Pathology 1 - Block 1 - Part 3

davidwurbel7's version from 2016-04-12 18:55

Outcomes of Chronic Inflammation

Question Answer
Remaining cells proliferate to replace dead cellsRegeneration
In tissues that can’t replicate or if tissue “scaffolding” is damaged. Fibrous tissue replacementScar
Control of proliferation. Capacities of different tissues to proliferate. Stem cells. Growth factorsCellular and Tissue Regeneration
Continuously dividing cells. Examples include Hemopoietic, epithelial, GI, UTLabile Cells
Minimal replication normally but have an enhanced replication when needed. Examples include Liver, kidney, pancreas, ECs, fibroblasts, smooth muscle Stable Cells
No replication abilities. Examples include Neurons and heart musclePermanent Tissues
Self renewal capacity and undergo asymmetric replicationStem Cell
Have self-renewal capacity. Are present among differentiated cells in organs. Limited capacity for differentiation. Can only become tissues within organ in which they resideAdult Stem Cells
In blastocyst inner cell mass. Extensive renewal capacity. Can be induced to mature into all three germ cell layersEmbryonic Stem Cells
Found in bone marrow. Can generate chondroblasts, osteoblasts, osteoclasts, myoblasts. May be useful in specific medical conditionsMesenchymal Stem Cell
Lack of bone break down enzymes resulting in very hard and dense bone but subject to spiral fracturesOsteopetrosis
Proteins that bind to a receptor that signal gene activation. Lead to proliferation, prevention of proliferation, synthesis of moleculesGrowth Factors
Macrophages, Lymphocytes at site. These cells are activated by other cytokines. Parenchymal cells and stromal cells that were damaged by the etiological agent release theseGrowth Factors for Repair
Collagens and elastins. Provides strengthFibrous structural proteins
Proteoglycans, hyaluronan. Provides resilience and lubricationWater – Hydrating Gels
Connect elements to each other and to cellsAdhesive Glycoproteins
Transmembrane heterodimers. Leukocyte adhesion. Cellular attachment to ECM. Platelet aggregation. Mediate transmembrane signaling. Not on RBCsIntegrins
Occurs in lesions that involve connective tissue framework. Cell regeneration inadequate. Deficit filled in by collagenScar Formation
Growing of new blood vessels. Part of the healing process. Development of collateral circulations. Tumor progressionAngiogenesis
Proliferation of ECs behind leading front. Remodeling into tubes. Recruitment of peri-enothelial cells are steps in thisAngiogenesis
Production is induced by hypoxia. Bind to VEGFRs on cell surface. Stimulates proliferation and migration. Stimulates nitric oxide productionVEGF
Exuberant proliferation of granulation tissue. Prevents epithelializtion and has to be surgically removedProud Fresh
Excess production of type III collagen. Overproduction of collagen that overflows the original borders of the injury siteKeloid
Maximum tensile strength of a scar is this70%-80%

Tissue Renewal And Repair

Question Answer
Ability to replace damaged components and return to normal state. Occurs in cells that survive the injury & retain the capacity to proliferate. Examples: skin, intestines, liverRegeneration
Occurs in tissue which are incapable to complete restitution, or if the supporting structures of the tissue is severely damaged. Repair occurs by laying down of fibrous tissueScar Formation
Scar formation is the same as thisFibrosis
Extensive deposition of collagen. Damage to ECM cause loss of framework. ECM components are important for maintaining structural frameworkScar Formation
Continually dividing cells. Examples are surface epithelium (skin, oral cavity). Mature cells are derived from adult stem cells which has high proliferative capacityLabile Cells
Low level of replication. However, can undergo rapid proliferation following stimuli. Examples of this are liver, kidney, pancreas, mesenchymal cells (fibroblasts), endothelial cells, lymphocytesQuiescent Cells
Cannot undergo mitosis in postnatal life. Examples include neurons, skeletal muscle, cardiac muscleNondividing Cells
Growth factor produced by platelets, macrophages. Functions: mitogenic for keratinocytes, fibroblasts helps in granulation tissue formationEpidermal growth factor (EGF)
Growth factor produced by macrophages, T lymphocytes, keratinocytes. Functions: mitogenic for keratinocytes, fibroblasts helps in granulation tissue formationTransforming Growth Factor- α (TFG-α)
This is the receptor for EGF and TGF-αHER-2/Neu Receptor
ERB B2 receptors also referred to asHER-2/Neu Receptors
HER-2/Neu is over expressed in this type of cancerBreast Cancer
Growth factor produced by platelets, endothelial cells, lymphocytes, & macrophages. Functions: binds to 2 cell surface receptors (types I & II), triggers phosphorylation of cytoplasmic transcription factors called Smads plays numerous roles: Act growth inhibitor: by increasing the expression of cell cycle inhibitors. Loss of this role helps tumor proliferation. Fibrogenic agent: fibroblast chemotaxis, production of collagen, fibronectin, proteoglycans. Inhibits collagen degradation. Anti-inflammatory: limit & terminate inflammatory responseTransforming Growth Factor- β (TGF- β)
Growth factor produced by mesenchymal cells. Functions: inducing endothelial cell permeability, and vasodilation (ref: acute inflammation), formation of blood vessels in early development (vasculogenesis). Growth of new blood vessels (angiogenesis in cancer), lymphogenesis. hypoxia (hypoxia inducible factor)Vascular Endothelial Growth Factor (VEGF)
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Question Answer
Collagen found in bone, tendon (high tensile strength)Type I
Collagen found in cartilage, intervertebral disc, vitreousType II
Collagen found in blood vesselsType III
Collagen found main component of basement membraneType IV
Genetic condition more than half are Autosomal Dominant, several variants are seen. Types - affects commonly Type 1 and Type III collagen synthesis. Molecular genetics: mutations in structural genes for collagens. Clinical signs and symptoms - Skin: thin, velvety, hyperextensible, easily traumatized, poor wound healing. Ligaments and joints: laxity, and hypermobility, mild to irreducible hip dislocation. CVS - Mitral valve prolapse, aortic dissectionEhlers-Danlos Syndrome
Genetic condition also called “brittle bone disease”, Autosomal Dominant. Deficient synthesis of type 1 collagen mostly bones. Molecular genetics: AD mutation in genes that encode for α1 and α2 chains of collagen. Type I form have normal life span, but have childhood fractures. As the child grows, incidence of fractures reduce. Blue sclera: reduced collagen content hearing loss: conduction through ossicles in middle ear. Dental: small, blue-yellow misshapen. Due to deficiency in dentinOsteogenesis imperfecta
Genetic condition Autosomal dominant, 1 in 5000 live births. Age of onset of symptoms vary, cardiac problems begin by 3rd to 4th decade of life defect in extracellular glycoprotein “fibrillin-1”. FBN1 mutations are associated with Marfan syndrome. Fibrillin is a major component of microfibrils seen in ECM microfibrils provide scaffolding on which tropoelastin gets deposited to form elastic fibers. Morphology: Skeletal system: unusually tall, long extremities, long tapering fingers, ligament laxity, kyphosis, scolosis, pigeon-breast deformity. CVS: mitral valve prolapse, aortic dissection, aortic valve incompetence. Eye: subluxation of lens (ectopia lentis - bilateral, symmetrical, and supertempora dislocation)Marfan Syndrome
Form highly hydrated compressible gels, act as lubricant. Examples are seen in joint cartilageProteoglycans and Hyaluronan
Ability of a cell to maintain shape, polarity, organize, and shift depends on intracellular scaffolding of proteinsCytoskeleton
Intermediate filament seen in nuclear lamina of all cellsLaminin
Intermediate filament seen in mesenchymal cellsVimentin
Intermediate filament seen in muscle cellsDesmin
Intermediate filament seen in axons of neuronsNeurofilament
Intermediate filament seen in glial cellsGlial fibrillary acidic protein (GFAP)
Intermediate filament seen in epithelial cellCytokeratin
Tissue composed of proliferating capillaries (microscopically characterized by plump endothelial cells), fibroblasts producing collagen (spindle cells with pink background), red cells, inflammatory sells (including macrophages), necrotic materialGranulation Tissue
Wounds with opposed edges. clean, uninfected, surgical incision approximated by surgical sutures. Incision causes death of limited number of epithelial and connective tissue cells, disruption of basement membraneHealing by First Intention
By day 3, neutrophils are replaced by macrophages to remove the debris. Fibroblast lay down Type III collagen. This is then replaced by Type I collagenHealing by First Intention
This fibrogenic agent plays a role in bringing fibroblast into the area and laying down collagenTGF-β
From Day 3 to Day 5 during the healing processMaximum Granulation
Wounds with wide edges with larger amount of granulation tissue wound contraction caused by myofibroblasts. Large amount of scar formationHealing by Second Intention
Degradation of collagen and other ECM proteins is done by this family of moleculesMatrix Metalloproteinases (MMP)
Actions of MMPs can be inhibited by these moleculesTissue Inhibitors of Metalloproteinases (TIMPs)
Blood supply (lower limbs in diabetics, varicose veins), Local infection, Foreign body and Hematoma are local factors that effect thisWound Healing
Varicose veins is due to failure of the valves in these veinsSaphenous Vein
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Question Answer
Astrocyte (glial cell) proliferate in response to injury. Responsible for repair and scar formation. This process is calledGliosis
The excessive deposition of collagen and other ECM components in a tissue. A pathologic process induced by persistent injurious stimuli such as chronic infections and immunologic reactions. The major cytokine involved in this is TGF-βFibrosis
The major cytokine involved in fibrosis is thisTGF-β
Wound healing complications in which there is inadequate formation of granulation tissue can lead to thisWound Dehiscence
Scar tissue grows beyond the boundary of the original wound, and do not regressKeloid
Excessive amount of collagen producing a raised scar that stays within the boundary of the original woundHypertrophic Scar
Dense proliferating fibrous tissue with entrapped skeletal muscle bundles usually seen in anterior abdominal wall and Cesarean sectionDesmoid Tumor
Excessive contraction of wound results in deformities. Frequently involves the palms, soles, anterior aspect of thorax. There is an impairment of joint movementsContracture

Hemodynamic Disorders Part 1

Question Answer
Severe and generalized edemaAnasarca
Protein poor fluid, seen in body cavities (effusions), dependent pitting edemaTransudate
Protein rich fluid, high LDH, example - inflammationExudate
Ascites is due to low amounts of this in the bloodProtein
Protein rich fluid. Non-pitting edemaLymphedema
Local: results from impaired venous outflow example: deep vein thrombosis. Generalized: congestive heart failure leading to pulmonary edemaHydrostatic Edema
Caused by Ischemic heart disease, Hypertension, aortic and Mitral valvular diseases and Myocardial diseases. Morphology: Hypertrophy of the heart and Pulmonary edema. Clinical - cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, atrial fibrillation, pre-renal azotemiaLeft-Sided Heart Failure
Commonly follows left-sided failure. pure right-sided failure happens in patients with lung pathology (COPD), pulmonary hypertension, pulmonary thromboembolism. Morphology Liver and Portal system: congestion of liver, portal venous hypertension. Clinical: congestive hepatomegaly, ascites, raised JVPRight-Sided Hearth Failure
Edema characterized by heavy proteinuria (proteinuria more than 3.5g / 24 hrs.) and hypoalbuminemia. Examples of this can be seen in nephrotic syndrome and liver cirrhosis seen as ascitesReduced Plasma Osmotic Pressure Edema
Edema characterized by blockage of inguinal lymph vessels by parasite worms (Filariasis)Elephantitis
Plugging of superficial breast lymphatics by tumor cells that cause this appearance of the of the breastPeau d' Orange
“Batwing” sign on x-ray chest indicatesPulmonary Edema
Caused by traumatic brain injury (TBI), ischemic stroke, tumors, meningitis. brain is swollen, narrowed sulci, distended gyri, signs of flattening against the rigid skullBrain Edema
Optic disc blurring on fundoscopy. Due to elevated intracranial pressure (ICP). Increase in intra-axonal pressure due to edema.Papilledema
Papilledema is an indication of thisIncreased Intracranial Pressure
Hemosiderin laden macrophages see in the lungsHeart Failure Cells
Heart failure cells are also called thisHemosiderin Laden Macrophages
If iron is suspected on the slide, this stain is usedPrussian Blue
Central regions of hepatic lobules are red brown due to hypoxia surrounded by uncongested tan brown caused by fatty change due to anoxiaNutmeg Liver
Accumulation of blood within tissuesHematoma
1 to 2 mm hemorrhages. Can be due to locally increased intravascular pressure or low platelet countPetechiae
≥3mm hemorrhages. Can be due to low platelet count, trauma or vascular inflammation (vasculitis)Purpura
Subcutaneous hematomas (bruises)Ecchymoses
Hemorrhage in the pericardical sac causing compression of the heartCardiac Tamponade
Patients presents with muffled hearts sounds, increase in JVP and narrowing pulse pressureCardiac Tamponade