03 - September 17, 2013.docx

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Department
Laboratory Medicine and Pathobiology
Course
LMP299Y1
Professor
All Professors
Semester
Fall

Description
LMP402 September 17, 2013 Read paper before Thursday lecture 38 year old male Symptoms of lymphoma; underwent treatment; as result of treatment, good response, mass disappeared; developed generalized nausea, vomiting; ER visit, where lob consolidation where air space filled with fluid as seen on X-ray; developed respiratory failure; death Left upper lobe – area of hemorrhage Microscopic section – make out the alveolar walls; most air spaces filled with blood; blood has albumin and fibrin that coagulates once blood reaches extravascular tissues Higher magnification – gram stain – microorganiss throughout the lungs – rod shaped, consistent with pseudomonas Invading the walls of the vessels, accounting for hemorrhage Pneumonia and septicemia Due to pseudomonas aeruginosa Patient was immunosuppressed – as result of therapy for his therapy of lymphoma – patient able to mount inflammatory response that would readily control this infection at the early stages Very frequent opportunistic infection Aquatic environments – hospitals are cesspools of infection – ill patients shed their bacteria; and where they can survive, they will survive there anywhere in hospital; especially places where have water Bacteria will infect lungs – when in intensive care, intubated, which can be source of infection from upper respiratory tract into lower respiratory tract Aspirate gastric contents before getting intubated but the main culprit is the fact that this patient has bone marrow that is depleted of myeloid cells – this makes the patient susceptible to opportunistic infections Another example – HIV – CD4 positive cells destroyed by virus – these patients are predisposed to opportunitist cinfections, but not by this bacteria; HIV predisposed to viral infections, TB infections, crytobacteria – not bacterial infections because it’s the innate immune system that are most critical for that; slight differences between different types of immunosuppression and the type of opportunistic pathogen that is susceptible to Another example – Cystic fibrosis – vulnerable to psenumonas, other bacterial infectiosn – CF patients cannot clear mucus in lungs – susceptible to bacterial infections in bronchii of lungs Another example – organ transplantation – these patients susceptible to – less so innate immunity??? Genetic conditions of immunosuppression – could affect acquired immune system and/or innate immune system – ex. Conditions like genetic deficiency of integrin, ex beta2 integrins, these patients lack leukocyte adhesion type 1 – have circulating myeloid cells, because integrins are key molecules required for exit of cells into tissues, these patients predisposed to bacterial infections Genetic infections affecting bacteria killing, etc. 70 year old male Developed pneumonia after surgery for femur fracture Decreased level of consciousness Radiological features of pseuomenaous colitis Arrow pointing to colon – wall is thick as compared to wall of small intestine Thickness in bowel wall – Air fluid level in bowel – colon is quite dilated Colon dilated and long – Pseudomembraneous – pseudomebrane attached to mucosa – pus being deposited and adherent to surface of bowel Section through colon – normal looking mucosa; destruction of mucosa, leukocytes and fibrin deposited there Higher magivication – still remnants of mucosa – top of mucosa been destroyed and see neutrophils – this is what caused the pseudomembrane A lot of edema – on radiological study, there is fluid that exits from the blood vessels, causing dilation of submucosa – this is why radiologically, the wall looks so thick on CT scan Mechanism of pseudomembraneous colitis Broad-spectrum antibiotics cause destruction of normal bacterial flora in bowel Clostridium usually resistant to antibiotics – now less competition for nutrients and if patient is infected with clostridium – different in balance between normal microbiota versus pathogen – allows pathogen to proliferate and to take over Spores can survive for months in hospital environment – hard to eradicate If thesepatients exposed to antibiotics – decrease normal flora – clostridium will grow and take over Clostridium – makes two toxins – entertoxins – they disrupt the barrier function of colonic mucosa – some subset of clostridium that makes binary toxin – some studies that suggest particularly severe cases of this disease also associated with this binary toxin – another example to reinforce the normal microbiota in this intestine What causes these patients to die? Can produce various factors/cytokines that are released into Low blood pressure – blood vessels become leaky, but more importantly, ther ies decreased peripheral vascular resistance; cardiac output of blood – what maintains the blood pressure at certain level is the ability of the blood to exit from those arteries – this is regulated at level of arterioles; if dilate arteirioles, more blood let into a particular tissues; if dilate all arterioles, the heart in these patients pumping very fast (cn get cardiogenic shock – if infarction, the pump doesn’t work very well), get low blood pressure Resistance decreased- blood into tissues at higher rate Learning objectives: Mechanisms of inflammation Rapidly destroy dilute or isolate the injurious agent or infectious agent – the inflammatory response, evolutionarily goes all the way back to beginning – even unicellular organisms have ability to combat various pathogens Amoeba can phagocytose bacteria, destroying it Higher organisms with vascular system, this sytem used for inflammatory response Vascular system undergoes number of different changes that promotes inflammation Chronic can go on for the entire life of the patient If take histological section or biopsy of tissue from infalmamtory region, can subclassifity that inflammatory response as either acute or chronic Causes of acute inflammation Extracellular – infections – most are extracellular Trauma or cold or frostbite or burn – all can cause inflammatory response, initially that inflammatory response is sterile – but if have condition that can damage surface epithelium – if damge surface epithelium, have exposure to bacteria to enter – get infection on top of one of these conditions Antigen, antibody complexes – can lead to acute inflammatory response Cell necrosis – important cause of acute inflammation – ex heart attack/myocardial infarction; chronic inflammatory disease in artery (atherosclerosis) lead to plaque sdisruption, thrombus, acute ischemia in regions supplied by artery – get inflammatory response; aptoptosis does not lead to inflammation because it is a regulated process, involing caspase 3; disruption of proteins, and as the cell undergoes apoptosis, vesicles produced; contents encapsulated in vesicles, and these vesicles cleared by neighbouring cells; during normal development; significant number of cells that die, no inflammatory response to that; as evolutionary response, to develop normally, cells must die In necrosis, cell membrane permeable; calcium enters cell; cell releases products into extracellular environment and pro-inflammatory componets of these cells are various proteins that are released; some are localized to nucleus; other to mitochondria; these proteins incite inflammatory response; some of these proteins have been termed danger-associated molecular patterns Acute inflammation can be part of chronic inflammation – autoimmune disease can have flare-ups, so have acute inflammation response that becomes chronic; or intersitital lung disease, have flare-up and then it settles down and it progressively gets worse Acute bacterial pneumonia – histological section of patient who has pneumonia – Acute myocardial infarction – myocyte fibres – spaces between fibres – indicating edema, fluid that has leaked out and separated the fibres – infiltration of cells – myocytes show changes in ischemia – bands known as contraction bands – because of ischemia damage causes calcium to leak out of cells – rigor mortis that sets in after death Same mechanism – permeability of cell membrane, influx of calcium, hypercontraction of muscles Etiology of chronic inflammation Organisms that invade into cells – intracellular – tend to cause chronic inflammation Ex. Tuberculosis, leprosy, salmonella, Viruses – tend to be intracellular – best example of viral infection wuld be viruses that infect liver – hepatitis virus, hepatitis B virus – look at section of hepatitis B – tons of mononuclear cells – mostly lymphocytes invading liver and causing destruction of indiivdiual hepatocytes – inaddition to viuses, various toxic agents Endogenous – wall of ???????????????? Group of autoimmune diseases – lupus, Multiple sclerosis, etc – effect different tissues, organs, associated with chronic inflammatory changes In r arthritis – take section of joint, in synovial of joint, filled with lymphocytes – known as pans?? Vascular changes in inflammation Vascular changes critical to inflammatory response Initially, change in blood flow to the site of inflammation – a little bit about arterioles – what regulates the blood flow to a particular site and if the
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