Dear Followers and Visitors,
I am happy to inform you that the blog "Pathology: You Can Do It" has grown out into the website "M.Y. Pathology Project" located at http://sites.google.com/site/mypathologyproject/home. I am updating and transferring all material to the website, and I hope you will like it.
See you there,
Dr. Y.
Monday, January 11, 2010
Wednesday, November 25, 2009
Pathology Club Conference “Nutritional Ways to Prevent Cancer: Dietary Factors that May Be Causative or Protective Agents”
On Tuesday, November 24th, the Pathology Club had the last conference for this September-December 2009 Semester with the topic “Nutritional Ways to Prevent Cancer: Dietary Factors that May Be Causative or Protective Agents”.
We had ten excellent presentations of based on literature research where contributors tried to disclose a possible role of dietary factors in carcinogenesis and also to give an answer to the exciting question "can dietary modification inhibit neoplastic transformation and growth?"
We had ten excellent presentations of based on literature research where contributors tried to disclose a possible role of dietary factors in carcinogenesis and also to give an answer to the exciting question "can dietary modification inhibit neoplastic transformation and growth?"
“Fruit and Vegetable Consumption in the Prevention of Cancer” by Lindsey Haga
“Beneficial Role for Folate in the Prevention of Colorectal and Breast Cancer” by Robert McEvoy
“Selenium in Cancer Prevention: a Review of the Evidence and Mechanism of action” by William Bradford
“Chemoprevention of Lung Cancer: The Rise and Demise of Beta-Carotene” by Rachel Lacy
“Vitamin D, Calcium Supplementation, and Colorectal Adenomas” by Rebecca Charland
“Effect of Dietary Flaxseed on Serum Levels of Estrogens and Androgens on Postmenopausal Women” by Nathan Amrine
“Multi Targeted Therapy of Cancer by Omega-3 Fatty Acids” by Richard Chan
“Meat, Meat Cooking Methods, and Preservation, and Risk for Colorectal Adenoma” by Latha Jayakumar
“Overview of the Risks and Benefits of Alcohol Consumption” by Aisha Wafa
“Apoptosis by Dietary Factors: the Suicide Solution for Delaying Caner Growth" by Glynn Faircloth
The presentations were very welcome by the audience; each report raised a wave of questions, which from time to time grew in shot discussions.
The End
Monday, November 23, 2009
SJS, TEN, & SSSS
Steven-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe life-threatening conditions with morality rate of ≈5% and ≈30% correspondingly. They belong to a group of so-called dermatologic emergencies which also encompasses such horrifying maladies like cutaneous anthrax, necrotizing fasciitis, meningococcemia, staphylococcal scalded skin syndrome, etc.
Both SJS and TEN, as well erythema multiforme (EM) per se, represent a cluster of skin diseases known as interface dermatitides with characteristic damage of dermal-epidermal junction and formation of subepidermal blisters. For years dermatologists regarded SJS and TEN as severe variants of erythema multiforme. It sounds quite reasonable because despite of certain difference in etiology and presentation, the pathogenesis of all three diseases overlaps in many aspects:
1) Hypersensitivity reaction to an exogenous antigen, either drug or infection
2) Epidermal infiltration with CD8 lymphocytes and macrophages, and dermal infiltration with CD4 lymphocytes
3) Cell-mediated cytotoxicity affecting keratinocytes
• Perforin-granzyme and/or FAS-FAS ligand mechanisms
4) Apoptosis (sometimes named as necrosis or dyskeratosis) of keratinocytes often affecting the full thickness of the epidermis
5) Vacuolization and formation of subepidermal blisters
What is the difference? What is the matter to distinguish these conditions?
The answer is simple: erythema multiforme is a benign, self-limited disorder with excellent prognosis. On the opposite side, SJS and TEN are rapidly developing and potentially fatal diseases and their prompt diagnosis and treatment can greatly improve outcome and reduce mortality rate. Below you can find a brief presentation of each of these diseases oriented mainly toward their differential diagnosis.
Erythema multiforme
1) Precipitating factors: infections (HSV, EBV, histoplasma, Mycoplasma pneumonia, etc)
2) Skin rash characteristics: three-zone target lesions – centrally located necrotic area or vesicle, intermediate zone of edema and blanching, and peripheral hyperemia;
3) Location of skin rash: extremities are mostly affected
4) Mucosal involvement
a) Without oral cavity lesions: erythema multiforme minor
b) With oral bullae and erosions: erythema multiforme major (bullous erythema multiforme)
SJS
1) Provoking factors
a) Drugs: sulfonamides, anticonvulsants, NSAIDs, aminopenicillins, cephalosporins, etc
b) Infections: viral, bacterial, or fungal
o A history of infection alone, without medication treatment, may direct the diagnosis toward bullous EM
c) Graft-versus host disease (bone marrow transplantation)
d) Malignancies
2) Skin rash characteristics: two-zone target (targetoid) lesions – confluent erythematous macules with purpuric centers which rapidly evolve into flaccid blisters (full-thickness epidermal necrosis); later blisters rupture with denudation of red oozing dermis. Total area of detached or “detachable” epidermis with positive Nikolsky sign is less than 10% of body surface area (BSA).
3) Location of the rash: the lesions appear on the face and upper trunk and then extend to the abdomen, back and proximal extremities; distal extremities are relatively spared.
4) Mucosal involvement: erythema, blisters and erosions affecting the lips, oropharynx, conjunctiva, esophagus, trachea, bronchi, urethra, etc; hemorrhagic crusts over the lips.
TEN
Provoking factors, skin lesion characteristics and location, and mucosal involvement are the same as in SJS with only exception of the area of affected epidermis: bullous changes are seen over 30% of BSA and more.
When blistering eruptions are found over from 10 to 30% of the BSA, the condition is referred to as SJS/TEN overlap syndrome.
Because SJS, TEN, and SJS/TEN overlap syndrome have similar precipitating factors, identical pathomorphologic features and comparable clinical patterns, they conventionally considered as different representatives of the same disease process.
Staphycoccal Scalded Skin Syndrome (SSSS) is a rare type of staphylococcal infection characterized by an extensive detachment of the epidermis, which clinically can resemble TEN. But opposite to TEN, SSSS affects predominantly neonates and infants and is associated with much lower mortality rate. This condition occurs in children with a history of staphylococcal infection and fully blown clinical presentation: focus of pyogenic inflammation, fever, positive bacterial culture, etc.
The pathogenesis of SSSS is linked to staphylococcal exotoxins, which damage desmosomes of keratinocytes in the stratum granulosum with subsequent detachment of stratum corneum. Characteristically, inflammatory infiltration and apoptosis/necrosis of keratinocytes are not seen.
Even gross appearance of the SSSS blisters is similar to that seen in SJS and TEN (flaccid bullae, positive Nikolsky sign), the diagnosis is usually made based on clinical findings and biopsy is rarely required. With prompt recognition and administration and proper antibiotics, the prognosis is good, and the lesions will heal without scarring.
Finally, I would like to explain why I wrote so long article about these relatively rare skin diseases. The first of all, there are not so many potentially fatal skin diseases and, I believe, a future physician has to be at least aware of them. The second, the dermatopathologist plays a crucial role in rapid recognition of SJS and TEN: characteristic skin biopsy findings (a combination of dyskeratosis, subepidermal blisters and sparse mononuclear infiltrate) along with macroscopic appearance of skin rash directly prompt diagnosis toward these pathologies. With early diagnosis followed by aggressive treatment the patients have great chances to recover.
Both SJS and TEN, as well erythema multiforme (EM) per se, represent a cluster of skin diseases known as interface dermatitides with characteristic damage of dermal-epidermal junction and formation of subepidermal blisters. For years dermatologists regarded SJS and TEN as severe variants of erythema multiforme. It sounds quite reasonable because despite of certain difference in etiology and presentation, the pathogenesis of all three diseases overlaps in many aspects:
1) Hypersensitivity reaction to an exogenous antigen, either drug or infection
2) Epidermal infiltration with CD8 lymphocytes and macrophages, and dermal infiltration with CD4 lymphocytes
3) Cell-mediated cytotoxicity affecting keratinocytes
• Perforin-granzyme and/or FAS-FAS ligand mechanisms
4) Apoptosis (sometimes named as necrosis or dyskeratosis) of keratinocytes often affecting the full thickness of the epidermis
5) Vacuolization and formation of subepidermal blisters
What is the difference? What is the matter to distinguish these conditions?
The answer is simple: erythema multiforme is a benign, self-limited disorder with excellent prognosis. On the opposite side, SJS and TEN are rapidly developing and potentially fatal diseases and their prompt diagnosis and treatment can greatly improve outcome and reduce mortality rate. Below you can find a brief presentation of each of these diseases oriented mainly toward their differential diagnosis.
Erythema multiforme
1) Precipitating factors: infections (HSV, EBV, histoplasma, Mycoplasma pneumonia, etc)
2) Skin rash characteristics: three-zone target lesions – centrally located necrotic area or vesicle, intermediate zone of edema and blanching, and peripheral hyperemia;
3) Location of skin rash: extremities are mostly affected
4) Mucosal involvement
a) Without oral cavity lesions: erythema multiforme minor
b) With oral bullae and erosions: erythema multiforme major (bullous erythema multiforme)
SJS
1) Provoking factors
a) Drugs: sulfonamides, anticonvulsants, NSAIDs, aminopenicillins, cephalosporins, etc
b) Infections: viral, bacterial, or fungal
o A history of infection alone, without medication treatment, may direct the diagnosis toward bullous EM
c) Graft-versus host disease (bone marrow transplantation)
d) Malignancies
2) Skin rash characteristics: two-zone target (targetoid) lesions – confluent erythematous macules with purpuric centers which rapidly evolve into flaccid blisters (full-thickness epidermal necrosis); later blisters rupture with denudation of red oozing dermis. Total area of detached or “detachable” epidermis with positive Nikolsky sign is less than 10% of body surface area (BSA).
3) Location of the rash: the lesions appear on the face and upper trunk and then extend to the abdomen, back and proximal extremities; distal extremities are relatively spared.
4) Mucosal involvement: erythema, blisters and erosions affecting the lips, oropharynx, conjunctiva, esophagus, trachea, bronchi, urethra, etc; hemorrhagic crusts over the lips.
TEN
Provoking factors, skin lesion characteristics and location, and mucosal involvement are the same as in SJS with only exception of the area of affected epidermis: bullous changes are seen over 30% of BSA and more.
When blistering eruptions are found over from 10 to 30% of the BSA, the condition is referred to as SJS/TEN overlap syndrome.
Because SJS, TEN, and SJS/TEN overlap syndrome have similar precipitating factors, identical pathomorphologic features and comparable clinical patterns, they conventionally considered as different representatives of the same disease process.
Staphycoccal Scalded Skin Syndrome (SSSS) is a rare type of staphylococcal infection characterized by an extensive detachment of the epidermis, which clinically can resemble TEN. But opposite to TEN, SSSS affects predominantly neonates and infants and is associated with much lower mortality rate. This condition occurs in children with a history of staphylococcal infection and fully blown clinical presentation: focus of pyogenic inflammation, fever, positive bacterial culture, etc.
The pathogenesis of SSSS is linked to staphylococcal exotoxins, which damage desmosomes of keratinocytes in the stratum granulosum with subsequent detachment of stratum corneum. Characteristically, inflammatory infiltration and apoptosis/necrosis of keratinocytes are not seen.
Even gross appearance of the SSSS blisters is similar to that seen in SJS and TEN (flaccid bullae, positive Nikolsky sign), the diagnosis is usually made based on clinical findings and biopsy is rarely required. With prompt recognition and administration and proper antibiotics, the prognosis is good, and the lesions will heal without scarring.
Finally, I would like to explain why I wrote so long article about these relatively rare skin diseases. The first of all, there are not so many potentially fatal skin diseases and, I believe, a future physician has to be at least aware of them. The second, the dermatopathologist plays a crucial role in rapid recognition of SJS and TEN: characteristic skin biopsy findings (a combination of dyskeratosis, subepidermal blisters and sparse mononuclear infiltrate) along with macroscopic appearance of skin rash directly prompt diagnosis toward these pathologies. With early diagnosis followed by aggressive treatment the patients have great chances to recover.
Thursday, November 19, 2009
Acute Nephritic Syndrome vs Hematuria
In our reputed recommended Pathology texts, clinical presentation of glomerular diseases usually starts with either nephritic (Robbins’) or nephrotic (Rubin’s) syndrome. As a rule, nephrotic syndrome, a condition commonly seen in clinical settings, is relatively easy to explain, comprehend, and diagnose, therefore I won’t talk about it today.
On the opposite side, nephritic syndrome is not so common, and its full-blown clinical picture is not often seen nowadays. One hundred years ago a patient with acute poststreptococcal glomerulonephritis would present with gross hematuria, hypertension edema, and oliguria, usually followed by azotemia/uremia. Today, for diagnosis of acute nephritic syndrome, presence of only two out of four signs (edema, hematuria, hypertension and oliguria) is required. That means if you have a patient manifesting edema and hematuria, or hematuria and hypertension, you can proceed with the diagnosis of nephritic syndrome. Oliguira is not a common component of acute nephritic syndrome nowadays, and if azotemia develops, it is usually mild and transient. Classical causes of acute nephritic syndrome are acute diffuse proliferative (poststreptococcal) glomerulonephritis and rapidly progressive glomerulonephritis. Besides, the syndrome can manifest membrano-proliferative glomerulonephritis, and focal and diffuse proliferative lupus nephritis (1, 2).
What is much more commonly seen in the patients with glomerulonephritis that is hematuria. Glomerular hematuria is usually classified into four categories (3, 4, 5):
1) Gross hematuria. Brown-smoke urine with dysmorphic RBCs and RBC casts is usually accompanied by non-significant proteinuria, but not by any clinical sign or symptom of glomerulonephritis. As a rule, gross hematuria is seen in patients with IgA nephropathy and Alport syndrome.
2) Asymptomatic microscopic hematuria without proteinemia is often related to with strenuous physical exercises, fever, trauma, but not to glomerular injury. The diagnosis of this condition is made when more than two RBCs are found per one high power field in spun urine sediment. If the glomerulus is involved, biopsy will detect thin basement membrane disease, or mild forms of Alport syndrome and IgA nephropathy.
3) Asymptomatic microscopic hematuria with proteinuria is a rare condition, but is associated with a higher risk for a significant glomerular pathology. Among common causes of this type of hematuria there are more severe variants of thin basement membrane disease, Alport syndrome and IgA nephropathy. In addition, this laboratory sign can be seen in patients with membrano-proliferative glomerulonephritis, acute diffuse proliferative glomerulonephritis, and mesangial proliferative and focal proliferative lupus nephritis.
4) Symptomatic microscopic hematuria; this term is used when the patient presents with detectable clinical signs and symptoms:
a. Systemic: fever, fatigue, malaise, perspiration, loss of weight and appetite, etc
b. Extrarenal: cough and hemoptysis, GI bleeding, purpuric skin rash, etc
c. Renal: edema, hypertension, oliguria, uremic manifestation, etc. When hematuria presents along with
edema or hypertension, or oliguria, the term “acute nephritic syndrome” will be more relevant.
References
1. http://emedicine.medscape.com/article/240337-overview
2. http://www.uptodateonline.com/online/content/topic.do?topicKey=glom_dis/11292&selectedTitle=1%7E150&source=search_result
3. http://www.uptodateonline.com/online/content/topic.do?topicKey=renldis/7627&selectedTitle=1%7E150&source=search_result
4. http://www.uptodateonline.com/online/content/topic.do?topicKey=pedineph/18271&selectedTitle=3%7E150&source=search_resul
5. http://www.uptodateonline.com/online/content/topic.do?topicKey=pedineph/12709&selectedTitle=2%7E150&source=search_result
On the opposite side, nephritic syndrome is not so common, and its full-blown clinical picture is not often seen nowadays. One hundred years ago a patient with acute poststreptococcal glomerulonephritis would present with gross hematuria, hypertension edema, and oliguria, usually followed by azotemia/uremia. Today, for diagnosis of acute nephritic syndrome, presence of only two out of four signs (edema, hematuria, hypertension and oliguria) is required. That means if you have a patient manifesting edema and hematuria, or hematuria and hypertension, you can proceed with the diagnosis of nephritic syndrome. Oliguira is not a common component of acute nephritic syndrome nowadays, and if azotemia develops, it is usually mild and transient. Classical causes of acute nephritic syndrome are acute diffuse proliferative (poststreptococcal) glomerulonephritis and rapidly progressive glomerulonephritis. Besides, the syndrome can manifest membrano-proliferative glomerulonephritis, and focal and diffuse proliferative lupus nephritis (1, 2).
What is much more commonly seen in the patients with glomerulonephritis that is hematuria. Glomerular hematuria is usually classified into four categories (3, 4, 5):
1) Gross hematuria. Brown-smoke urine with dysmorphic RBCs and RBC casts is usually accompanied by non-significant proteinuria, but not by any clinical sign or symptom of glomerulonephritis. As a rule, gross hematuria is seen in patients with IgA nephropathy and Alport syndrome.
2) Asymptomatic microscopic hematuria without proteinemia is often related to with strenuous physical exercises, fever, trauma, but not to glomerular injury. The diagnosis of this condition is made when more than two RBCs are found per one high power field in spun urine sediment. If the glomerulus is involved, biopsy will detect thin basement membrane disease, or mild forms of Alport syndrome and IgA nephropathy.
3) Asymptomatic microscopic hematuria with proteinuria is a rare condition, but is associated with a higher risk for a significant glomerular pathology. Among common causes of this type of hematuria there are more severe variants of thin basement membrane disease, Alport syndrome and IgA nephropathy. In addition, this laboratory sign can be seen in patients with membrano-proliferative glomerulonephritis, acute diffuse proliferative glomerulonephritis, and mesangial proliferative and focal proliferative lupus nephritis.
4) Symptomatic microscopic hematuria; this term is used when the patient presents with detectable clinical signs and symptoms:
a. Systemic: fever, fatigue, malaise, perspiration, loss of weight and appetite, etc
b. Extrarenal: cough and hemoptysis, GI bleeding, purpuric skin rash, etc
c. Renal: edema, hypertension, oliguria, uremic manifestation, etc. When hematuria presents along with
edema or hypertension, or oliguria, the term “acute nephritic syndrome” will be more relevant.
References
1. http://emedicine.medscape.com/article/240337-overview
2. http://www.uptodateonline.com/online/content/topic.do?topicKey=glom_dis/11292&selectedTitle=1%7E150&source=search_result
3. http://www.uptodateonline.com/online/content/topic.do?topicKey=renldis/7627&selectedTitle=1%7E150&source=search_result
4. http://www.uptodateonline.com/online/content/topic.do?topicKey=pedineph/18271&selectedTitle=3%7E150&source=search_resul
5. http://www.uptodateonline.com/online/content/topic.do?topicKey=pedineph/12709&selectedTitle=2%7E150&source=search_result
Friday, November 13, 2009
A Few Questions about Acute Renal Failure
Acute Renal Failure (ARF) is not a topic that creates serious problems for medical students, but a novice while working with this subject will definitely face a few pitfalls. Below you can find some questions (with answers, of course, :-) which can confuse beginners in nephrology.
Q: Is oliguria an immanent sign of ARF?
A: No, it is not.
Comment: ARF is referred to a rapid decline in renal filtration, but a decline in filtration does not automatically imply a reduction in urinary output. Urinary output depends on two processes: filtration and reabsorption, therefore if both processes are affected, a patient may develop non-oliguric ARF.
Q: Is serum creatinine level always elevated in patients with ARF?
A: No, it is not.
Comment: A well know fact is that creatinine is filtered through the glomerulus, partially secreted by renal tubules, and almost non-reabsorbed. These features of creatinine metabolism are used in determination of a major parameter of renal function: glomerular filtration rate. Because serum creatinine level is inversely proportional to glomerular filtration rate (GFR), we can expect all ARF patients to have an increased concentration of serum creatinine. But during the first few hours of acute renal failure, when glomerular filtration was shut down recently, there would be a gradual increment in serum creatinine and a single measurement might produce normal figures. Moreover, certain pathologic conditions, like acute glomerulonephritis, are associated with activation of tubular secretion of creatinine; therefore even in the situation when GFR significantly falls down, serum creatinine level will only slightly raise.
Because ARF is a dynamic pathologic process, which can require different approaches in management at different stages of pathogenesis, the specialists in renal diseases prefer the term “acute kidney injury” (AKI) instead of “acute renal failure”. In widely accepted RIFLE (2004) classification of AKI, the whole process of kidney damage is divided in five stages: Risk of renal dysfunction, Injury to the kidney, Failure or Loss of kidney function, and End-stage kidney disease. Each stage of AKI is characterized by a certain set of urinary output, glomerular filtration rate, and creatinine concentration (1).
Q: If urinary output and serum creatinine remain WNL how are we able to diagnose AKI?
A & Comment: It is unusual that both indexes stay unaffected in the patient with AKI. Besides we can also use some more parameters like
1) Pace of serum creatinine elevation, e.g. from 0.7 to 1.2 mg/dL during a day
2) An increase in BUN concentration
3) Casts in urinary sediment (dirty-brown granular casts in ATN)
Q: Do elevated levels of serum creatinine and BUN always indicate AKI?
A: No, they do not
Comment: We always have to keep in mind other reasons for elevation of these nitrogen compounds. E.g., some drugs like trimethoprim and cimetidine may decrease creatinine secretion with subsequent rise in serum creatinine in patients with normal renal function. An increment in BUN can be associated with severe burns, GI bleeding, steroid use, tetracycline administration, or dietary protein overload, not only with GFR decline.
Why we use BUN/creatinine ratio?
A & Comment: Both creatinine and urea are products of protein metabolism and are excreted with urine. Definitely, blood levels of both substances will be higher in patients with renal failure. But from the course of physiology we remember two characteristic features of urea behavior within the kidneys: 1) a significant proportion of filtered urea is reabsorbed in the proximal tubules; 2) process of urea reabsorption is influenced by two factors: velocity of urinary flow through the tubular system and a tone of the renal microvasculature. In early stages of pre-renal AKI, when filtration is inhibited and urinary flow is diminished, there is a burst in vasodilatory mediators with subsequent rise in tubular reabsorption of BUN and elevation of its plasma level. BUN/creatinine ratio, which in normal individual fluctuates from 10:1 to 15:1 (2), in patients with pre-renal AKI is usually higher than 20:1. If severe pre-renal AKI stays untreated, it will eventually progress to renal AKI when tubular epithelium gets badly damaged and vasodilation turns to vasoconstriction. In such conditions urea reabsorption slows down and ratio may turn to ordinary figures.
For differential diagnosis of pre-renal and renal AKI, besides BUN/creatinine ratio we can use the following indices: urine specific gravity, urine osmolarity, urine sodium, urine-plasma creatinine ratio and, of course, fractional excretion of sodium, but that will be another story.
References
1. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P. Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. Aug 2004;8(4):R204-12.
2. Balogun RD, Ocusa MA. Diagnosis of acute tubular necrosis and prerenal disease.
Monday, October 19, 2009
Pathology Club Conference "Does Screening Prevent Cancer?"
The conference began with Rachel Lacy’s introduction where she stressed two major issues in modern Oncology: an impact of cancer on American society and necessity of screening and early detection of malignant neoplasms and their precursors. Below you can find a brief summary about the presentations we had.
“Breast Cancer Screening” by Rebecca Charland: American Cancer Society no longer recommends breast self examination.
“Lung Cancer Screening” by William Bradford: Systematic screening for lung cancer is not currently recommended by any major medical professional organization. Why?????
“Skin Cancer Screening” by Lindsey Haga: One American dies of melanoma almost every hour.
“Prostate Cancer Screening” by Glynn Faircloth: Until there is clear evidence to show that a national screening program will bring more benefit than harm, the NHS will not invite men who have no symptoms for prostate cancer screening.
“Cervical Cancer Screening” by Christopher Bierman: Doctors believe that woman must have been infected with HPV to get cervical CA…Not everyone with HPV will get cervical CA.
“Endometrial Cancer” by Rachel Lacy: In 2001, American Cancer Society concluded that there was insufficient evidence to recommend screening for endometrial cancer at any risk.
“Colorectal Cancer Screening” by Robert Mc Evoy: Colonoscopy remains a golden standard for detection of colon adenomatous polyps and early colon carcinomas.
“Run for the Cure” organized by Canadian Breast Cancer Foundation in Toronto on October 04, 2009” by Dr. Yakubovskyy: Please see the previous post “Toronto Report”.
All reports were well received by the audience, many students and faculties participated in the discussion of the topics raised.
The Pathology Club members agreed that if they survived the next Mini, they would prepare another conference with a tentative title “Cancer Prevention”.
“Breast Cancer Screening” by Rebecca Charland: American Cancer Society no longer recommends breast self examination.
“Lung Cancer Screening” by William Bradford: Systematic screening for lung cancer is not currently recommended by any major medical professional organization. Why?????
“Skin Cancer Screening” by Lindsey Haga: One American dies of melanoma almost every hour.
“Prostate Cancer Screening” by Glynn Faircloth: Until there is clear evidence to show that a national screening program will bring more benefit than harm, the NHS will not invite men who have no symptoms for prostate cancer screening.
“Endometrial Cancer” by Rachel Lacy: In 2001, American Cancer Society concluded that there was insufficient evidence to recommend screening for endometrial cancer at any risk.
“Colorectal Cancer Screening” by Robert Mc Evoy: Colonoscopy remains a golden standard for detection of colon adenomatous polyps and early colon carcinomas.
“Run for the Cure” organized by Canadian Breast Cancer Foundation in Toronto on October 04, 2009” by Dr. Yakubovskyy: Please see the previous post “Toronto Report”.
All reports were well received by the audience, many students and faculties participated in the discussion of the topics raised.
The Pathology Club members agreed that if they survived the next Mini, they would prepare another conference with a tentative title “Cancer Prevention”.
The End
Sunday, October 18, 2009
Toronto Report
City Center
A storm coming from Lake Ontario
A night view from the 23rd floor of Metropoliten Hotel
A morning view from the 23rd floor of Metropoliten Hotel
A rainy day in the Bay Street
On Octover 4, 2009 a meeting and Run for the Cure organized by the Canadian Breast Cancer Foundation got together about 170,000 people and ...
... and 30,000 of them ran
People, who (as your humble narrator) did not run, enjoyed "Jersey Boys" show
Locals had fun too
Jonas Brothers also were there
Physicians again and again stood for sreening...
...and people again and again beg for cure
The last cup of coffee in Toronto
The end of the story
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