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MCPHS Pathophys Test 1 Questions And
Accurate Answers
Pathophysiology - Answer The study of the disordered physiological processes associated with disease or injury Etiology - Answer Cause of disease, can be genetic (inherited mutations or variants) orAcquired (Infection, nutrition, chemical, physical). Usually multifactorial
Pathogenesis - Answer sequence of cellular, biochemical, and molecular events thatfollow exposure to an injurious agent
Cellular Housekeeping - Answer Normal cell function including protection, movement,nutrition, communication, catabolism, and energy generation. These genes are constantly active Plasma Membrane - Answer Phospholipid bilayer for protection and nutrient acquisition.passive diffution of small nonpolar molecules (O2, CO2, Steroids)
Channel Protein - Answer Hydrophillic pores in membrane that allow passive diffusion ofsolutes
Carrier protein - Answer Protein in cell membrane the changes conformation to permitactive diffusion across membrane
Receptor mediated transport - Answer Endocytosis, exocytosis, transcytosis Answer Microtubules: Cytoskeletal protein, thickest, most versatile; maintains cell
shape; mitosis aide; able to form flagella/cilia Intermediate filaments: Answer: Cytoskeletal protein, medium size, maintains cell shape Actin microfilaments: Answer: Cystoskeletal protein, thinnest, provides shape, permitstransport between organelles
Occluding Junction (tight junction): Answer: Blocks diffusion of molecules between cells(paracellular)
Anchoring junctions (desmosomes) - Answer Attach cells and intracellularcytoskeletons to other cells or the ECM. Small gap between cells allowing substances to pass in between Communication Junctions (gap junctions) - Answer 1/5-2nm pores (called connexons)allowing cell to cell communications
Endoplasmic Reticulum (ER) - Answer Site of synthesis of transmembrane proteins andlipids (Rough ER has ribosomes)
Chaperone Molecules - Answer retain proteins in ER until protein folding is complete Smooth ER - Answer Synthesize steroid hormones (in gonads/adrenals), catabolize lipidsoluble molecules (in liver), and sequester intracellular calcium (for apoptosis)
Sarcoplasmic Reticulum - Answer Smooth ER in muscle cells holding calcium for musclecontration
Golgi Apparatus - Answer process and pack secretory proteins
Cell signalling types- Answer Autocrine- self Endocrine- distant cellParacrine- neighbor cell
Intracellular receptors- Answer Include transcription factors activated by lipid solubleligands
Cell surface receptors-Answer transmembrane proteins that bind extracellular ligands Cell receptor actions- Answer open ion channels, activate G protein,activate enzyme (RTK), or initiate proteolytic event to activate transcription factor
Growth Factors- Answer Promote celly cycle entry and progression. Prevents apoptosis Extracellular Matrix (ECM)- Answer Interstitial proteins that support tissue. Critical forcell healing, architecture scaffolding and control cell proliferation
Interstitial matrix - Answer Space between cells produced by cells such as fibroblasts Basement membrane - Answer ECM tissue that surrounds cells to separate fromconnective tissue. Usually made from collagen and laminin
Cell cycle - Answer G1.presynthetic growth, S- DNA replication, G2. premitotic growth,M -Mitosis. Cycle can be activated or halted
Stem cells - Answer Self renewing, clonogenic, and multipotent. Performs asymmetricdivision where one daughter remains a stem cell and the other differentiates
Embryonic stem cells - Answer Totipotent, present in blastocyst Tissue stem cells - Answer Found in stem niches, quiescent until needed, mostlyoligopotent
Stem cell balance - Answer Self renewal/ proliferation versus cell death/differentiation Noxious stimuli - Answer reduced oxygen, chemical injury, microbial infection Adaptation - Response stress induced change in cell, viability preserved Reversible injury - Response Can return to steady state Irreversible injury - Response permanent damage leading to cell death Hypertrophy - Response Increase cell size, no new cells. Caused by synthesis ofaddition intracellular components Physiologic - muscle building Pathologic - Hypertension induced Cardiac hypertrophy Hyperplasia-Answer Increased cell division in cells capable not nerve or cardiac cells.Results from Growth Factor or stem cell proliferation. Physiologic- liver, bonePathogenic- BPH
Atrophy- Answer reduction of cell size and/or number caused by decreased workload,loss of inervation/blood supply, protein degradation/no more protein synthesis
Metaplasia - Answer Change in cell type in response to change in environment, ex:
substance accumulation from inability to degrade Lipid accumulation - Answer Steatosis - fat accumulation in liver causing inflammationNiemann-pick disease - lysosomal storage disorder
Protein accumulation - Answer excessive synthesis, reabsorption, or defectivetransport. Amyloidosis- misfolded protein accumulation in multiple organs Accumulation of: Glycogen accumulation - Answer caused my Diabetes or lysosomaldisorder Pigment accumulation - Answer Exogenous-carbon dust Endogenous- melanin, homogentisic acid (alkaptonuria causes this buildup, ochronosisis the deposit), Hemosiderin is hemoglobin derived deposit Calcification accumulation - Answer Dystrophic- cell death increases calcium in blood Metastatic- parathyroid hormone elevation, bone destruction, vitamin D disorder, renalfailure (increased phosphate binds to calcium) Inflammatory sequence - Answer 1) recognition of offending agent 2)Recruitment of Leukocytes and plasma protein3) Leukocyte activation and proteins
- Reaction termination
- Tissue Repair Causes of Inflammation Answer Necrosis, foreign bodies, and immune reactions 2 major components of inflammation Answer 1) vascular wall response- vasodilation andpermeability 2)inflammatory cell response- leukocytes recruitment and activation
Mediators of inflammation Answer initiates and controls inflammation secreted by cells or plasma short lived Histamine Answer Source: Mast CellsAction: Vasodilation, increased vascular permeability
Prostaglandins Answer Source: Mast CellsAction: Vasodilation, pain, fever
Leukotrienes - Answer Source: Mast CellsAction: Increase vascular permeability
Cytokines (TNF, IL-1) - Answer Source: Macrophages and helper T cellsAction: Local-endothelial activation, Systemic- fever
Chemokines - Answer Source: Leukocytes, activated macrophagesAction: Chemotaxis
Platelet Activating Factor (PAF) - Answer Source- Leukocytes and mast cellsAction- platelet aggregation and degranulation
Complement system - Answer Source: PlasmaAction: direct target killing
Kinins - Answer Source: Plasma Action: smooth muscle contraction and pain
infiltrate, severe fibrosis Exudate Edema - Answer Exudate- inflammatory extravascular fluid with high proteincontent. Pus is example
Transudate Edema - Answer extravascular fluid with low protein content Lymph response - Answer Increased flow/filtering. in severe injuries can havelymphangitis (lymph vessel) and lymphadenitis (lymph node)
Acute inflammation leukocyte-Answer first 6-24 hours, roll and adhere to vascularendothelium (1), Diapedesis through endothelium (2), and migration to tissue through chemotaxis (3) Phagocytosis -Answer Recognize, engulf, and kill by ROS or lysosome Outcomes of acute inflammation -Answer complete resolution, replacement withfibrosis, or progress to chronic inflammation
Causes of chronic inflammation-Ans acute inflam., persistent/repeated stimuli, orflaming response w/o prior acute inflammation (persistent infection, allergy/autoimmune, toxic chemical exposure) Cells of chronic inflammation-Ans macrophages derived from hematopoietic stem cell inbone marrow or progenitor cells in yolk sac and fetal liver. phagocytosis and cytokine secretion (excessive may lead to prolonged inflammation and tissue injury) Lymphocytes (T cells) in chronic inflammation - Answer Propagates inflammation byactivating macrophages which in turn activate more lymphocytes
Granulomatous Inflammation - Answer Chronic inflammation where activated
macrophages accumulate and are surrounded by lymphocytes with central necrosis Foreign Body Granuloma - Answer incited by particles not easily phagocytized Immune Granuloma - Answer Formed by T cell mediated responses to persistentmicrobes or self antigen (Tuberculosis and Crohn disease)
Systemic effects of inflammation - Answer Called "acute phase response" - cytokinemediated fever, increased plasma proteins produced by liver (C-reactive protein), and leukocytosis (increased leukocyte number) Excessive inflammation consequences - Answer allergies, autoimmune, cancer,atherosclerosis
Defective inflammation consequences - Answer susceptibility to infection, delayedhealing of wounds, tissue damage
Tissue repair Answer rebuild architecture and tissue function. Regeneration(proliferation of surviving cells and maturation of stem cells) and Connective tissue depostion (deficient function scar formation) Tissue proliferation activity Answer Labile (proliferate throughout life ex: stem)Stable (divide in response to stimuli ex: liver/kidney) Permanent (cannot divide postnatal ex heart/brain) Mild tissue injury Answer regeneration and return of function Tissue injury - Answer injury to parenchyma and stroma repair by fibrous connectivetissue
Edema cause-Answer accumulation of fluid in tissue or body cavity (effusion) increasedhydrostatic pressure (ex heart failure), decreased colloid osmotic pressure (low plasma protein), increase vascular permeability (inflammation), Lymphatic blockage, orsodium/water retention (ex renal failure)
Increase hydrostatic pressure diseases-Answer Congestive heart failure, ascites (livercirrhosis), venous obstruction, thrombosis
Reduced plasma osmotic pressure diseases-Answer nephrotic syndrom, liver cirrhosis(ascites), malnutrition
Lymphatic obstruction-Answer Inflammation, neoplasm Disease of sodium retention- Answer Increased tubular reabsorption of sodium, increadrenin-angiotensin-aldosterone secretion
Agranular Leukocytes- Answer no granules- lymphocytes (T,B,NK) and monocytes(macrophages)
Granular Leukocytes- Answer Basophils, neutrophils, eosinophils, mast cells B Lymphocytes- Answer Source: Bone marrow Action: differentiate into plasma cells that mass produce antibodies Helper T Lymphocytes (CD4+) - Answer Recognize antigens from antigen presentingcells (APC's) then activate macrophages, release cytokines, and activate differentiation/proliferation of T and B lymphocytes Cytotoxic T Lymphocytes (CD8+) - Answer recognize antigen on infected cell andcauses the cell to go through apoptosis (perforin).
IMPORTANT: fights against virus, tumor, and role in transplant rejection Regulatory T lymphocyte - Answer Suppress T lymph replication Dendritic Cells-Answer Antigen presenting cell that secrete cytokines and activate NKcells and aide differentiation of helper and cytotoxic T cells
Macrophages-Answer Antigen presenting cell, clears antigen/antibody complexes toreduce inflammation, wound healing, phagocytosis
MHC facts-Answer on chromosome 6Human Leukocyte Antigen (HLA) in humans Helps T cell recognize antigens Polymorphism between individual people MHC Class I - Solution Expressed on all nucleated cells, recognised by CYTOTOXIC TCELLS (CD8+) AND NK CELLS. low class receptor
MHC Class II - Solution Expressed on antigen presenting cells (macrophage/dendritic)and recognised by HELPER T CELLS (CD4+) high class receptor
NK cells- Lympohcyte that fights virus, tumors and transplant. Inhibited by normal MHCI, Activated by virus infected cell expressing activation ligand and not expessing MHC I
Neutrophils- During acute inflamation phagocytose and destroy foreignantigens/microbes
Eosinophils- Parasite fighting using inflammatory factors and histamine release frommast cells
Innate immunity mechanisms - Answer ready to react to pathogens, first 6-12 hours ofinfection
Adaptive immunity mechanisms - Answer Stimulated by microbes and foreignsubstances. 1-5 days after infection
Toll Like Receptors (TLRs) - Innate immunity - Answer Cytoplasmic and plasmamembrane receptors recognize DAMPs (Damage associated molecular pattern molecules) released from damaged (necrotic, stressd, inflammed) cells. TLRs increasecytokines
Adaptive Immunity - Humoral - Answer Fluid immunity mediated by B cells andantibodies
Adaptive Immunity - Cellular - Answer Cell immunity mediated by T cells Lymph cascade in primary adaptive immunity - Answer antigen recognition; activation ofT cells and elimination of intracellular antigen; Activation of B lymphocytes and elimination of extracellular antigen; decline of response Secondary adaptive immunity - Answer Memory B cells last decades Humoral Immunity - Answer Naive B cell recognizes antigen (helper T or other stimuli),activate, proliferate, and differentiate to antibody secreting plasma cells. Memory B cellsIgG, IgM- activate complement IgA- mucosal immunity IgE-mast cell and eosinophil activation Class switching - Answer Antigens cause production of different class of antibodies (bcell)
Affinity maturation - Answer Helper T cells cause production of high affinity antibodies Cell mediated Immunity - Answer 1)Dendritic cells transport antigen to lymph, expressMHC II
- naive T cell recognize, proliferate, and differentiate into effector and memory cells.3) T cell enter circulation
- T cell migration to site5)CD4 - activate phagocyte/ recruit leukocyte CD8 - kill intracellular pathogens Atopy - Answer increased susceptibility to develop immediate hypersensitivity reaction Antibody functions - Answer 1) Enhance phagocytosis by: Neutralize virus/bacteria,agglutinate (clump) microbes, precipitate dissolved antigens 2)Cell lysis: activation of complement IgG Immunoglobulins - Answer most abundant, late immune response, can betransported across placenta
IgM Immunoglobulins - Answer predominates in primary immune response, strongcomplement relation
IgA Immunoglobulins - Answer abundant in mucosal secretions (saliva, bile) IgE Immunoglobulins - Answer protect against parasites. RESPONSIBLE FOR ALLERGICREACTIONS
Hypersensitivity Type I Immediate (first hour) - Answer Mast cell coated in IgE
Requirements: Specific immune reaction to self antigen or self tissue, Primarypathologic cause, and Lack of other pathological cause. Can be organ specific (DM I) or Systemic (SLE) Immunologic Toleranc - Answer Unresponsiveness to antigen even though lymphocytesare exposed to the antigen
Central Tolerance - Answer In central lymphoid tissue -bone marrow/thymus. Immaturelymphocyte may encounter self antigen and either perform apoptosis, B cell change receptor specificity, or regulatory T cell development Peripheral Tolerance - Answer Tolerance in peripheral tissue where maturelymphocytes may be inactivated, deleted, suppressed by regulatory T cells, or ANERGY -functionally unresponsive due to lack of co-stimulation Genetic Mechanism of Autoimmunity - Answer Mutation causing self tolerance failure.HLA genes have greatest contribution
Environmental factors of autoimmune disease - Answer Infections, injury, inflammationcauses entry of lymphocytes to tissue, activation of self-reactive lymphocytes, and tissue damage. Usually a chronic disease process Difference between tolerance and activation: LOCATION - Answer Self antigens ingenerative organs induce tolerance
Microbial antigens accumulate in blood and peripheral lymphoid organs Difference between tolerance and activation : COSTIMULATION - Answer Withoutcostimulation self antigens are subject to all mechanisms of tolerance
Microbes have costimulators that promote lymphocyte survival and activation
Difference between tolerance and activation: DURATION OF ANTIGEN EXPOSURE -Answer Self antigens are long lived and may induce TCR anergy and apoptosis
Foreign antigens have short exposure reflected by effective immune response Systemic Lupus Erythematosus (SLE) - Answer Systemic autoimmune disorder (Type III)with autoantibodies (Antinuclear Antibodies "ANAs") that bind to DNA, RNA, and proteins. immune complex deposition leads to tissue injury Smith (Sm) Antigen - Answer Antigen used in diagnosis of SLE SLE Etiology - Answer HLA gene, defective elimination of self reactive B cells anddefective peripheral tolerance, and UV light induced inflammation causing damage to DNA Pathogenesis of SLE (Environmental) - Answer External trigger causes cell apoptosis,large amount of antigen formed due to inadequate clearing - APC activates B cell inducing persistent high level antinuclear IgG production Pathogensis of SLE (Genetic) - Answer Mutation causing survival of self reactivelymphocytes - produce lots of IgG ANAs
Clinical features of SLE - Answer Vary, Butterfly rash is big, hematologic symptoms,arthritis, fever, fatuige
Autograft - Answer Transplantation of tissue from one site to another site on the sameindividual
Isograft - Answer Transplantation between 2 genetically identical individuals twins
