Pathology (phase A)
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What are forensic pathologists?
CSI - what the public thinks they do. A small part of their practice.
List and describe the types of pathology.
- Anatomical: surgical, cytology, autopsy
- Clinical: hematology, clinical chem and microbiology
What is fine-needle aspiration?
disease detection by the study of individual cells
What does a coroner do?
establish Who the deceased was and Where, When, and How the death occurred.
What is hematology?
The study of blood in health and disease
What is disease?
An abnormal condition affecting the body (& mind) of an organism
Difference between irreversible and reversible cell damage
- Reversible: can be healed, usually deals with the cytoplasm, cell adapts to fix damage (think of cell adaption slide)
- Irreversible: usually severe and long lasting problem, generally problems with the nucleus (fading, shrinking, or fragmentation)
List seven cell adaptations:
- The plasias:
- -Hyperplasia: increased number of cells
- -Hypoplasia (aplasia): decreased (no) number of cells
- -Normoplasia: normal number of cells
- -Metaplasia: reversible change from one tissue type to another
- The trophy's:
- -atrophy: shrinking cells
- -hypertrophy: expanding cells
List 9 causes of cellular injury
- -hypo/anoxia: (no oxygen) (also reoxygenation injuries)
- -microbial pathogens
- -physical agents
- -immunologic injury
- -genetic factors
- -nutritional factors
- -social factors
describe the three types of cell death:
- 1) necrosis: exogenously induced
- 2) apoptosis: programmed cell death
- 3) autolysis: death of cells after death of organsim
What are the 5 types of necrosis?
- 1) coagulative: Proteins are coagulated like in a fried egg
- 2) Liquefactive: dissolving of tissue (pus)
- 3) caseous: cheesy necrosis, usually found in TB, dry and wet gangarene
- 4) fat: what happens when fatty tissue is injured (traumatic or enzymatic)
- 5) Fibrinoid: Looks like the deposition of on BV walls (e.g. rhematoid arthritis)
Name some intracellular accumulations
- 1) Glycogen
- 2) Proteins
- 3) Lipids
- 4) Hyaline
- 5) Lipofuscin
- 6) Pigments
- 7) Calcium
Trace the path of disease development
- 1) Cause
- 2) Pathogenesis
- 3) Morphological changes
- 4) clinical expression
Describe vascular changes and chemical activity in acute inflammation
- 1) arteriole and capp. bed dilation (increased blood flow)
- 2) increased vascular permeability (tissue edema)
- 3) Leukocytes (initially neutrophils) leave the vasculature via diapedesis migrate to site of injure (lured by chemotatic agents)
- 4) activation of leukocytes
- 5) phagocytosis, killing, and degradation of offending agent
- 6) termination: resolution, scar, chronic inflammation
What are the 5 cardinal signs of inflammation?
- 1) heat
- 2) redness
- 3) swelling
- 4) pain
- 5) loss of function
Describe the steps in extravation of leukocytes from blood
- 1) margination and rolling along vessel wall
- 2) firm adhesion to endothelium
- 3) transmigration between endothelial cells
- 4) migration to site of infection via chemotaxis
What characterizes a chronic inflammation?
- 1) infiltration with mononuclear cells (including macrophages, lymphocytes, and plasma cells)
- 2) tissue destruction because of inflammatory cell byproducts
- 3) repair: angiogenesis; fibrosis
what is a granuloma and what causes it?
- granuloma: chronic inflammation with char. aggregates of activated macrophages with scattered lymphocytes (walls off the offending agent)
- Happens in 3 settings
- 1) persistent T-cell response to certain microbes (e.g. TB, leprosy,)
- 2) Immune-mediated inflammatory disease (e.g. Crohn's disease)
- 3) inert foreign bodies
growth of cells and tissues to replace lost structures. Requires an intact connective tissue scaffold
differences between and examples of labile, stable (quiescent), and permanent cells
- labile: continuously dividing (epithelium, blood cells)
- stable: can divide if necessary (liver, kidney)
- permanent: non-dividing and peprmanently differentiated (myocytes, neurons)
what factors influence wound healing?
- 1) tissue environment and extent of tissue damage
- 2) intensity and duration of stimulus
- 3) presence of foreign bodies or inadequate blood supply
- 4) diseases (e.g. diabetes) that inhibit repair
4 sequential processes in CT tissue repair (fibrosis)
- 1) angiogenesis
- 2) migration and prolif. of fibroblasts
- 3) collagen synthesis
- 4) CT remodeling
4 steps in angiogenesis
- 1) vasodilation (due to VEGF and NO)
- 2) migration of endothelial cells
- 3) proliferation of endothelial cells
- 4) Inhibition of endothelial cells
Compare wound healing by first and second intention
1) first: knife cut, focal disruption, regeneration is the principal method of repair,
2) second: ulcer, widespread disruption, more macrophages, heavy wound contraction, more granulation
Which cells participate in wound healing?
- polymorphonuclear leukocytes (e.g. neutrophils)
Compate dihiscence to keloid formation
1) dihiscence: the wound opening after suturing
2) keloid formation: accumulation of excess collagen
What is the pathogenesis of amyloidosis.
misfolding of proteins. The misfolded proteins cannot be degraded via the body's normal mechanisms. Can happen with any protein but often associated with SAA (becomes AA) and immunoglobulin light chains (becomes AL)
Describe the morphological appearance of an amyloid
Gross: waxy pale in organs
Histo: Looks apple green when using congo red stain (specific stain used for this)
Clinical features and diagnosis of amyloidosis
- depends on where it is located.
- heart: arrythmia, conductive disturbances, cardiomyopathy
- kidney: renal failure
- brains: role in Alzheimer's
- Diagnosis: usually an abdominal fat pad biopsy
How can you classify amyloidosis?
- 1) systemic:
- -primary: immunocyte-associated (e.g. multiple myeloma)
- -secondary: AA-associated (e.g. chronic inflammation diseases like TB)
- 2) localized:
- -senile cerebral: Alzheimer's disease
Name three basic things about atheriosclerosis
- 1) present in intimal layer
- 2) Chronic inflammation
- 3) multiple attempts to heal inflammation
name some risk factors for atherioscleorsis
Describe the pathogenesis of atheriosclerosis
- 1) Monocytes (in the blood) enter the BV intima and become macrophages (in the tissue) because of cytokines
- 2) These macrophages take up oxidized LDL (low density lipoprotein) and become foamy macrophages which in turn release cytokines that bring in more monocytes and bring in smooth muscle cells from the tunica media
- 3) The proliferation of these SM cells and the macrophages cause the plug to grow and release HDL over time
Describe the morphology of atheriosclerosis
- 1) fatty streak: collection of foamy macrophages in the intima
- 2) fibrofatty atheroma
What is the difference between a stable and a vulnerable plaque?
stable: thick fibrous cap, small lipid core, minimal inflammation
vulnerable: thin fibrous cap, large lipid core, increased inflammation
Describe the clinical presentation of atheriosclerosis
stenosis (chronic narrowing): stable angina, ischemia, small amount of flow getting through
acute plaque changes: rupture, ulceration, hemorrhage, thrombosis-embolism
Can later lead to an aneurysm (like a hernia of a blood vessel) in front of the blockage
Key roles of pathology in patient care
- 1) Diagnosis
- 2) Prognosis: how will the patient do given the diagnosis?
- 3) Prediction: how will the disease respond to a specific treatment?
- 4) Follow-up
- 5) Experimental therapy
Describe three specimens in pathology
- 1) cytopathology: fine needle aspirates; fluids
- 2) Surgical pathology: biopsies; resections
- 3) Autopsy: post-mortem organ/tissue examination
Three types of surgical pathology specimens
- 1) core biopsy
- 2) excision biopsy
- 3) resection
Describe specimen processing
- 1) cyto and surgical specimens
- -send fresh specimen to lab
- -fixed for the microscope
- -alive for flow cytometry
- -frozen for molecular studies
- -touch imprints for FISH
- 2) Autopsy specimens
- -integrity depends on death-postmortem interval
What is synoptic reporting?
a standardized template for reporting data for different sites/different centres, etc
Key issues in pathology reporting
- 1) accuracy and conveying uncertainty
- 2) turnaround time
- 3) Quality
What are you looking for in an autopsy?
- 1) Cause: Immediate and underlying cause
- 2) Manner: accidental, homicidal, suicidal, natural
- 3) mechanism: pathophysiologic explanations
What is quality of care?
degree to which health services increase the likelihood of desired health outcomes
What are the domains in quality of care?
- 1) Safety: avoid injuries to patients
- 2) Effective: provide services based on good science
- 3) Patient-Centred: each patient is an individual and needs to be treated with respect
- 4) Efficiency: avoid wasting resources
- 5) Equitable
- 6) Access: physical/geographic access to health facilities
Describe the characteristics of an error.
- -non-random (in a recurrent pattern)
- -Circumstances and not practitioners influence errors
- -dependent on error-provoking factors in system
- -most are systemic
What contributes to medical error?
- 1) Organization (e.g. hierarchy) contributes to:
- 2) Environmental factors (e.g. fatigue) Contributes to:
- 3) Individual (e.g. mistakes, negligence) contributes to:
What are some barriers of disclosure?
- 1) tort culture
- 2) regulatory issues
- 3) no uniform policies
- 4) fear of peer review
- 5) ignorance of benefits
Where do histamines and serotonin come from and what are their functions?
- -both are cell-derived amines
- -Histamine (mast cells, basophils, platelets)
- -vasodilation, increased BV perm, endothelial activation
- -serotonin (platelets)
Where do prostaglandins and leukotrines come from and what are their functions?
- -They are cell-derived
- -both come from mast cells and leukocytes
- -prostaglandins: vasodilation, pain, fever
- -leukotrines: increased vasc perm, chemotaxis, leukocyte adhesion and activation
Where do reactive Oxygen species originate and what are their functions?
- -cell derived
- -come from leukocytes
- -kill microbes and cause tissue damage
Where was NO come from and what is its function?
- -comes from endothelium and macrophages
- -kill microbes, SM relaxation in BVs
Where do cytokines come from and what are their functions?
- -.e.g. TNF, IL-1, IL-6
- -macrophages, endothelial cells, mast cells
- -local: activate endothelial cells
- -systemic: fever, shock, metabolic abnormalities (think of cytokine cascade)
Where do complements come from and what do they do?
- - they are plasma-derived (in the liver)
- -leukocyte chemotaxis and activation
- -Membrane attack complex
- -opsonization (mark for phagocytosis)
Where do kinins come from and what to they do
- - they are plasma-derived (produced in liver)
- -this group mediates vascular reaction and pain
Where do coagulation proteins come from and what do they do?
- -they are plasma-derived (produced in liver)
- -activate clotting, endothelial activation, leukocyte recruitment
What chemical mediators are responsible for Vasodilation?
- nitric oxide
What chemical mediators are responsible for increased vascular permeability?
- histamine and serotonin
- C3a and C5a
What chemical mediators are responsible for chemotaxis, leukocyte activation and recruitment?
- -TNF IL-1
- -C3A, C5a
- -bacterial products
What chemical mediators are responsible for fever?
What chemical mediators are responsible for pain?
What chemical mediators are responsible for tissue damage?
- lysosomal enzymes from leukocytes
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