Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

153 Cards in this Set

  • Front
  • Back
Squamous Metaplasia
Bronchial epithelium of a smoker from columnar to squamous.
Glandular Metaplasia
(Barrett Oesophagus); squamous epithelium of oesophagus goes to columnar due to reflux.
Disordered cell growth; a step towards malignancy.
1.) pleomorphism
2.) Enlarged, hyperchromic, irregular nuclei.
3.) Disordered arrangement/maturation.
Squamous Metaplasia
Bronchial epithelium of a smoker from columnar to squamous.
Glandular Metaplasia
(Barrett Oesophagus); squamous epithelium of oesophagus goes to columnar due to reflux.
Disordered cell growth; a step towards malignancy.
1.) pleomorphism
2.) Enlarged, hyperchromic, irregular nuclei.
3.) Disordered arrangement/maturation.
Mallory bodies
Protein accumulations of cytokeratin filaments in hepatocytes.
Russell Bodies
Protein accumulation of Ig in plasma cells.
α1-antitrypsin (abnormal type)
Protein accumulation; a "permanently misfolded" protein that gets sequestered and accumulates in hepatocytes. Normally an acute phase reactant protease inhibitor.
pigment accumulation; sign of cell "wear and tear", from peroxidation of mem. lipids. Stains darkly with haematoxylin.
Pigment accumulation: aggregates of ferritin micelles due to ↑absorption, ↓usage, or ↑RBC degradation.
Prussian Blue
A stain that turns iron blue, used for visualising iron pigment accumulation in tissue slides.
Congo Red
A stain that distinguishes amyloid (pos.) from other hyaline substances like collagen and fibrin.
Marker for melanomas, 50% of malignant peripheral nerve sheath tumors, and clear cell sarcomas
Reperfusion Injury
Reoxygenation after ischemia may cause O2 free radicals, influx of neutrophils (who produce lytic enzymes and O2 free radicals). Causes lipid peroxidation of mems, modification of proteins, and DNA damage.
Reversible Injury
Hallmarks: hydropic change (influx of water), fatty change, ultrastructural alterations.
Coagulative Necrosis
Usu. caused by ischemic damage.

Denaturation > digestion; basic cell outline preserved as cell ghost.
Cytoplasm: ↑eosinophilia
Nucleus: pyknosis (shrinkage, ↑basophilia), karyorrhexis (fragmentation), karyolysis (loss of sustainable nuclear material).
Ex: MI, Kidney infarct
Liquefactive Necrosis
Enzymatic digestion > denaturation
Cells → viscous fluid.
Ex: Bacterial infxn abscess, brain infarct
Caseous Necrosis
Yellow-white, "cheesy" friable granular mass. Amorphous, eosinophilic, no cell outlines. Loss of tissue architecture. Epithelioid macs surround necrotic region. Multinucleated Giant cells may be present. A cell-mediated hypersensitivity.

Ex.: TB, histoplasmosis (fungal)
Fat Necrosis
Lipases (from pancreas) released into abdominal cavity, releasing FAs from adipose. Causes saponification (FA combine with Ca2+).

Gross: Chalky white
Hist: necrotic fat cells.

Ex.: Pancreatitis, traumatic injury to adipose tissue.
Apoptotic Bodies
Pieces of an apoptotic cell that break off, containing organelles and other components. Express new ligands for binding and uptake by phagocytes.
Pro-apoptotic Factors
Bax, Bak, Bad, Bik
Anti-apoptotic Factors
Bcl-2, Bcl-XL, A1
Creatine Kinase MB
An isoform of CK that's enriched in the cardiac myocyte mems. Presence in serum diagnostic of damage.
Tissue Plasminogen Activator
Clot-dissolving factor made by endothelial cells; levels highest in afternoons, lowest in the mornings (MIs likely), due to levels of inhibitor.
Advanced Glycosylation End-Products (AGEs)
A type of cumulative damage related to aging. Nonenzymatic glycosylation of proteins leads to AGEs that X-link cellular proteins (Maillard/Browning Rxn), occurs more freq. when [glucose] is high.
Retinoic Acid
Inhibits AP1, a TF that activates collagenases/elastases that degrade dermal matrix. AP1 is activated by UVB rays.
mouse gene encoding a secreted β-glucosidase. Mice with homozygous deletion of this gene display progeria.
"I'm not dead yet"; fruit fly Kreb cycle intermediate transporter gene. Heterozygous loss of fxn doubles lifespan by ↓g met?
Fruit fly gene for G-protein coupled transporter. Loss of this gene ↑s resistance to oxidative stress, and lifespan by 35%.
Yeast gene; heterozygous loss of fxn ↓s lifespan by 60%
Cellular senescence
Mortality of human cells; can divide ~50x max. Mediated by P53, which recognises exhaustion of telomere supply. Senescence is dominant and requires the nucleus.
Crisis (in cell aging)
When a cell runs out of telomeres, chr.s become unstable. Ultimately the cell stops dividing.
histamin, bradykinin
Chemical mediators in acute inflammation that cause contraction of endothelial cells, creating gaps and ↑g perm.
IL-1, TNF, INF-γ
Cytokines that reorganise cytoskeleton to produce endothelial gaps during inflammation.
Vascular Endothelial Growth Factor (VEGF)
Causes ↑'d transcytosis across endothelial cells during inflammation by putting in channels. Also ↑angiogenesis, endothelial cell prolf.
Leukocyte Extravasation
1.) Margination
2.) Rolling (selectins)
3.) Adhesion (Integrins; LFA-1, MAC-1)
4.) Transmigration (diapedesis): PECAM-1
5.) Interstitial Migration (chemotaxis): C5a, leukotriene B4, IL-8
Enzyme that makes H2O2 into reactive halide to kill bacteria in phagosomes.
Fever cytokines
Plasma proteases
1.) complement system
2.) kinin sys
3.) coagulation sys
4.) Fibrinolytic sys
Zeta Potential
Negative charge of RBCs that is ↓'d by fibrinogen, γ-globulins etc., facilitating the formation of rouleaux, which sediment faster than monodisperse RBCs.
Erythrocyte Sedimentation Rate (ESR)
Measure distance RBCs sediment in a fixed time period (mm/hr). ↑'d sed rate is nonspecific evidence for inflammation.
C-Reactive Protein (CRP)
an opsonisation factor made rapidly by liver in response to inflammation; nonspecific lab marker, esp. of atherosclerosis.

CRP causes flocculation (precipitation) when mixed with capsular polysaccharide of pneumococci.
Serum Protein Electrophoresis (SPEP)
Method used to measure changes in conc. of acute phase reactants and Igs to determine severity of inflammation or presence of "gammopathy".
Acute Phase Reactants
CRP: Oponsonisation (↑s 100-500x with inflammation)
Fibrinogen: coagulation
α1-antitrypsin: protease inhibitor
hatpoglobulin: binds Hb, forming biliverdin (eventually biliruibin)
C3: complement
Ceruloplasmin: binds copper
α2-macroglobulin: protease inhibitor
Trichrome Stain
Stains collagen blue; diagnostic of inflammatory ECM deposition due to fibroblast proliferation.
Histamine and Serotonin
Acute Inflam. mediators
Source: Histamine: mast cells, platelets. Serotonin: platelets.
Effect: ↑vascular leakage.
Acute Inflam. mediators
Source: plasma substrate
Effect: ↑vascular leakage, pain!
Acute Inflam. mediators
Source: plasma protein via liver
Effect: ↑vascular leakage, C3b is opsonic.
Acute Inflam. mediators
Source: Macs
Effect: ↑vascular leakage, chemotaxis of neutrophils.
Acute Inflam. mediators
Source: Mast cells, mem. phospholipids.
Effect: potentiates other mediators; vasolidation, pain, fever.
Leukotriene B4
Acute Inflam. mediators
Source: Leukocytes
Effect: Neutrophil chemotaxis.
Granulation Tissue
On the 3rd day of healing, this tissue begins to form in wound space. Pink, soft, granular, mixture of BVs and fibroblasts laying down collagen in haphazard fashion (not parallel).
Collagen Fibrils
On day 5 of wound healing, fibrils begin to bridge the wound.
Fresh granulation: type III
Day 7-8: Type I collagen
2-3 months: Max accumulation
Evenutally fibres are reoriented along lines of stress.
Collagenous Scar
By year 1 of wound healing, collagen has been re-organised into parallel strands, and the scar is hypovascular, hypocellular.
Wound Contraction
Feature of secondary union/intention of large, contaminated wounds. Mediated by myofibroblasts. Contraction starts 5 days post-injury.
Labile Cells
Continuously dividing tissue with stem cells; most capable of repair. Include epidermis, bone marrow, lymphoid tissue, and GI mucosa.
Quiescent/Stable cells
Little, if any replicative activity, but has potential to divide if stimulated. Include: hepatocytes, renal tubular epithelium, endocrine cells, endothelium, CT, bone, sm mm.
Permanent Cells
Cannto divide; if cell dies, it is replaced by CT. Ex: neurones, cardiac myocytes, sk mm. (Caveat: portion of the cell may regenerate).
Type I collagen
Most abundant form; found in bone, skin, tendon, fascia, and mature scars. Fibrillar
Type II collagen
Found in cartilage, nucleus pulposus, and vitreous body. Fibrillar
Type III collagen
Abundant in pliable organs such as BVs, uterus, GI tract, skin. Important in early wound healing. Fibrillar.
Type IV collagen
Found in BMs. Forms sheets.
Elastic Fibres
Very long half-life, provide recoil to tissue. Contains elastin and fibrillin, found in BVs, skin, lung, uterus (cf. Type III collage).
Glycoprotei that binds other macromolecutes. Involved in migration, adhesion, stabilisation of early wound, opsonisation, chemotaxis (macs/fibroblasts)
Glycosaminoglycan bound covalently to proteins; like a sponge. Involved in ECM organisation.
Basement Membrane
Seperates cell from stroma, composed of Type IV collage, heparan sulfate proteoglycan, and Laminin.
Involved in cell-cell and cell-matrix binding, inhibits angiogenesis.
Activates leukocytes, endothelium, ↑s adhesion molecules, fever. Acute phase cytokine.
Source: Macs
Effect: Angiogenesis, chemotaxis
Effect: ↑IL-1 and bFGF, chemotaxis, collagen syn.
EGF (epidermal GF)
aka TGF-α
Effect: ↑cell division, angiogeneis.
TGF-β (transforming GF)
Effect: chemotaxis of macs and fibroblasts. ↑collagen syn., inhibits prolif. of certain cells.
bFGF (basic fibroblastic GF)
Effect: ↑cell division, angiogeneis. (same as EGF)
Healing with restoration of normal structure and function, with little or no scarring. Requires stromal framework to be intact.
Healing with loss of normal sxr and fxn, with marked scarring. Usu. due to prolonged infxn/inflam., sig. necrosis, destruction of stromal framework, or injury involving permanent cells.
Hypertrophic scar
Type of a scar characterised by excessive granulation, persistant collagen arranged in nodular whorls, but flatten spontaneously over 1+ years. Nodules eventually shrink and straighten out. Tends not to recur if excised.
Scar of persistant collagen nodules that extend beyond site of original injury, and will rarely regress. Tends to recur if excised. Higher incidence in dark-pigmented individuals.
Profileration of fibroblasts in wound repair, resulting ind deposition of ECM.
assoc. with noninflammatory conditions; fluid is an acellular ultrafiltrate with low protein content and low specific gravity (<1.015)
Usu. associated with an inflammatory condition. Fluid has lots of cells and cellular debris, high protein content, and high specific gravity (>1.015)
Active Hyperaemia
↑'d volume of blood in tissue due to BV (arteriolar) dilation, mediatedy by neurogenic or chemical stimulation. Blood is more oxygenated than passive hyperaemia due to ↑'d inflow of blood.
Passive Hyperaemia
Congestion caused by impaired venous drainage and backing up of blood. Systemic (CHF) or localised (thrombosis). Blood more deoxygenated. "Nutmegging" of congested liver, necrosis of central lobules. Can result in atrophy, poor wound healing.
Prostacyclin (PGI2) [↓s platelet aggregation, vasodilator) thrombomodulin (regulates thrombin), tissue factor pathway inhibitor (TFPI)
Tissue Plasminogen Activator (tPA)
Profibrinolytics that is the first line of anti-clot therapy in most hosptials.

Made by endothelial cells. Converts plasmalogen to plasmin. Potentiated by fibrin, low at nigh.
von Willebrand factor (vWf)
Procoagulant syn.'d by endothelial cells and megakaryocytes, stored in Webel-Palade Bodies (endothelial) and α-granules (platelets). Missing in classic haemophilia. high MW spp mediate platelet adhesion and factor VIII transport.
Thromboxane A2 (TXA2)
Mediates platelet aggregation. Released from platelets, whose COX-2 and PL systems cleave it from mem. phospholipids.
dense granules
found in platelets; contains ATP, ADP, serotonin, Ca2+, etc.
found in platelets; contains fibrinogen, vWf, fibronectin, etc.)
Aspirin (acetylsalicylic acid)
irreversible inhibitor of COX-2, "anti-platelet". Lasts lifetime of platelet (7-10d), prolonging bleeding time.
gpIIb/IIIa inhibitors
anti-coagulative drugs that inhibit platelet mem. glycoproteins used as RR for adhesive plasma proteins (vWf, fibrinogen). Ex.: ReoPro, Integrilin.
Intrinsic Clotting Pathway
Activated by conact with clotting factors with negatively charged "activating" surfaces. Players: XII, XI, IX, VIII, kallikrein, HMWK.
Extrinsic Pathway
Believed to be initiated by "tissue factor" liberated from damaged extravascular tissue. Players: VII
Factor XIII
Transglutaminase clotting factor of the common pathway taht stabilises fibrin by catalysing cross-linking.
Vitamin K-dependent clotting factors
II (thrombin), VII (extrinsic), IX (intrinsic), X (common), protein C, and protein S
Antithrombin (AT)
Serine Proteinase Inhibitor (SERPIN) made in liver that inhibits all clotting factors save VIIa (extrinsic).
Protein C
Made by hepatocytes (mostly) and endothelial cells. Vit-K dependent; inhibits Va and VIIIa (intrinsic+common). Half-life is 5-10hrs, cf. VII.
Protein S
Made by hepatocytes and other cells; Vit.-K depenedent cofactor of Protein C, helping to inhibit Va/VIIIa. Free form is active. Bound inactive form is complexed to C4b-binding protein, an acute phase reactant. Thus, acute inflamm. increases clotting.
Tissue Factor Pathway Inhibitor (TFPI) aka Lipoprotein-Associated Coagulation Inhibitor (LACI)
Made by endothelium, binds to and inactivates Xa, then VIIa (extrinsic+common). If VIII and IX are present though, VIIa/tissue factor complex is protected from TFPI.
Annexin V
Cell-bound protein that seems to inhibit tissue factor (extrinsic)
Warfarin (Coumadin)
Anti-coagulating drug that prevents Vitamin K from being recycled to its reduced form, rendering it unable to help carboxylate factors II, VII, IX, X, protein C, and S.
Highly sulfated linear glycosaminogglycan that binds to antithrombin, potentiating its inhibition of IIa and Xa.
Only acceptable anticoagulant for test tubes. Chelates Ca2+, preventing clot until exogenous Ca2+ is added.
Prothrombin Time (PT)
Asseses the extrinsic and common pathways (VII), can monitor Warfarin therapy.
Fibrin Degradation Product (FDP)
Pieces of cross-linked fibrin broken up after fibrinolysis. Breakup is mediated by plasmin.
Urinary-type Plaminogen Activator (aka urokinase, uPA)
Converts plasminogen into active plasmin, like tPA. Source unknown, but abundant in urine. Potentiated by fibrin.
Plasminogen Activator Inhibitor-1 (PAI-1)
SERPIN like antithrombin. Inhibits tPA, high at night. Platelets are rich source. ↑ clotting.
Inhibitor of plasmin, syn.'d by liver.
Vitamin A
Sources: green leafy vegetables, eggs, butter, meat, milk, fish liver.
Fxns: maintenence of specialised epithelia, enhance immunity, antioxidant, reg. cell growth.
Vitamin C
Sources: citrus fruits, leafy green vegetables, peppers, tomatoes.
Fxn: powerful antioxidant, free radical scavenging. Keeps ferrous iron reduced for collage hydroxylation.
Vitamin E
4 related tocopherols and tocotrienols; α-tocopherol most potent.
Sources: vegetables, grains and their oils, fish
Fxn: antioxidant
Thiamine (B1)
Source: unrefined foods.
Antithiamines: raw fish, strong tea, coffee.
Fxns: ATP syn (oxidative decarboxylation), pentose phosphate pathway (transketolase), maintence of neural mems and normal nerve conduction.
Gene that causes cancer if "turned on" by being translocated into the transcription millieu of another more active gene. Ex.: abl gene, when under transcriptional control of bcr.
mutator gene
Gene in which loss of fxn leads to genomic instability and ↑ mutations. Participates in "two-hit" mechanism. Ex. hMSH2 gene of HNPCC
tumour suppressor gene
Gene which normally prevents overproliferation. Loss of fxn causes overproliferation and ↑ mutations. Participates in two-hit mechanism. Distinction from mutator gene unclear.
Oncogene that binds GTP and participates in signal transduction. Gain-of-fxn produces protein with ↓'d intrinsic GTPase activity, thus longer GTP binding and ↑'d cellular proliferation.
Classic tumour suppressor gene that prevents cells with unrepaired DNA damage from entering S phase, and stimulates transcription of DNA repair genes. Induces apoptosis in tumours that outgrow their blood supply. Dominant negative; even one mutated allele will result in nonfunctional dimer.
dominant negative
Loss of fxn in even one allele is enough for disease phenotype. Classic example is p53.
a tissue with all the characteristics of malignancy, but has not yet metastisised. Technically not yet cancer.
Downregulation of this gene results in ↓'d cohesiveness of tumour cells.
matrix metalloproteinases (MMP)
Mediates degradation of ECM in tumour cells so they can invade.
entry of tumour cells into lymphatic or vascular vessels.
Circulating tumour cells enter distant tissue sites.
Cetuximab (Erbitux)
monoclonal Ab drug against EGFR (epidermal growth factor); some efficacy against metastatic colorectal cancer, targetting an oncogene.
Bevacizumab (Avastin)
humanised Ab against VEGF, ↓tumour-stimulated angiogenesis in colon cancer.
oncogene that is activated by amplification in neuroblastoma.
cell surface growth factor oncogene that is overexpressed in some breast/ovarian cancers
Mutator genes involved in repair of dsDNA, implicated in some familial breast/ovarian cancers.
Rb (retinoblastoma) gene
tumour suppressor gene involved in cell cycle checkpoint. Familia (two-hit) or somatic.
Tumour suppressor gene; neg. regulator of Ras; del permits unchecked ras-induced proliferation and neurofibromatosis.
factors that produce irreversible DNA damage but themselves don't produce neoplasms.
Factors that can cause tumours in "initiated" cells (by stimulating cell proliferation, leading to further genetic damage)
Direct-acting chemical carcinogen
covalently modifies target molecule, typically DNA.
Indirect-acting chemical carcinogen
requires metabolic conversion to "ultimate carcinogen", which is direct acting.
Anticancer alkylating agents
Direct-acting carcinogens that can cause 2° iatrogenic malignancies such as leukaemia.
Polycyclic aromatic hydrocarbons
Chemical carcinogens including tobacco smoke, smoked meats, broiled animal fat.
Aromatic amines/azo dyes
Chemical carcinogens found often in dye and rubber industry, causing bladder cancer.
Chemical carcinogens that cause GI cancer
Vinyl chloride
chemical carcinogens that cause liver haemangiosarcoma.
chemical carcinogens that cause lung cancer.
UV light
forms pyrimidine dimers in skin, causing squamous cell and basal cell carcinoma, and malignant melanoma.
Human Papillomavirus
DNA oncogenic virus whose protein product inactivates p53, causing uterine, cervical, anogenital, oral, and laryngeal cancers.
Epstein-Barr Virus (EPV)
DNA oncogenic virus that has B-cell mitogenic effects; linked to Burkitt's Lymphoma.
Hepatitis B virus
DNA oncogenic virus associated with hepatocellular carcinoma. Viral protein HBx inhibits p53
Kaposi sarcoma herpesvirus (KSHV), aka human herpesvirus type VIII
DNA oncogenic virus associated with Kaposi sarcoma and B-cell lymphoma in HIV pts. Virus encodes homologues of human GFs.
Human T-cell Leukaemia Virus Type 1 (HTLV-1)
RNA oncogenic virus associated with T-cell leukaemia/lymphoma and tropical spastic paraparesis (deymyelinating disorder). Virus induces IL-2 and IL-2 R, causing polyclonal proliferation of T-cells. In small cases, T-cells progress to monoclonality and malignancy.
Hepatitis C virus
RNA oncogenic virus that ↑s risk of hepatocellular carcinomas due to chronic cirrhosis triggering cellular proliferation.
Helicobacter pylori
Oncogenic gram neg spiral/rod bacteria associated with large percentage of gastric lymphoma; may stimulate proliferation of B-lymphocytes.
extent to which a malignant neoplasm resembles normal tissue; "well-differentiated" to "poorly differentiated".
extent of spread of cancer, independent of grading. Codified by TNM system (Tumour size, Node involved, Metastases)
Tumour Markers
PSA - prostate cancer
CEA - GI, breast cancer
AFP - liver, germ cell cancers
CA 125 - ovarian cancer
hCG - trophoblastic/germ cell tumours
Asbestos/Feruginous body
Asbestos fibres coated by iron-protein complex, characteristically found in asbestosis. Caused by Macs engulfing asbestos and dying. Fe then attaches to asbestos.
Aflatoxin B1
Product of Aspergillus Flavus; contamination of food by fungus; peanuts/grains esp. Metabolism of Aflatoxin B1 yields reactive electrophilic epoxide, covalently binds to DNA; tumour initiation. HBV may be synergistic.