Showing posts with label Pathology. Show all posts
Showing posts with label Pathology. Show all posts

29 July 2012

Benign fibrous histiocytoma



Soft Tissue Tumors
Lucy H. Liu, M.D.
http://www.uic.edu

Soft Tissue Pathology
Richard Anderson, MD
http://www2.uic.edu

Bones, Joints, Soft Tissue Tumors
http://faculty.ccc.edu/
http://faculty.ccc.edu/

Reactive and Benign lesions of Fibroblastic and Histiocytic Origin
http://student.ahc.umn.edu

Soft Tissue Swellings Parulis
Gum Boil
http://dental.case.edu

Case Study
Kenneth Clark, MD
http://neuro.pathology.pitt.edu

Case Study
Harry Kellermier
http://neuro.pathology.pitt.edu/

Bone and Soft Tissue Sarcomas
http://www.mcw.edu

Dermal and Subcutaneous Tumors
Adam Wray, D.O.
http://www.atsu.edu

Dermatoses Resulting from Physical Factors
http://www.atsu.edu

Tumor Pathology and Histology 
Carleton T. Garrett, MD, PhD
http://www.pathology.vcu.edu

Pathology of the Larynx
Nikolay Popnikolov M.D., Ph.D
http://www.utmb.edu

Oncology Basics
Lorin A. Hillman, DVM
https://netfiles.uiuc.edu

125 Published articles list on Benign fibrous histiocytoma

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04 June 2012

Plasmapheresis



Cast Nephropathy & Plasmapheresis
Alicia Notkin
Multiple_Myeloma.ppt

Acquired Cystic Kidney Disease
Alicia Notkin
Acquired_Cystic_Renal_Disease.ppt

Molecular Mechanisms of Antidiuretic Effect of Oxytocin
Alicia Notkin
Oxytocin.ppt

Therapeutics of Autoimmune Diseases
Autoimmune_Rx_4_3_06.ppt

Clinical Pathology Conference: to plasmapheresis or not?
Bill Zaloga, DO
ToPlasmapheresisOrNot.ppt

Cold Agglutinin Disease
Daniel K. Noland MD
CAD82004.ppt

Chronic Inflammatory Polyradiculoneuropathy (CIDP)
CIDP.ppt

Blood & Blood Component Donor Selection and Collection
Bill Zaloga, D.O.
Donorselectionandcollection.ppt

Renal Disorders in Multiple Myeloma
Hematology Grand Rounds, Tom Fong, MD
Renal Disorders in Multiple Myeloma.ppt

Morbidity and Mortality Conference
Brian J. Schwender, M.D.
Morbidity and Mortality Conference.ppt

Anemia
Anemia.ppt

Cryoglobulinemia
Cryoglobulinemia.ppt

Small- Vessel Vasculitides
Small- Vessel Vasculitides.ppt

Human Lupus
Human Lupus.ppt

Coping with Changing Controlled Vocabularies
James J. Cimino, M.D., Paul D. Clayton, Ph.D.
Coping with Changing Controlled Vocabularies.ppt

Coagulation Emergencies
How to deal with/avoid a bloodbath
CoagulationEmergenciesPathology.ppt

Autoimmune Inner Ear Disease
Robert H. Stroud, M.D., Jeffery T. Vrabec, M.D.
Autoimmune-Inner-Ear.ppt

Blood Collection
Terry Kotrla, MS, MT(ASCP)
DonorBloodCollection2011.ppt

Guillain-Barre Syndrome
Lisa Rose-Jones, MD
Guillain-Barre Syndrome.ppt

Gemcitabine-induced Hemolytic Uremic Syndrome
Xiaoyi (Sherry) Hu
Gemcitabine-induced Hemolytic Uremic Syndrome.ppt
Free 200 full text articles

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20 May 2012

Skin Pathology



Skin Pathology Presentations from Loyola University Health System
Skin Pathology, Case 1
http://zoomify.lumc.edu/path/skin/skincase1.ppt

Skin Pathology, Case 2
http://zoomify.lumc.edu/path/skin/skincase2.ppt

Skin Pathology, Case 3
http://zoomify.lumc.edu/path/skin/skincase3.ppt

Skin Pathology, Case 4
http://zoomify.lumc.edu/path/skin/skincase4.ppt


Free published articles

Ilkovitch D.
J Leukoc Biol. 2011 Jan;89(1):41-9. Epub 2010 Jul 13. Review.
Biggs L, Yu C, Fedoric B, Lopez AF, Galli SJ, Grimbaldeston MA.
J Exp Med. 2010 Mar 15;207(3):455-63. Epub 2010 Mar 1.
Jiménez N, Escalante T, Gutiérrez JM, Rucavado A.
J Invest Dermatol. 2008 Oct;128(10):2421-8. Epub 2008 May 1.
OLIVER JO.
Br Med J. 1954 Feb 27;1(4860):511-4.

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Renal Pathology



Renal Pathology Presentations from Loyola University Health System

Renal Pathology case-1
http://zoomify.lumc.edu/path/urogen2/renalpath1.ppt

Renal Pathology case-2
zoomify.lumc.edu/path/urogen2/renalpath2.ppt

Renal Pathology case-3
http://zoomify.lumc.edu/path/urogen2/renalpath3.ppt

Renal Pathology case-4
http://zoomify.lumc.edu/path/urogen2/renalpath4.ppt

Male Genital  Tract 1 case-1
http://zoomify.lumc.edu/path/urogen1/malegent1case1.ppt

Male Genital  Tract 1 case-2
http://zoomify.lumc.edu/path/urogen1/malegent1case2.ppt
Male Genital  Tract 1 case-3
http://zoomify.lumc.edu/path/urogen1/malegent1case3.ppt

Male Genital  Tract 1 case-4
http://zoomify.lumc.edu/path/urogen1/malegent1case4.ppt
54 scholarly articles free access

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09 March 2010

The Liver and the Biliary Tract



The Liver and the Biliary Tract
By:Brando Cobanov, M.D.
Department of Pathology
UMDNJ-RWJMS

Hepatic Injury
* Inflammation = hepatitis
o Portal tracts, lobules
* Degeneration
o Damage from toxic or immunologic insult
o Accumulation of substances, e.g., steatosis
* Cell death
o Centrilobular, submassive, massive necrosis
* Fibrosis
o Usually irreversible
* Cirrhosis

Bile
Jaundice
* Excessive production of bilirubin
o Hemolytic anemias, ineffective erythropoiesis
* Reduced hepatic uptake
* Impaired conjugation
o Physiologic jaundice of the newborn
o Crigler-Najjar syndromes types I and II
o Gilbert syndrome
o Viral or drug-induced hepatitis, cirrhosis
* Decreased hepatocellular excretion
o Dubin-Johnson syndrome, Rotor syndrome
* Impaired bile flow

Cholestasis
* Systemic retention of not only bilirubin but also other solutes eliminated in bile, particularly bile salts and cholesterol
* Due to hepatocellular dysfunction or biliary obstruction
* Accumulation of bile pigment within the hepatic parenchyma – Kupffer cells
* Bile ductular proliferation
* Bile lakes
* Portal tract fibrosis

Hepatic Failure
Clinical Features
* Jaundice
* Hypoalbuminemia
* Hyperammonemia
* Fetor hepaticus
* Palmar erythema
* Spider angiomas
* Hypogonadism
* Gynecomastia

Complications
* Multiple organ failure
* Coagulopathy
* Hepatic encephalopathy
* Hepatorenal syndrome

Cirrhosis
* Bridging fibrous septa
* Parenchymal nodules
* Disruption of the architecture of the entire liver
* Etiologies

Portal Hypertension
* Prehepatic
* Intrahepatic
* Posthepatic

Clinical Sequelae
* Ascites
* Portosystemic venous shunts
* Splenomegaly
* Hepatic encephalopathy

Drug Induced Liver Disease
* Liver is the major drug metabolizing and detoxifying organ in the body
* Direct toxicity
* Hepatic conversion of a xenobiotic to an active toxin
* Immune mechanisms
* Table 16-6

Alcoholic Liver Disease
* Hepatic steatosis
* Alcoholic hepatitis
* Alcoholic cirrhosis
o Micronodular

Pathogenesis
* Shunting of normal substrates away from catabolism toward lipid biosynthesis
* Induction of cytochrome P-450
* Free radicals generated by microsomal ethanol oxidizing system
* Alcohol directly affects microtubular and mitochondrial function
* Acetaldehyde induces lipid peroxidation
* Neutrophil infiltration
* Immunologic attack of hepatocytes

Causes of Death
* Hepatic failure
* Massive GI hemorrhage
* Infection
* Hepatorenal syndrome
* Hepatocellular carcinoma

Nonalcoholic Fatty Liver
* Elevated serum aminotransferase levels
* Low risk for development of hepatic fibrosis or cirrhosis
* Associated with obesity, type 2 DM, hyperlipidemia
* Need to exclude other causes


Hemochromatosis
* Primary or hereditary
* Secondary
Pathogenesis
Morphology
Clinical Features
Wilson Disease
Morphology
Clinical Features
α1-Antitrypsin Deficiency
Morphology
Neonatal Hepatitis
Reye Syndrome
Morphology
Obstructive Biliary Tract Disease
Secondary Biliary Cirrhosis
Primary Biliary Cirrhosis
Primary Sclerosing Cholangitis
Circulatory Disorders
Hepatic Artery Inflow
Portal Vein Obstruction
Impaired Blood Flow Through the Liver
Hepatic Vein Thrombosis
Veno-Occlusive Disease
Hepatic Neoplasms
Benign Tumors
Focal Nodular Hyperplasia
Liver Cell Adenoma
Hepatocellular Carcinoma
Pathogenesis
Morphology
HCC
Clinical Features
Disorders of the Gallbladder
Cholelithiasis
Clinical Features
Cholecystitis
Choledocholithiasis
Cholangitis
Biliary Atresia
Gallbladder Carcinoma
Cholangiocarcinoma

The Liver and the Biliary Tract.ppt

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08 October 2009

Differentiating Babesia from Malaria



Differentiating Babesia from Malaria
By:Devak Desai

Case Presentation
* Middle aged hypertensive and asplenic man presented with a pruritic rash on his right buttock accompanied by flu-like symptoms.
* 1010, arthralgias, myalgias, some nausea, and general malaise, and decreased appetite.
* Reports walking through a wooded area on Martha’s Vineyard, an island off the coast of Mass.
* PE shows a well nourished man with no significant findings other than an erythmatous oropharynx without exudate.

Laboratory Data
* Normal WBC differential
* Blood smear: numerous intraerythrocytes involving 2.7% of RBCs
* Direct Combs test was negative
* Positive serologic test for Lyme Disease

Peripheral Blood Smear
* Numerous erythrocytes are infected with the predominantly ring or pear-shaped form of Babesia microti.
* Pleomorphic rings with 1-3 chromotin dots per parasite.
* 3 dots is unique for Babesia.

Host Infection Cycle
* Infection begins when sporozoites are released from the deer tick’s salivary gland during a blood meal.
* Sporozoites replicate directly in RBCs.
* Attachment and adsorption seems mediated through the C3b receptor.
* During invagination a clear vacuole appears.
* Babesia divided by asynchronous budding.
* The replicating structures are now called trophozoites.
* This is an asynchronous process with varying degrees of hemolysis.

Life cycle of Babesia spp. in the tick and vertebrate hosts
High Power
* Ring shaped trophozites
* The intraerythrocytic trophozoites multiply by binary fission or schizogony, forming two to four separate merozoites.
* White eccentric “food vacuole” in a ring form.
* Very transient stage in Malaria. Very rarely seen.

the famous Maltese Cross
* Presence of 4 daughter merozoites in a tetrad is pathomnemonic.
* However, rarely seen.
* Never seen in malaria.

Multiply infected RBCs
* RBCs can be infected with multiple organisms at the same time. Up to 12 parasites may infect a single RBC.
* Plasmodium has up to 3 parasites/RBC.
* Unremarkable RBCs.

Other Sightings
* Parasite with a peripheral nuclear band
* Basket cell
* Syncytium of extracellular parasites
* Far more common in Babesia infections

Malaria Review
Epidemiology
* There are >100 specicies of this intracellular parasite.
* Babesia microti is the predominant human pathogen, endemic to the NE and Midwest.
* 10-20% of adults are seropositive in endemic areas
* Natural parasite reservoir is rodents
* Carried by the hard-bodied Ixodes Deer tick.
* Also carries agents for Lyme Disease, and Ehrlichoisis.
* Can also be transferred transplacentally and through blood transfusion.

Clinical presentation
* Ranges from asymptomatic infection to fatal illness (rare)
* No direct correlation between parasitemia and severity.
* More severe infection tends to occur in immunnocompromised, elderly, and the very young.
* The extreme end of the spectrum is often described as a malaria-like infection; symptoms may include malaise, chills, mylagia, anemia, fatigue, and fever (as high as 1040).
* Some cases also described emesis, night sweats, weight loss, and hematuria.

Special Case – Splenectomy
* Most important risk factor for infection, esp. severe.
* Illness appears suddenly, with hemoglobinuria as the presenting symptom followed by jaundice due to severe hemolysis.
* Parasitemia can reach 80% of RBCs
* Can be a medical emergency.
* In the most severe cases, patients develop a shock-like picture, with renal failure and pulmonary edema.
* Chronic disease with many relapses over months to years may occur if not treated.

Co-Infection
* It is estimated from serologic surveys that as many as 13% of Lyme disease patients in babesia-endemic areas are coinfected with B. microti
* The initial symptoms of both babesiosis and Lyme disease overlap significantly.
* Like babesiosis, Lyme disease also presents with nonspecific symptoms of fever,fatigue, and other flu-like symptoms.
* Patients coinfected with B. microti and B. burgdorferi experience more severe symptoms, but does not increase the duration of Babesia parisitemia.
* Doxycycline will not kill Babesia.

Diagnosis
* Diagnosis is based on clinical suspicion and history of exposure.
* Thick and thin smears remain most clinically used
* However, it is necessary to examine 200 to 300 oil immersion fields before declaring a specimen negative.
* Various PCR detection assays are available for detection of B microtic and other species.
* More sensitive but also more time consuming and expensive.
* Indirect fluorescent antibody test can also be used as a confirmatory test.
* Can have false negatives (HIV) or false pos (autoimmune)

Treatment
* Current treatment is Quinine plus Clindamycin
* Better alternative treatment is Atovaquone plus Azithromycin
* This combo is almost as effective with fewer side effects.
* 72% receiving quinine and clindamycin had side effects attributed to the drugs—diarrhea, tinnitus, or vertigo
* 15% receiving atovaquone plus azithromycin experienced side effects (usually diarrhea or rash).
* For severe cases (asplenic) with high levels of parasitemia, RBC exchange transfusions may also be necessary.

Summary
* History: check for recent travel
* Symptoms: Babesia is milder and tends not to be cyclic.
* Smear: Babesia has no schizonts, gametocyes, or ameboid trophozoites.
* Lab tests: PCR or indirect antibody test.

Conclusion
* Major deterrents to the diagnosis of babesiosis include the low index of suspicion by physicians (except in endemic areas), non-specific flu-like signs, and the use of automated cell readers that cannot detect merozoites in erythrocytes
* Disease is increasing in prevalence due to more people living in rural tick infested areas and as the number of immunocompromised in increasing.
* Also environmental such as the exponential rise in deer populations.
* Blood transfusion risk becoming an increasing problem.
References

Differentiating Babesia from Malaria.ppt

Read more...

27 September 2009

Occupational Exposures to Bloodborne Pathogens



Occupational Exposures to Bloodborne Pathogens
By:Arjun Srinivasan
Johns Hopkins Hospital

Outline
* What’s an exposure?
* 1st step in all exposures - Clean the site!!
* Specific pathogens
o Hepatitis C
o Hepatitis B
o HIV

Scope of the Problem
Impossible to measure the psychological stress that an exposure places on a health care worker
At Risk Exposures
1. Percutaneous injury
Hollow needle > Solid sharp
Visible blood
Deep injury
Device in patient’s artery or vein
2. Splash on non-intact skin
3. Splash on mucous membrane

Risks From Body Fluids
* Known to be infectious:
o Blood
o Any fluid visibly contaminated with blood
o Semen
o Vaginal secretions
o Concentrated virus (used in labs)
* Potentially infectious
o CSF
o Pleural fluid
o Pericardial fluid
o Peritoneal fluid
o Amniotic fluid
o Synovial fluid
o Tissue samples
* Not Infectious (if not visibly bloody)
o Tears
o Saliva
o Urine
o Feces
o Sweat
o Emesis

The Solution to Pollution . . .
* Exposure site should be cleaned IMMEDIATELY! This may be the most important part of PEP
* Skin wounds should be washed with soap and water
* No evidence that antiseptics are useful and caustic agents (bleach) may do more harm than good
* Mucous membranes should be flushed thoroughly with water
* Eyes should be irrigated with a liter of saline

A word from our lawyers . . .
* ALL exposures should be reported to the proper people (Occupational health, Employee health etc.)
* Disability claims can be denied if follow up reporting was not done right

Hepatitis C
Hepatitis C: Risk of Exposure
Hepatitis C: Risk of Disease
Post Exposure Recommendations
* Clean the site immediately
* Hepatitis B immune globulin has NOT been effective
* Interferon is NOT recommended at this time
Hepatitis C: Follow Up
* Enzyme linked immunoassay (EIA) is screening test of choice
* ALL exposed HCWs should have LFTs monitored
* Average interval between exposure and seroconversion with EIA is 8-10 weeks
* Follow up guidelines vary - CDC recommends follow up at 4-6 months
Hepatitis C: Follow up issues
* EIA is falsely positive in up to 50% of HCW and falsely negative in 5% - results must be confirmed by RIBA or VL
* PCR may catch infection earlier but detection is highly variable
* Immediate referral for treatment if HCW seroconverts
Hepatitis C: Counseling
* Risk of transmission to infants and partners is thought to be low
* Exposed HCW do not need to modify sexual practices, stop breast feeding or refrain from becoming pregnant
* Should not donate blood

Hepatitis B
Hepatitis B: Risk of Exposure
Hepatits B: Outcome of Infection
* In patients who are infected with Hep B:
o 25% get jaundice
o 5% require hospitilization
o 6-10% become chronically infected
o .125% die of fulminant hepatitis

Hepatitis B: Good News
* Most HCWs have been vaccinated and vaccine offers virtually complete protection to responders
Hepatitis B: Bad News
* Some employees are NOT vaccinated
* 6-10% of vaccinees do NOT develop antibody
* Really bad news:
CDC estimates that 50-75 HCW die from Hep B each year
Hepatitis B: Post Exposure
* Clean the site immediately
* Determine the vaccine status of the HCW
* Determine the surface antigen status of the source patient

Hep B: HCW Never Vaccinated
* HCW should receive vaccine ASAP
1. Source patient is sAg positive:
HCW should also receive one dose of Hep B immune globulin (HBIG) .06ml/kg (1 vial=5 ml) ASAP and absolutely within 7 days of exposure
2. Source patient sAg neg or unknown
Vaccine alone
Hep B: HCW Vaccinated (one or more doses)
* Source patient should be tested for sAg AND HCW should be tested for sAb
* If HCW has adequate Ab >10 IU/mL (now or at any time) then no additional treatment
* IF HCW has inadequate Ab:
1. If pt is sAg negative:
HCW should get booster dose of vaccine (or complete series)
2. If pt is sAg positive:
HCW should receive HBIG AND a booster dose of vaccine at different sites (complete series if necessary)
If HCW has inadequate Ab:
3. Unknown source:
Give vaccine booster or complete series
Vaccine non-responders
* If HCW has inadequate Ab after 3 dose series they should get another series: 30-50% chance of responding to 2nd series
* If no response to 2nd series HCW should be considered susceptible
* PEP for known non-responders exposed to Hep B positive or high risk unknown sources: 2 doses of HBIG- 1 at exposure then 4 weeks later
Hep B: Follow Up Testing
* Hepatitis B sAg is the test of choice as it rises in about 6 weeks
* LFTs should be monitored at regular intervals
Post Exposure Counseling
* Risk of transmission to infants and partners is thought to be low
* Exposed HCW do not need to modify sexual practices, stop breast feeding or refrain from becoming pregnant
* Should not donate blood
HIV
HIV: Risk of Exposure
* Risk of transmission from percutaneous expsosures involving HIV positive pts estimated at 0.3%
* Risk from mucous membrane exposure estimated at 0.1%
* As of 2000 there were 56 confirmed and 138 possible cases of occupational transmission in the US
Rationale for PEP
* HIV infects dendritic cells and then regional lymph nodes before becoming systemic
* AZT blocks infectivity of HIV infected dendritic cells
* Goal of PEP is to halt viral replication before systemic infection is established

Does It Work?
* Several animal studies showing efficacy
* Peri-natal prophylaxis has been effective
* Retrospective study showed that risk of seroconversion after exposure was 81% lower in HCWs who took AZT PEP.
Time is Virus
What To Use?
* Before: AZT+3TC +/- IDV or NFV
* Now: Becoming more difficult to answer!
* Regimens may need to be tailored based on the treatment history of the source patient -Surveillance study from 1998-1999 found that 39% of virus from source patients had some NRTI resistance and 10% had some PI resistance.

Nucleoside Reverse Transcriptase Inhibitors (NRTI)
* Still form the backbone of most regimens
* AZT has been formally studied thus it should be included if possible
* Addition of 3TC is recommended because:
1. It appears non-toxic
2. It has some synergistic effect with AZT with respect to mutations
* If source patient’s virus is felt to be resistant to AZT or 3TC alternatives include:
* d4T + 3TC
* d4T + ddI
* Role of abacavir?
* Role of tenofovir?
Protease Inhibitors (PI)
* Are very potent anti-virals and work very well in patients
* BUT they have significant side effects and can cause HCW to stop PEP altogether
* PI should be recommended primarily when the exposure is high risk
* Any PI can be used but indinavir and nelfinavir have been used the most
Non Nucleoside Reverse Transcriptase Inhibitors (NNRTI)
* Not much experience using these for PEP
* Use should be reserved for situations when source patient’s virus is thought to be resistant to all PIs
* Nevirapine should probably be avoided as PEP: from 1997-2000 there were 22 reports of serious toxicity in HCW taking it for PEP

Toxicity of PEP
Side Effects of PEP
PEP Counseling
* Clean the site immediately
* Determine the HIV status of the source
* Determine the extent of the exposure
PEP management: Source Patient Testing
* Crucial 1st step as most exposures do NOT involve HIV positive patients
* Rapid test kit (SUDS) is available and yields an answer in about 30 minutes
* Rapid test is an EIA that is >99.9% sensitive
* Testing of blood on sharps is NOT recommended
* Patient consent is required in Maryland
HIV RNA Testing of Source
* No official recommendations and test is not approved for this indication
* Should be reserved for cases where there is a suspicion of acute retroviral conversion

Source Patient
1. Patient HIV negative - No PEP
2. Patient HIV positive
Low viral load / high CD4 = class 1
High viral load / low CD4 = class 2
3. Patient HIV positive, unknown CD4, VL
Use best judgement - err towards class 2
4. Unknown source
Exposure Types
1. Non-infectious fluids - No PEP
2. Mucous membrane, non-intact skin
Small volume
Large volume
3. Percutaneous injury
Less severe
More severe
HIV PEP Recommendations
Percutaneous injuries
Less severe
* Source pt HIV negative - No PEP
* Source pt class 1 - Recommend 2 drugs
* Source pt class 2 - Recommend 3 drugs
* Source of unknown status- Consider 2 drugs in setting where exposure to HIV positive pt likely or if pt has HIV risk factors

HIV PEP
More severe injury
* Source pt HIV negative - No PEP
* Source pt HIV class 1 or 2 - Recommend expanded 3-drug regimen
* Source of unknown status - Consider 2 drugs in setting where exposure to HIV positive pt likely or if pt has HIV risk factors
HIV PEP
Mucous membrane exposures
Small Volume
* Source pt HIV negative - No PEP
* Source pt class 1 - Consider 2 drugs
* Source pt class 2 - Recommend 2 drugs
* Source of unknown status- Consider 2 drugs in setting where exposure to HIV positive pt likely or if pt has HIV risk factors
Large volume
* Source pt HIV negative - No PEP
* Source pt class 1 - Recommend 2 drugs
* Source pt class 2 - Recommend 3 drugs
* Source of unknown status- Consider 2 drugs in setting where exposure to HIV positive pt likely or if pt has HIV risk factors
Duration of Treatment
* Current recommendation is 4 weeks but this is an arbitrary selection
* Animal studies suggest 10 days is too short but 28 days conferred protection
Resistance
* Becoming a significant problem now that so many patients are getting treated
* Treatment history can be helpful in the acute setting
* Recent history may be more important than remote
Resistance Issues
* Full medical history often not available when the exposure occurs - PEP should NOT be delayed
* Data from maternal transmission studies shows viral resistance does not preclude benefit
* Consultation with someone experienced in HIV treatment is recommended in cases where HIV resistance is possible
* PEP may need to be modified once more history is available
* Resistance testing is too slow to be of use right now

PEP and Pregnancy
* Women of child bearing age should be offered a pregnancy test before starting PEP
* BUT, recommendations on starting PEP should NOT change just because HCW is pregnant

HIV medications to avoid in Pregnant HCW
* d4T, ddI: have been associated with severe lactic acidosis in pregnant women
* Efavirenz: is teratogenic in primates
* Indinavir: causes hyperbilirubinemia in newborns if given near time of delivery

Post Exposure Testing
* Testing should be done at regular intervals (eg 6,12 weeks and 6 months)
* Testing should continue for 12 months if the HCW contracts HCV from the exposure
* Unclear if testing should be prolonged in exposures to pts with HIV and HCV or in HCW who have history of impaired Ab responses
* EIA is test of choice
* Viral loads and p24 assays should be reserved for suspected cases of acute seroconversion given high false pos rate
Counseling
* For 3 months following exposure HCW should avoid:
-unprotected sex
-donating blood
-sharing razors, toothbrushes
* HCW should consider stopping breast feeding (risk of perinatal transmission and drugs may get into breast milk)

Time to Seroconversion
* Most HCW seroconvert in 6-12 weeks with median time of 46 days
* 95% seroconvert within 6 months
* 100% seroconvert in one year
* Co-infection with HCV may delay HIV seroconversion

Acute Retroviral Conversion
* Symptomatic seroconversion develops in 50-90% of cases
* Average time from exposure to symptoms is 2-6 weeks
* ANY HCW who develops a flu-like illness in the follow up period should be encouraged to get HIV RNA testing

Resources
Conclusion

* People react very differently to exposures - be prepared for anything!
* The psychological impact of an exposure can be enormous
* Your patience and understanding may be the best PEP of all

Occupational Exposures to Bloodborne Pathogens.ppt

Read more...

13 June 2009

Pathology and Neoplasia



Pathology and Neoplasia
Lesions of the Vulva

* Cysts
* Tumors
* Dermatological conditions
* VIN
* Condyloma acuminatum
* Nevus
* Psoriasis
* Seborrheic Dermatosis
* Hidradenitis Suppurativa
* Lichen planus
* Lichen Sclerosis
* Lichen Simplex Chronicus
* Urethral Diverticulum or Caruncle
* Trauma
* Vaginal intraepithelial neoplasia (VAIN)
* Condyloma
* Urethral Diverticulum
* Urethral Caruncle
* Dysontogenetic cysts
* VAIN

Lesions of the Cervix
* Polyps
* Nabothian Cysts-mucous retention cysts, translucent/opaque, caused by normal healing process or cervix
* Fibroids
* Cervical intraepithelial neoplasia (CIN)
* Condyloma
* CIN
* Polyps
* Fibroids

Lesions of the Uterus
* Intravenous leiomyomatosis
* Leiomyomatosis peritonealis disseminata
* Fibroids
* Adenomatoid Tumors

Lesions of the Ovary
* Functional cysts
* Theca lutein cysts
* Tumors
* Fibroma
* Dermoid (Mature Teratoma)
* Brenner’s Tumor (transitional cell tumor)

References

Pathology and Neoplasia.ppt

Read more...

24 May 2009

Renal Pathology



Renal Pathology
By:Kristine Krafts, M.D.

Renal Pathology Outline
* Introductory stuff
* Glomerular diseases
* Tubular and interstitial diseases
* Diseases involving blood vessels
* Cystic diseases
* Tumors
* Introductory stuff
* Functions of the kidney:
o excretion of waste products
o regulation of water/salt
o maintenance of acid/base balance
o secretion of hormones
* Diseases of the kidney
o glomeruli
o tubules
o interstitium
o vessels
* Azotemia: BUN, creatinine
* Uremia: azotemia + more problems
* Acute renal failure: oliguria
* Chronic renal failure: prolonged uremia
* Hematuria
* Oliguria
* Azotemia
* Hypertension
Nephritic syndrome
* Massive proteinuria
* Hypoalbuminemia
* Edema
* Hyperlipidemia/-uria

Nephrotic syndrome
Renal Pathology Outline
* Introductory stuff
* Glomerular diseases

Nephrotic Syndrome
* Massive proteinuria
* Hypoalbuminemia
* Edema
* Hyperlipidemia, lipiduria
* Adults: systemic disease (diabetes)
* Children: minimal change disease
* Characterized by loss of foot processes

Causes
* Introductory stuff
* Glomerular diseases
o Nephrotic syndrome

Minimal Change Disease
* #1 cause of nephrotic syndrome in children
* Loss of foot processes
* Pathogenesis unknown
* Good prognosis

Things you must know
Minimal change disease
Normal glomerulus
Minimal change disease
Focal Segmental Glomerulosclerosis
* Primary or secondary
* Some (focal) glomeruli show partial (segmental) hyalinization
* Unknown pathogenesis
* Poor prognosis

Things you must know
Focal segmental glomerulosclerosis
Membranous Glomerulonephritis
* Autoimmune reaction against unknown renal antigen
* Immune complexes
* Thickened GBM
* Subepithelial deposits/spikes
Things you must know
Nephritic Syndrome
Causes
Post-Infectious Glomerulonephritis
Mnemonic
IgA Nephropathy
Pyelonephritis
Acute pyelonephritis with abscesses
Pyelonephritis
Cellular cast
Pyelonephritis
Urinary Tract Infection
E. coli
uncomplicated complicated
Pyelonephritis
UTI: Causative Organisms
Urinary catheter colonized by Proteus
Chronic pyelonephritis
Drug-Induced Interstitial Nephritis
Acute Tubular Necrosis
Benign Nephrosclerosis
Malignant nephrosclerosis
Malignant Hypertension
Renal Pathology Outline
Adult Polycystic Kidney Disease
Childhood Polycystic Kidney Disease
Medullary Cystic Kidney Disease
Renal Cell Carcinoma
Bladder Carcinoma

Renal Pathology.ppt

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12 May 2009

Organ System Pathology Images



Organ System Pathology Images

Cardiovascular Pathology:

117 Images

The heart and arterial system.

Central Nervous System Pathology:

123 Images

The brain and spinal cord.

Endocrine Pathology:

70 Images

The thyroid, parathyroids, adrenal, pituitary, and endocrine pancreas.

Female Genital Tract Pathology:

80 Images

The female reproductive system.

Gastrointestinal Pathology:

118 Images

The digestive tract from esophagus to rectum.

Hematopathology:

68 Images

The peripheral blood, bone marrow, lymph nodes, and spleen.

Hepatic Pathology:

60 Images

The liver.

Male Genital Tract Pathology:

40 Images

The male reproductive system.

Pulmonary Pathology:

110 Images

The respiratory tract, including lungs and pleura.

Renal Pathology:

119 Images

The kidney.



Visit here

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02 May 2009

Laboratory Medicine and Pathology videos



Laboratory Medicine and Pathology video presentations
from University of Wisconsin

Date
Presentation
02/25/2008 Picture from Discovery of the Year Celebration: Honoring James Thomson video
R. Golden, J. Thomson, J. Wiley, W. Dove, L. Hogle, C. Gulbrandsen
02/07/2008 Picture from Development of Non-Viral Methods of Nucleic Acid Transfer video
J. Wolff
11/20/2007 Picture from Medical Student Oral Presentations - Session II video
N. Ankumah, B. Hilgeman, C. Czeczok, B. Frederick, M. Rhodes
View description
Hear the following presentations from the 2007 Medical Student Research Fall Forum: "Phenotype Segregation Network Analysis of Risks Associated with Low Birth Weight" Nana-Ama Ankumah, Mentor: Theresa Duello, PhD "Developing Interventions to Treat Tobacco Dependence in a Free Clinic" Brian Hilgeman, Mentors: Tom Jackson, MD; Bruce Christiansen; Jennifer Brown "A Novel Method for Classification of Lumbar Degenerative Disc Disease" Charles Czeczok, Mentor: Paul Anderson, MD "Utilizing Systems Engineering Applications to Improve HIV Flow Laboratory Capabilities in Nairobi, Kenya" Brian Frederick, Mentors: Harold Steudel, PhD; Barbara Payne, PhD; Judd Walson, MD, MPH "Little Association Between Choice of Chemotherapy Treatment and Self-Related Health Among Women Diagnosed with Invasive Breast Cancer" Mary Rhodes, Mentor: Amy Trentham-Dietz, PhD

Picture from Medical Student Oral Presentations - Session III video
A. Segal, B. Schmidt, S. Hoffman, O. Zaka, B. Vyas
View description
Hear the following presentations from the 2007 Medical Student Research Fall Forum: "Immunohistochemical Analysis of Oxidative Stress and Apoptosis in Pre-Isolation Pancreas Biopsies as a Predictor of Islet Isolation Outcome: Ann Marie Segal, Mentor: Luis A. Fernandez, MD "To Be or Not to Be...In a Clinical Trial: Improving Accural Rates in Cancer Clinical Trials at UWCCC" Brian Schmidt, Mentor: Kim McDowell, MD, PhD "Women's Knowledge of Commonly Used Contraceptive Methods" Sarah Hoffman, Mentor: Sarina Schrager, MD, MS "Effects of Iron Deficiency in Minority Mothers on Offspring" Olamide Zaka, Mentors: Pamela Kling, MD; Roseanne Clark, PhD "Development and Characterization of a Cultured Myofibroblast Model for Vocal Fold Scar Studies" Bimal Vyas, Mentor: Susan Thibeault, PhD
09/05/2007 Picture from Fifty-two Rats video
K. Kudsk
View description
Kenneth Kudsk , MD, FACS, FCCM, speaks on "Fifty-two Rats" at the Health Sciences Learning Center on September 5, 2007.
(email me when the video is available)
07/19/2007 Picture from Heart Disease in the Female Population: Prevalence, Presentation and Pathophysiology video
M. Zasadil
View description
Mary Zasadil, MD, faculty at the University of Wisconsin-Madison, speaks on "CT Angiography" at the Health Sciences Learning Center on July 19, 2007.
03/15/2006 Picture from How the Maternal Fetal Interface Influences the Development Programming of Adult Onset Disease video
R. Magness
View description

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26 April 2009

The Lymphoid Systems Pathology



The Lymphoid Systems
(Lymph nodes; Thymus; Spleen)

Lymph Nodes
Micro-architecture & functional anatomy
White Blood Cell Disorders
Lymphadenopathy (Lymph Node Enlargement)
Non-specific reactive hyperplasia
Reactive Leukocytosis
Specific Lymphadenitis
Granulomatous lymphadenitis
Necrotising lymphadenitis
Sinus histiocytosis
Paracortical hyperplasia
Infectious Mononucleosis
Viral transmitted via direct oral contact (kissing disease)
Morphology
Clinical Course
Complications
Human Immunodeficiency Virus
HIV transmitted sexually
Acquired immunodeficiency syndrome
Neoplastic Proliferations of White Blood Cells
Lymph Nodes Micro-architecture & functional anatomy
Malignant Lymphomas
Non-Hodgkin’s Lymphoma
Hodgkin’s Disease
Non-Hodgkin’s Lymphoma
Grade Classification
Small Lymphocytic Lymphoma
Follicular Lymphoma
Mantle Cell Lymphoma
Lymphoblastic Lymphoma
precursor B-lymphocytic lymphoma
Burkitt’s Lymphoma
(Small non-cleaved lymphoma)
Malt Lymphoma
Mycosis fungoides; Sezony Syndrome
Adult T-cell Lymphoma
Hodgkin’s Lymphoma
Rye Classification
Aetiology & Pathogenesis
Clinical Features
Nodular Sclerosis
Lymphocyte Predominance
Lymphocyte Depletion
Disorders of the Thymus & Spleen
Splenomegaly
Massive Splenomegaly
Moderate Splenomegaly
Mild Splenomegaly
Thymus

The Lymphoid Systems.ppt

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Osteoarticular & Connective Tissues Systemic Pathology



Systemic Pathology

Osteoarticular & Connective Tissues
Bone
Function of Bone
Structure of Bone
Bone Remodeling Cycle
Osteoclasts
Osteoblasts
Fractures & Their Healing
Healing of Fractures
Congenital & Hereditary Bone Disorders
Achondroplasia
Osteogenesis Imperfecta
Regulation of Calcium Metabolism
Role in metabolic bone disease
Osteoporosis
Aetiological Factors
Factors in the Development of Osteoporosis
Pathogenesis
Acquired or genetic aetiology
Clinical Features
Rickets & Osteomalacia
manifestations of Vitamin D deficiency
Clinical Features & Diagnosis
Bone Disease Associated with Hyperparathyroidism & Hypercalcaemia
Morphology
Renal Osteodystrophy
Mechanisms of Renal Bone Disease
Osteomyelitis
Pathogenesis
Acute Osteomyelitis
Chronic Osteomyelitis
Tuberculous Osteomyelitis
Paget’s Disease (Osteitis Deformans)
Pathogenesis
Morphology
The affected femur shows characteristic thickening & deormity
Bone Tumours
Disease of the Joints
Osteoarthritis
Fibrillation & fissuring seen in osteoarthritis
Rheumatoid Arthritis
Immunological Abnormalities
Infectious Agents
Pathogenesis Overview
Extra-Articular Features
Spondyloarthropathies
Infective Arhtritis (Sepetic arthritis)
Aetiological Organisms

* Staphylococcus aureus
* S. albus (prosthetic jnts); S. pyogens
* Diplococcus pneumoniae
* Neisseria gonorrhoeae (STD)
* Heamophilus influenza (children)
* Gram –ve organisms (drug addicts)
* Borrelia burgdorferi (Lyme disease
* Mycobacterium TB
* Brucella abortus (intervertebral discs)

Routes of infection

* Haematogenous
* Traumatic implantation
* Direct spread from adjacent tissue

Gout
Aetiology of Hyperuricaemia
CHRONIC TOPHACEOUS ARTHRITIS
Pathogenesis of Renal Involvement
Typical Clinical Presentations
Pyrophosphate Arthropathy pseudogout
Systemic Diseases & Joint Changes
Examples

Systemic Pathology.ppt

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24 April 2009

Diagnostic Tests and Specimen Collection



Diagnostic Tests and Specimen Collection

Diagnostic Testing and the Nursing Process
Planning
Diagnostic Tests
Laboratory Tests
Hematology Tests

* Complete blood count (CBC)
o Information about the state of health or presence of illness
o Number of red blood cells (erythrocytes)
o Type and number of white blood cells (differential)
o Platelet count, PT, PTT, INR
* During infection, the number and type of white blood cells increase.
* Neutrophil counts can be significant.
* In severe infections, bone marrow releases more granulocytes.
* Immature polymorphonuclear neutrophils are released (called bands).
* The result is a shift to the left (more bands).
* Drug therapy may cause leukopenia (a decrease in leukocytes).
* Hemoglobin shows the capacity of the blood to transport oxygen from the lungs to the tissues.
* A normal platelet count is essential to clotting.
* Coumadin therapy is guided by prothrombin time (reported in INR numbers).
* The erythrocyte sedimentation rate (ESR) gives clues about inflammatory conditions.


Chemistry Tests
* Whole blood, plasma, and serum
* Body fluids such as:
o Urine, spinal fluid, gastric contents
* Chemistry tests provide information about biochemical reactions such as electrolyte balances and organ function.
* Some institutions use automated computerized blood chemistry testing.
* Examples of tests available are:
o Serum albumin, alkaline phosphatase (ALP), aspartate aminotransferase (AST)
o Total bilirubin, serum calcium, cholesterol, glucose, LDH, phosphate, total protein, BUN, uric acid
Blood Glucose

* Blood glucose is a test commonly performed at the bedside or in the physician’s office by the nurse.
* Guides insulin therapy for diabetics
* Guidelines for performing test depend on manufacturer of testing equipment
* Requires a finger stick to obtain capillary blood

Serology Tests

* Based on analysis of serum
* Used to diagnose both viral and bacterial diseases or determine antibody levels for:
o Dysentery, rheumatic fever, typhoid, influenza, rubella, and syphilis
* Can also be used to determine titers in response to vaccines
* May use radionuclides such as iodine-125 and iodine-131
* Examples of serology tests ordered
* Agglutination test for specific organisms
* Antistreptolysin-O titer
* Blood typing: ABO groups and Rh
* Carcinoembryonic antigen assay (CEA)
* Coombs’ test
* C-reactive protein antiserum
* Heterophil antibody titer
* Tests for syphillis

Urinalysis

* Provides information about kidney function or other body functions and diseases
* Single, catheterized, or random specimens can be collected anytime, with no special preparation. First voided specimen is preferred.
* Urine deteriorates quickly and should be tested soon after collection.

Midstream collections

* External genitalia are cleansed
* A small amount of urine is passed.
* Urine is collected from midvoiding in a sterile container.
* Used for cultures when a bladder infection is suspected
Timed, long-period specimens

* Collected over 12- or 24-hour period
* Container may be kept on ice and has some form of preservative.
* Used to determine kidney function and possible glomerulonephritis or acute tubular necrosis

Other Laboratory Tests

* Bacteriology
* Histology
* Cytology
* Ova and parasites
* Cultures from specimens of feces, blood, urine, wound drainage, or samples of body tissue or fluids

Ultrasonography

* Records the reflection of sound wave directed into the tissues
* Used to diagnose pathologic conditions of
o Uterus, ovaries, prostate, heart, liver, kidneys, pancreas, gallbladder, lymph nodes, thyroid, eyes, and peripheral blood vessels
* Often used in conjunction with nuclear medicine scans
Radiology Procedures

* Most common test is radiation by x-ray
* Produces images in varying densities on film after it passes through the body
* Commonly performed radiology procedures:
o Chest x-ray
o Barium swallow and upper GI series
o KUB (kidneys, ureters, and bladder)
o Gallbladder series

* IVP (intravenous pyelogram)
* X-ray of bony skeleton
* Arthrogram
* Myelogram
* Radionuclide scan
* Computed tomography (CT) scan

Magnetic Resonance Imaging

* Noninvasive method of differentiating body tissue (commonly used for brain, knee joint, spine and spinal cord, and abdominal organs)
* Requires that all metal be removed from the patient
* Contraindicated in patients with hip prostheses, implanted pacemakers or defibrillators, artificial cardiac valves, or vascular clips or staples from recent surgery
* Patient teaching is very important before this procedure; patient needs to know the duration of the test and that it requires being in a noisy environment.
* Patient may become claustrophobic during test.
* Patient needs to know deep-breathing and relaxation techniques.


Cardiopulmonary Studies

EKG/ECG

* Diagnoses heart rhythms and heart disease; measures electrical activity of the heart

Cardiac catheterization

* An invasive procedure used to determine function of heart valves, coronary artery blood flow, and oxygenation at different points in the heart and to diagnose coronary artery disease
o Abnormal blood in cardiac vessels can be detected as can valvular dysfunction.

* Surgical procedure that requires consent
* Procedure is performed under sterile technique in radiology or a surgical suite.
* Postprocedure requires checking insertion site every 10 to 15 minutes for possible bleeding.
* If the femoral approach is used, the patient’s leg may be immobilized for several hours.
* New angioseal devices may preclude the need for post procedure pressure.
Treadmill Stress Test

* A cardiac-monitored ECG test
* Patient is on a treadmill, which is used to increase heart rate and blood pressure with controlled activity.
* Test may be done with radioisotope imaging
* Patient should avoid smoking, dairy products, or drinking caffeine for 4 hours before the test.
* Angiography/Arteriography
* Used to locate lesions, occluded vessels, tumors, and malformed blood vessels
* A contrast medium is injected during the procedure (check for allergies).
* Consent is required.
* Patient should be NPO for at least 6 hours before the test.
* Patient may be given preprocedure sedation.


Other Tests

* Endoscopic examinations of:
o The stomach (gastroscopy)
o The sigmoid colon (proctosigmoidoscopy)
o The entire colon (colonoscopy)
o The bladder (cystoscopy)
o The gallbladder and common bile duct (endoscopic retrograde cholangiopancreatograhy [ERCP])

Electroencephalography (EEG)

* Measures neurologic and physiologic activities of the brain via the electrical discharges from the brain
* Performed to localize and diagnose brain lesions, scars, epilepsy, infections, or clots
* Performed to determine brain death in comatose patients on life support

Things to Remember

* All invasive tests requiring injection of a medium require a consent.
* Tests requiring premedication or sedation usually require a consent.
* Many tests have some form of preparation; review the laboratory manual for your facility to determine what must be done before the patient has the test and after the patient has had the test.

Diagnostic Tests and Specimen Collection.ppt

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