Path Flashcards

Question

fibroblasts

Answer 1

primary and most abundant cell in connective tissues; spindle shaped but only nucleus = seen in stains --> oval shaped, finely granulated chromatin w/ 1-2 prominent nucleoli; responsible for fibers, glycoprotein and proteoglycan components of matrix

Answer 2

material that fills space b/w cells --> bulk of connective tissue mass. 1) ground substance - amorphous (w/o shape) material varying consistency from fluid to semisolid, sometimes solid in specialized connective tissue (ex: proteoglycans - large sugar/carb molec w/ some protein and lots of sulfate --> attracts H2O into matrix; nonfibrous glycoproteins - contain short branching carb chains attached to a protein --> mediate interaction b/w cells and extracellular matrix), and 2) fibers

Answer 3

all = glycoproteins made and secreted by fibroblasts. collagen - fam of 27+ diff proteins made into triple helical structure to produce collagenous fibers, provide tensile strength --> bind structures together w/in body; synthesis complex (both intra/extracellular steps) vs reticular fibers (Type III collagen) - fine branching fibers forming loose mesh --> provides scaffolding to support other cells and structure of certain organs, component of reticular lamina, requires special stain w/ silver impregnation, does scars vs elastic fibers - allows tissue to recoil after stretching, can be cross linked to form sheets or filaments, requires special stain w/ aldehyde fuschin or neg img w/ H&E stain if big enough, made and secreted by smooth muscle cells

Answer 4

bone, blood, cartilage

Answer 5

mesenchyme - progenitor of all other connective tissue, mucous tissue - similar to mesenchyme except small collagen fibers = present vs packing, anchoring and/or embedding material in almost every organ of the body; contains typical components of connective tissue w/ matrix made of fluid-like ground substance w/ random collagen and elastic fibers; can replace other tissues physically after injury --> fibrosis, keloids, scleroderma vs branching network or reticular fibers that form framework of certain organs; fibers secreted by reticulocytes but other functional cells suspended w/in meshwork vs made of lipid storing cells called adipocytes embedded w/in reticular framework; the only connective tissue lacking matrix; always found in loose connective tissue except nervous system, lungs, eyelid, ears, penis, dorsum of hand; energy storage, thermal insulation and shock absorption; have 2 types: unilocular and multilocular; can be stained w/ Sudan stains or osmium tetroxide vs great abundance of large collagen fibers arranged randomly; contains few elastic an reticular fibers w/ very little matrix; forms tough fibrous sheets vs densely packed fibers running parallel to e/o

Answer 6

yellow fat, lipids stored in 1 large vacuole that occupies majority of cell --> nucleus is pushed to the edge and cell has little cyto, more common in adults vs brown fat, lipids stored in small mult vacuoles --> cyto has FROTHY appearance, more common in babies, help w/ heat production since mito lacks ATPse and all energy production from Kreb's cycle = lost as heat

Answer 7

structural abnmllity responsible for ill health. gross lesion - you see w/ eyes, can make dx vs microscopic lesion - looking under microscope vs ultrastructural lesion - look under e- microscope vs molecular lesion - looking at molec level (DNA, protein)

Answer 8

objective evidence of dz by examining physician vs subjective evidence of dz by pt

Answer 9

congenital anomalies - occur before birth, happen in womb vs hereditary dzs - DNA abnmlities inherited from parent --> fhx vs inflamm dzs - immune system attacks own tissue (ex: graft rejection) vs degenerative dzs - tissue degenerates overtime (ex: arthritis) vs neoplastic dzs - ca, abnl growth

Answer 10

investigation and dx of dz from examining tissue; perform autopsies, microscopic exam of surgical biopsies, examine cytopath and hematology smear. surgical path, cytopath, forensic

Answer 11

study of tissue removed from living pts during surgery to dx dz, does bx's vs studies and dx dz on cellular level, does cell collection vs does autopsies and frozen sections

Answer 12

removing sample tissue from body of living pt. entire mass/suspicious area (including surround skin) = removed vs portion of lesion = removed --> purely diagnostic --> have to f/u and remove the rest later prn vs endoscope = used to visually examine interior of canal or organ and remove tissue w/ forceps vs small cylindrical tube of tissue = removed, similar to incisional bx b/c you remove portion of it, seen in derm vs surgical/razor blade shaves lesion on epidermis or upper dermis, mostly seen in derm. removal of tissue en masse, often after bx confirming a dx

Answer 13

cells shed spontaneously an collected in cytology specimen, specimen on glass slide => smear (ex: thoracentesis, paracentesis) vs cells manually scraped/brushed off surface of body (ex: pap smear) vs intervening into body to collect samples (ex: Fine Needle Aspiration - tissue sample = removed w/ thin hollow needle, US guided)

Answer 14

examining organs of dead body. pt dies in hosp from terminal illness, dz, or age; NOT suspicious of criminal background, performed w/ permission from deceased's relatives, identify dz/problem related to pt's death that may have been unresolved during hosp stay vs determine cause of death and/or collect evidence that may be used in prosecution; basically find cause and manner of death (ex: cause = GSW, manner = natural, artificial, suicide, homicide, undetermined)

Answer 15

1. examine docs (chart review) 2. examine external body 3. examine internal body (Y shaped incision, peel skin from chest wall, open rib cage and remove chest plate, remove thoracic and abd organs in 1 block => Rokitansky method, organs sampled for microscopic exam, organs = returned and body = reconstructed)

Answer 16

autopsy exam = limited to certain areas of body, can be requested by fam; not done for criminal cases

Answer 17

type of tissue processing; surgeon does procedure and wants immediate eval --> calls pathologist to take tissue and make dx in 20min

Answer 18

study and dx of dz from chemical change in tissues and fluids. clinical chemistry, hematopath, clinical microbio, blood banking - transfusion medicine, molecular (genetic) path

Answer 19

measure conc of substances like sugars, lipids, proteins, ab, enzymes, hormones, electrolytes; automated vs study dz and d/o w/in blood cells and organs involved w/ hematopoiesis like peripheral blood smears, flow cytometry, immunohistochemistry vs identify organisms responsible for infection vs store and maintain blood and blood products to be transfused, type & crossmatch blood products vs isolate DNA or RNA from pts' blood or tissue samples to dx dz and predict course of illness

Answer 20

etiology (causes), pathogenesis (mechanisms), morphology (structural change), functional change (clinical significance), clinical manifestations (s/s), clinical course - acute/subacute/chronic, complications

Answer 21

inherited medical condition caused by DNA abnllity (ex: sickle cell anemia, CF) vs physical (burns), chemical (lead, mercury, arsenic), nutritional (deficiency, obesity, malnutrition), infectious (strep, TB), immunological (hay fever)

Answer 22

something that inc risk or susceptibility to dz vs dz w/ unknown cause; also called idiopathic, essential, or cryptogenic

Answer 23

inadequate oxygenation of tissues; most common cause of cell injury; can be generalized or localized. healthy individuals do anaerobic glycolysis --> activated 100x more rapidly, less efficient than [O] phosphorylation --> makes 2 ATP

Answer 24

lung-related hypoxia, hgb-related hypoxia, circulatory hypoxia, histotoxic hypoxia, tissues susceptible to hypoxia

Answer 25

ventilation effects: impaired O2 delivery to alveoli (atelectasis, pna), perfusion defects: absence of blood flow to alveoli (air going in but no O2 exchange), diffusion effects: dec O2 diffusion thru alveolar capillary membrane (ex: pulm edema, pulm interstitial fibrosis), right-to-left shunt: blood shunts from R to L side of circ (ex: tetralogy of Fallot, cyanosis)

Answer 26

anemia: dec # in RBC and [hgb], PaO2 and SaO2 = still nml. methemoglobinemia: ferric iron instead of ferrous iron, doesn't bind O2 --> can't deliver O2 to tissues --> cyanosis, PaO2 = still nml but SaO2 = dec; caused by benzocaine and lidocaine (topical anesthetics) exposure. CO intoxication from housefire or suicide: CO has 250x more affinity for hgb --> carboxyhemoglobin (HbCO) --> bright red color; coma, incontinence, sz, death; CT shows globus pallidus and nucleus caudatus of basal ganglia

Answer 27

blood flow compromised --> can't deliver O2 to tissues; caused by L heart failure from dyspnea, cyanosis, pulm edema or paroxysmal nocturnal dyspnea, or shock by persistent hypotension w/ reduced perfusion of organs and inadequate O2 in tissues;

Answer 28

inactivation of cytochrome C oxidase (complex IV in ETC) d/t binding of cyanide --> pink skin color; causes coma w/ sz, apnea, cardiac arrest. uncoupling of oxidative phosphorylation; uncouplers prevent using chemical energy from mito e- transport to make ADP to ATP, they don't inhibit ETC or ATP synthase; natural coupler = thermogenin in brown adipose tissue, synthetic coupler = 2,4-dinitrophenol (DNP) as insecticide

Answer 29

brain neurons die in 8min, cardiac myocytes die in 30-40min, kidney and liver epithelial cell die in 90-120min; watershed area b/w 2 blood supplies (are b/w anterior and middle cerebral arteries), subendocardial tissue, renal cortex and medulla

Answer 30

aka ischemia; most common cause of hypoxia; caused by arterial obstruction by thrombi or emboli --> interrupts blood flow/insufficient blood supply --> ischemic necrosis (infarct) of organ/tissue supplied by that blood vessel --> lost supply of O2, supply of substrates for metabolic and synthetic processes and removal of waste prod

Answer 31

absence of O2: loss of [O] phosphorylation --> anaerobic glycolysis = main energy source. depletion of glycogen and ATP: loss of cell fxn, accumulation of lactic acid and H+ => acidosis, Na-K pump fails, dispersion of cytoskeleton, cell swelling. These are all reversible if O2 = restored vs ischemia in myocardium: dmg to plasma membrane, mito swelling, large amorphous densities in mito matrix. calcium: loss of ATP --> no active extrusion of Ca2+ from cell, no sequestration of intracellular Ca+ in ER and mito --> rapid influx of Ca2+ in cell --> cell loses viability

Answer 32

lysosomes digest own cell (autolysis), and denaturation of dead cell protein --> dead tissue becomes firmer and pale 24hrs post ischemia; as cell = dying, cyto becomes hypereosinophilic (more pink), nuclear changes appear in karyopyknosis (smaller nucleus), karyorrhexis (nuclear fragments/dust), or karyolysis (dissolution of nucleus --> no longer visible) vs programmed, enzyme-mediated cell death, basically cell suicide; process = divided into 2 phases (initiation phase (to start) and execution phase (to do/die))

Answer 33

outline of dead cell = preserved, caused by ischemia --> denaturation of intracellular enzymes and structural proteins; firm in texture, cells show cytoplasmic hypereosinophilia and absent nuclei; ex: myocardium, kidney and spleen vs hydrolytic/lysosomal enzymes from necrotic cells or neutrophils dissolve cells --> dead tissue softens and liquifies; ex: abscess, infarct of brain or spinal cord, pancreatic infxn vs release of lipids from cell walls of mycobacterium tuberculosis or fungi after destruction by macs --> cheese like caseous material; yellowish-white, soft, granular like dry cheese, cells show amorphous, eosinophilic, granular focus in center of granuloma vs enzymatic fat necrosis: pancreatic enzyme lipase hydrolyzes TAG to produce free FA --> FA combine w/ Ca2+ to make soaps => saponification; grossly visible white chalky deposits in adipose, fat cells show pale outline filled w/ basophilic-staining calcified areas; trauma fat necrosis: physical injury --> dmg to adipocytes --> release of TAG and hydrolysis by lipase vs accumulation of homogenous fibrin-looking acellular material d/t dmged basement membranes in HTN or vasculitis; injured blood vessels like arterioles/venules/capillaries, cells show vessel walls really stained w/ eosin vs dry: dead tissue not removed b/c leuks can't reach site --> dessicated --> black tissue --> pt can't go to sepsis and die; wet: when dry gangrene = infected --> pt can go to sepsis and die

Answer 34

hypoxia, infarction, ischemia

Answer 35

1. cell shrink and cyto becomes dense 2. chromatin becomes dense mass against nuclear membrane 3. nucleus breaks up into round fragments 4. cell emits protrusions that break off small round apoptotic bodies 5. macs phagocytize apoptotic bodies

Answer 36

death receptor-mediated pathway: extracellular signals like toxins, hormones, growth factors and cytokines bind to death receptors of TNF receptor fam; ex: FAS ligand binds to FAS receptor --> trimeriztion of Fas receptor --> clustering of death domains --> FADD binds to trimerized domain --> FADD+domain binds to procaspase 8 or 10 --> become caspase 8 or 10 --> activate executioner caspases vs mito pathway: DNA dmg, free radical dmg, hypoxia, misfolding, growth factor deprivation --> trigger antiapoptic Bcl-2 proteins to dimerize and fxn, proapoptic Bcl-2 proteins to dimerize or fxn, or sensors (they promote proapoptic Bcl-2 proteins and suppress antiapoptic Bcl-2 proteins (they stop apop by binding and sequestering proapop proteins)); p53 induces apop by interacting w/ proapop Bcl-2 fam members - Bak and Bax; oligomerized Bak and Bax form a channel => mitochondrial apoptosis-induced channel --> release cytochrome C from intermembrane space to cytosol --> cytochrome C binds to Apaf-1 --> formation of apoptosome (consists of 7 Apaf-1 and 7 cyto C) --> activate procaspase 9 --> become caspase 9 --> activate executioner caspases

Answer 37

BH1-4 vs BH1-3 vs BH3

Answer 38

enzymes that play a role in apop; start as procaspase that later become active caspase via proteolysis prn; initiator caspases: 8, 10 for extrinsic and 9 for intrinsic; executioner caspases: 3, 6, 7

Answer 39

executioner caspases (primarily 3) cleaves nuclear lamin, DNA fragmentation, chromatin margination and nuclear collapse; generally these caspases target proteins for controlled proteolysis --> prevents immunostimulatory molec and minimize disruption of neighboring cells

Answer 40

ca, autoimmune dz, virus vs AIDS, neurogenerative d/o, myelodysplastic syndromes, ischemic injury, toxin-induced liver dz

Answer 41

Tdt-dependent UTP biotin nick end labeling: staining method that allows recognition of apoptotic nuclei in tissue sections; broken DNA ends in nucleus of apoptotic cells = visualized by horseradish peroxidase --> enzyme Tdt (terminal deoxynucleotid transferase) binds and adds biotinylated nucleotide to broken DNA --> biotin labels nucleic acid broken ends --> horseradish peroxidase binds to biotin --> visible in light microscopy

Answer 42

any species that contains single/unpaired valence e- in outermost orbital --> unstable --> highly reactive. superoxide radical (O2.), hydroxyl radical (OH.), H2O2, hypochlorous acid (HOCl); there are 2 major free radical groups: oxygen-free radicals and nitrogen-free radicals

Answer 43

when 1 e- = added to diatomic O2, primary reactive O2 species that interacts w/ secondary ROS, produced in mito, Haber-Weiss rxn: H2O2 + O2. --> O2 + OH. + OH- vs very reactive; Fenton rxn: Fe2+ + H2O2 --> Fe3+ + OH.; UV radiation splits H2O2 into OH. --> aging; ionizing radiation: gamma radiation splits H2O into OH. --> dmg protein and DNA, trigger lipid peroxidation vs involved in free radical theory of aging; peroxisomes produce H2O2 for phagocytosis (neutrophils and macs use H2O2 kill phagocytosed bacteria) vs produced by myeloperoxidase (MPO) of azurophilic granules of neutrophils to kill bacteria

Answer 44

8-oxoguanine: mimics thymine --> binds to adenine --> transversion mutation; OH. and peroxynitrite attacks DNA; lipid peroxidation targets cell membranes: lipid radical --> lipid peroxyl radical --> lipid hydroperoxide --> unstable and yields isoprostanes (IP), malondialdehyde (MDA) and 4-hydroxy-2-nonenal (HNE) --> cell membranes lose integrity; 3-nitrotyrosine = bio marker for peroxynitrite

Answer 45

nitrous oxide (NO) + O2. --> ONOO.; powerful reactive radical --> cytotoxicity; reacts w/ lipids (lipid peroxidation), DNA (fragmentation), proteins (convert to 3-nitrotyrosine, which is a biomarker for peroxynitrite --> loss of protein fxn d/t enzyme inactivation)

Answer 46

catalyze dismutation of superoxides: O2. + O2. --> O2 + H2O2; SOD1 has Cu prosthetic group (so if you're Cu-deficient --> dec SOD), in cyto; SOD2 has Mn, in mito; SOD3 has Zn, 3 in extracellular vs 2H2O2 --> O2 + 2H2O vs 2H2O2 + 2GSH --> 2H2O + GSSG; GPx1 removes H2O2 from mito and ER to cyto, GPx4 removes lipid peroxides; GPx contains Se in active site vs scavenges superoxide, hydroxyl radical, and peroxynitrite --> stops lipid peroxidation vs majorly stops lipid peroxidation

Answer 47

acute radiation syndrome, carbon tetrachloride intox, acetaminophen intox, ischemia/reperfusion injury vs hereditary hemochromatosis and Wilson dz

Answer 48

complex bio response of vascularize tissues to harmful stimuli like pathogens, dmged cells, irritants. acute inflamm - early short response by body, mainly neutrophils; chronic inflamm - occurs after delay, longer response, mainly mono/macs and lymphocytes

Answer 49

non specific response of vascularized tissue injury. infxn, physical trauma, chemical trauma. redness, heat, swelling, pain, loss of fxn

Answer 50

injury --> vasodilation --> inc permeability --> exudate leakage --> margination, rolling, adhesion --> transmigration/diapedesis --> chemotaxis --> neutrophil activation --> phagocytosis --> termination of inflamm response --> resolution or scar or chronic inflamm

Answer 51

initial vasoconstriction: stop spread of injury, transitory & reflexive, lasts up to 30s; gradual vasodilation of arterioles and capillaries: relaxation of reflexive spasm, CAUSED BY HISTAMINE, causes bleeding to start (d/t inc blood flow); vasodilation: causes endothelial gap --> permeability changes, slowing of blood flow --> hemostasis, EXUDATE LEAKAGE (MOSTLY HIGH PROTEIN CONTENT AND CELLULAR DEBRIS); permeability changes: from inflamm chemical, occur in capillaries & small venules, junctions b/w epithelial cells loosen, fluid leak --> deliver necessary proteins to injury site and facilitate margination vs mast cells: already present in connective tissue, RELEASE HISTMINE AND HEPARIN, dmg to connective tissue leads to activation & degranulation; circulating leuks: neutrophils - arrive min post-injury, phagocytose bacteria, release chemical mediators, mono/mac - ARRIVE 24-48HRS POST INJURY, phagocytose and release chemical mediators & cytokines, remove dead tissue debris, basophils - release anti-coagulants

Answer 52

margination: leuks line vascular wall rolling: mediated by L selectins and Sialyl-Lexis X on leuks binding to E and P selectins on endothelium adhesion: tight adhesion = mediated by integrin family (LFA-1) on leuks binding to ligand ICAM-1 on endothelium diapedesis: leuks emigrate across endothelium from circ chemotaxis: leuks move toward chemotactic stimulus

Answer 53

cells (phagocytes = neutrophils and mono/mac) engulf and elim solid particles; degranulation and oxidative burst destroy engulfed particles. 1. recognition and attachment - opsonization (C3b, Fc fragment, IgG), 2. engulfment - phagocytic vacuole formation, 3. killing and degradation/digestion - ROS, lysozymes/lactoferrin/defensin, major basic proteins, nitric oxide

Answer 54

triggered by offending stimuli to: produce eicosanoids (prostaglandin, thromboxanes, leukotrienes, lipoxins), undergo degranulation (ROS, proteolytic enzymes), secrete proinflamm cytokines (chemokines, colon stimulating factor, TNF-alpha, INF, interleukins)

Answer 55

from plasma or cells in response to injury/triggering stimulus; short-lived. histamine - from mast cells, causes vasodilation and inc vascular permeability; seratonin - in GI tract/mast cells/PLTs, causes vasodilation and smooth muscle contraction; bradykinins - in liver/blood; inc vascular permeability and pain (activate prostaglandins); prostaglandins - released from phospholipids for pain/fever/clotting, target of NSAIDS & steroids; complement - in liver/blood; opsonization, direct target killing, vasodilation; free radicals - released from endothelium (ex: NO2), causes vasodilation; PLT activating factor - phospholipid released from many cells, activates clotting; lysosomes - digestive enzyme breaking down ingested particles inside phagocytes

Answer 56

proteins involved in acute inflamm; produced primarily by liver and released in response to neutrophil and mac products like IL1, 6, 8; fxn: inc body temp and bp, dec appetite, cause somnolence (sleepiness)

Answer 57

C-reactive protein - opsonin binds to phophocholine on surface of dead cells and bacteria --> activate complement and enhance phagocytosis by mac. Haptoglobin (Hp) - binds free hgb released from RBC. Serum amyloid A (SAA) - recruit immune cells to inflamm sites; transport cholesterol to liver for secretion into bile. Fibrinogen - forms fibrin for blood clot, traps invading microbe in blood clot, cause chemotaxis. Albumin - main protein of plasma; regulates oncotic pressure of blood compartment; carriers for hydrophobic molec like free FA, lipid soluble hormones, and bile salts; saves aa for producing "pos" acute-phase proteins. Transferrin - iron-binding plasma glycoproteins controlling lvl of free Fe in biological fluid; sequesters iron complexes from bacteria depriving them of growth. Transthyretin - serum carrier of thyroid hormone thyroxine (T4); releases free T4 in plasma as anti-inflamm self defense mechanism; saves aa for producing "pos" acute-phase proteins

Answer 58

simple, inexpensive, nonspecific lab test --> screening test NOT diagnostic. anticoagulated whole blood stands in narrow vertical tub --> erythrocytes settle out from plasma d/t gravity --> plasma at top, RBC at bottom --> measure by mL of clear plasma/1hr. fibrinogen has high affiity for RBC membrane --> RBC form stacks => Rouleaux (assoc w/ mult myeloma) --> sink faster --> sediment more rapidly; inc fibrinogen --> inc ESR

Answer 59

neutrophilia = neutrophils inc (bacterial), lymphocytosis = lymphocytes inc (viral), monocytosis = mono inc (TB, syphillis), eosinophilia = eosinophils inc (asthma, allergies, parasites), leukopenia = dec WBCs (typhoid fever, some viral, rickettsiae, protozoa, ca, alcoholism, rampant TB)

Answer 60

"bands" = immature neutrophils w/ band shaped nuclei (not like multi lobed nuclei found in mature neutrophils); inc bands d/t bacterial infxn --> "left shift" b/c %age of bands = reported on L side of blood chart --> bone marrow = making neutrophils at inc pace; greater shift to L --> more severe infxn; L side = immature side

Answer 61

proteins produced by immune cells, support cells, endothelial cells; does autocrine, paracrine, endocrine communcation (know defs); ex: interleukins - produced by WBC to affect behavior of other WBC, interferons - produced by WBC to interfere w/ replication and spread of infectious agents, chemokines - cytokines involved in chemotaxis, growth factors - proteins stimulating cell growth. TNF and IL-1

Answer 62

DILATION OF SM BLOOD VESSELS AND ACCUMULATION OF LEUKS AND FLUID IN EXTRAVASCULAR TISSUE. serous - watery (plasma), exudation of cell poor fluid in to spaces created by cell injury, ex: skin blisters (fluid accumulated under dmged epidermis); fibrinous - hemorrhagic, rich in fibrin, develops when vascular leaks = large or local procoagulant stimulus, fibrinous pericarditis (fibrin deposited in pericardium); suppurative - pus (dying neutrophils), abscess = localized collection of pus, ex: bacterial abscesses in the lung; ulcerative - dmg below basement membrane, local defect/excavation of surface of organ/tissue produced by sloughing of inflamed necrotic tissue, ex: duodenal ulcer

Answer 63

resolution - if little to no dmg --> inflamm resolves, return of fxn. repair and regeneration (replacement w/ same kind of tissue) - if sig dmg --> labile regeneration (fully regenerates like epithelium), stable regeneration (partially regenerates like bone), or permanent (does not regenerate like muscle)

Answer 64

forming granulation tissue (fibrous connective tissue + vessels). neovascularization - capillary budding results from mitogens, fibroplasia - mesh framework for scar development (type III collagen = laid down RANDOMLY --> not strong --> later manipulated in remodeling process to be more organized w/ type I collagen), mature scars not as strong as orig healthy tissue

Answer 65

complete recovery, sequelae (consequence from prev dz), recurrence, remission, death

Answer 66

respiratory/oxidative burst generates reactive oxygen species (i.e., superoxide anion) that are important in destruction of engulfed bacteria

Answer 67

1. heart dz 2. ca 3. covid in USA