually a large dose but it comes in small volumes


so have to usually open up 5 bottles and it comes in poder and
it comes like sand; takes a while; dilutes like sand; very difficult
to administer

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Propofol
Friday, March 07, 2008
10:23 AM

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Halothane
Friday, March 07, 2008
10:24 AM

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Midazolam
Friday, March 07, 2008
10:30 AM

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

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

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

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11_Pre-Op Prep
Friday, February 29, 2008

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

• What are the downsides of doing a CT


○ CT is not insignificant radiation
○ Time

• LFT is so low in healthy people that it wouldn't be useful to do


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

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 Wound infection: 5 to 10% of patients who have appendectomies
 Will likely heal secondarily
 Perforation during surgery: cecum, terminal ileum
 Also talk about complications that are rare but important
○ Talk about risks and benefits ultimately then: risks of not having operation
○ If it hasn't perforated, then will have risk of perforation
 Appendix will perforate and get gram negative bacteria and develop
intraabdominal abscess and then travel through portal vein and settle into
liver abscesses
• What would you do differently if patient was a 12 week pregnant
19 year old woman?
○ No CT US instead
○ 10-11,000 normal WBC for woman

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

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

• What if guy is 82, diabetic, leg amputation, dbtc, tumor in rectum


○ Ablation! Can do endoscopic ablation; or cryotherapy (don't have seame durative bneefit);
so other options besdies abdominal curative resection

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

palliation

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

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

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

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• Mnemonic for post op order is DAVID
• Crepitus for wound is feeling of subcutaneous emphysema
• D: Diet
• A: Acitivity
• V: Vitals
• I: Investigations/nursing orders
• D: Drugs

• Physical exam: start with vitals; temp: 39.2; looks sick


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

• Post-op: hypotensive with oligouria:

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Abdominal perineal resection

• Hypovolemia: related to bleeding


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

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(from Tuesday case)

• NPO, NG tube stays in!


• Will have significatn gastric ileus

• DDx: PE, PE, PE!


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

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Answers to Pre- Post- Op Scenario Seminars

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Week 11 Review Questions

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1_Intro Trauma
Friday, March 14, 2008

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2_Mgm Airway Breathing
Friday, March 14, 2008

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3_Hypotx in Trauma
Friday, March 14, 2008

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4_Thracic and Abd Trauma
Friday, March 14, 2008

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• Can get lots of false positives and negatives

• Injury to
spleen often
accumulates
between
spleen and
kidney

• Usual way assess abdomen in trauma room

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• Never used to diagnose specific injury; looking for
free fluid (blood)!

• Need 400cc of blood in abdomen


for it to be seen on FAST; so what
you can do is repeat it

• CT: SHOULD NEVER BE IN


A CT SCAN WITH A (and you have an
HYPOTENSIVE patient
indication that
there's blood in the
abdomen)

• Excellent for solid organ; not that good for hollow


organ injuries
• May see extravasation of contrast; need to go to OR or
do angio suite since surgeon can embolize it

• If gunshot has penetrated peritoneum, then the


patient needs surgery; incidence of intra
bdominal surgery to some structure is very high
so need surgery

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

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

• Become now a role for non-surgical manamgent; if


hemodynamically stable, then can admit to icu

• Usually leave packs in abcomen in damage control


lapartotomy

• Increased abdomeinal pressure: usually 20-25 mmHg


• And end organ dysfunction
• Treatment for ACS is open abdomen, fasciaand skin and put some dressing on it

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

• In blunt trauma, the overall incidence of inuries to the c-


spine specifgically is about 2 to 3 percent
• Includes fender benders s and all other kinds of trauma • Missing an injury to c-sine: disastrous consqcs
• 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

Common reasons
why people miss
c-spine injuries

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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
• Chin lift or jaw thrust DO cause movement of c-
HAVE NO INJURIES
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

If CT scan normal, can


still have a ligamtneous
injury; must examine
again to make sure
don't have any
ligamentous injury; this
• No pain with rotation, flexion, • Remember CT scan is done IN AXIAL PLANE; cuts maybe in the is not common but big
extension of same plane as cuts or between cuts; but can now reconstruct problem is that the
the c-spine images; so if have qualified neurosurgeon or orthopedic or consequences of
radiologist, then radiologically, that spine doesn't have any bony missing it is that the
injuries; BUT you can have a normal CT scan but can have a consequences are
ligamentous injury; SO NOT ENOUGH TO JUST DO A CT scan 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

key is loss of reflexes; with complete


Level of lesion; inuries, have the reflexes but are
overactive often

• With vulvar cavernosus reflex, lose the reflex of


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

• 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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6_Neurotrauma - Brain Injuries
Friday, March 14, 2008

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

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

• It strips the dura off inside of skull but held in place


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

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SUBDURAL HEMATOMA CONTUSION; really hematomas in the brain

• Look at diff: instead of being lens shaped, here dura is still


attached to inner table of cortex; usually due to bridging
veins; from inner table of skull into brain; get torn and you White: skull (bone), blood, or contrast
get subdural hematoma • So if you're doing an abdominal CAT scan, do head ct
first because…

Diffuse axonal injury

• Diffuse axonal injury: shearing of the


brain; disrupt millions of axons; CT
scan can be very normal
• GCS: devised in 70's
• Normal CT with bad neuro
• Very useful to follow patient's progress
• Also great for communication

• CRUCIAL TO KNOW THIS; use it not only for brain


injuries BUT ANY NEUROLOGICAL IMPAIREMENT, IE.
STROKE
• Supraorbital pressure best to assess pain; sternal rub
leaves marks

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

• Hypoxemia and hypotension together in a


patient with severe TBI, then 80 to 100%
death

• By the time see them in the hospital, they've already had their injury
• Maintain CPP (Mean arterial presure - ICP); normal CPP = 90 mmHg; normal ICP about
10mmHg

• How opitimize cerebral perfusion pressure?

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If ICP increases, you can herniate

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

• If you're hyperthermic, then need to prevent and treat hyperthermia


• Remember CAN HAVE NON-CONVULSIVE SEIZURES!

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7_Organ_Tissue Donation
Friday, March 14, 2008

Within the context of


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

• Hospitals DON't accept spinal cord donations following death


• Donation can come from anyone who dies from any cause

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

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

Clinical examination for


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

T/F: Ancillary testing


is done IN
CONJUNCTION
WITH and NOT AS A
SERIES OF STAND-
ALONE
CONFIRMATORY
TESTS for NDD?

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

Week12 Page 45
TGLN = Trillium
Gift of Life
Network

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

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

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8_Tues Sem
Friday, March 14, 2008

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

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

List 3 common reasons


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

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

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09 FMP 2008 THURS Trauma Radiology Seminar Notes.pdf

<file://C:\Documents and Settings\Mr. Intensity\My Documents\1Medicine\2ndYearFiles\1FMP-2007\Week12\09


FMP 2008 THURS Trauma Radiology Seminar Notes.pdf>

Week12 Page 55
FMP 2008 Trauma Week Q & A - PART 1.pdf
Tuesday, April 01, 2008
10:20 PM

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

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

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

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00 FMP 2008 Week 13 Intro Pages.pdf

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Pain Week Student Manual 2008
Saturday, March 22, 2008

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

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

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