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Path Exam 1 "Things To Know"

Amyloid Group of fibrillar proteins w/ a common physical conformation (beta-pleated sheet)
Amyloidosis Extracellular accumulation of an amorphous eosinophilic (hyaline) substance
Atrophy A decrease in the size and/or number of cells usually with consequent decrease in the size of an organ or tissue and a decrease in function
Dysplasia Disordered cell growth and maturation
Dystrophic calcification Deposition of calcium in necrotic or damaged tissue
Hemochromatosis Marked accumulation of iron with damage/impairment of function
Hemosiderin Aggregates of ferritin micelles
Hemosiderosis Mild accumulation of iron with no damage or impairment
Hyperplasia Increase in the NUMBER or cells in an organ or tissue
Hypertrophy Increase in the SIZE of cells with consequent increase in the size of an organ or tissue
Metaplasia Replacement of one mature cell type by another mature cell type
Metastatic calcification Deposition of calcium in normal tissues
Primary (genetic) hemochromatosis Due to gene mutation (short arm of chromosome 6) that results in excessive intestinal absorption of iron
Coagulative necrosis - Change in cytoplasm Increased eosinophilia
Coagulative necrosis - Changes in nucleus Pyknosis - Karyorrhexis - Karyolysis
Do cells shrink or swell when ATP is depleted? Cells swell b/c Na-K ATPase no longer functions -> Na+ diffuses in and K+ diffuses out -> net gain of solute -> osmotic swelling
Extrinsic pathway of apoptosis Receptor-mediated - Important for the control of inflammation - Tumor Necrosis Factor (TNF) or Fas ligand (FasL) interact with their receptors -> receptors activate intiator caspases
Fat necrosis - Gross Images Chalky white areas
Fat necrosis - Micro Images Necrotic fat cells associated with calcium deposits
How does cell size change due to necrosis or apoptosis? Cell swells in necrosis - Cell shrinks in apoptosis
Intrinsic pathway of apoptosis Stree-mediated - Important for the removal of damaged cells - DNA damaged by free radicals or increased mitochondrial permeability -> Cytochrome c or other pro-apoptoic mediators like p53 released -> initiator caspases activated
Karyolysis Loss of sustainable nuclear material
Karyorrhexis Fragmentation of the nucleus
Pyknosis Shrinkage of the nucleus with increased basophilia
Sources of free radicals Exogenous sources (neutrophils during acute inflammation ) - Generation within affected cells (ionizing radiation : metabolism of exogenous chemicals and drugs : abnormal accumulation of iron or copper : NO production by some cells) - Reperfusion injury
What are the 2 hallmarks of reversible cell injury? Cell swells - Ribosomes dissociate from ER
What are the 3 hallmarks of irreversible cell injury? Irreversible mitochondrial dysfunction - Membrane damage - Nuclear damage (pyknosis - karyorrhexis - karyolysis)
What should think if you see a bunch of gram positive cocci in a micro image? Liquefactive necrosis - Lung abssess as a result of infection
What type of necrosis results from a lung infarct? Coagulative necrosis (lung infection -> absess/liquefactive ::: TB -> granulomatous)
What's saponification and what's it associated with? Free fatty acids combine with calcium to form chalky white deposits - Occurs in fat necrosis
Average lifespan (ALS) Steadily increasing - More old, old people
Biological age Reflects the progressive accumulation of age-associated changes in tissues and organs - Modified by diet, socio-economic factors and the environment
Cellular quiescence Withdrawal from the cell cycle into G0
Chronological age The time elapsed since birth
Maximum lifespan Has not increased significantly over time - Hypothetical maximum is approx 110-120 years
Progeria Lamin A gene mutation
Replicative cell senescence Cells cannot be stimulated to re-enter the cell cycle
Werner's syndrome WRN gene mutation
Alpha1-antitrypsin Acute phase protein - A proteinase inhibitor
Alpha2-macroglobulin Acute phase protein - A proteinase inhibitor
C3 Acute phase protein - Complement component
Ceruloplasmin Acute phase protein - Binds copper
Coagulation system Plasma protease
Complement system Plasma protease
C-reactive protein (CRP) Acute phase protein - Involved in opsonization - Secreted rapidly by the liver in response to inflammation - Elevation persists as long as there is inflammation - Levels decrease when inflammation resolves
Erythrocyte Sedimentation Rate (ESR) An increased "sed" rate is considered non-specific evidence of an inflammatory process - Rouleaux of RBCs (stack of coins) sediments more rapidly than dispersed individaul RBCs - RBC rouleauxs involved in blood stasis in vascular response causing inflamma
Fibrinogen Acute phase protein - Involved in coagulation
Fibrinolytic system Plasma protease
Haptoglobin Acute phase protein - Binds hemoglobin
Histamine Vasoactive amine
IL-1 Cytokine that causes fever
IL-6 Cytokine that causes fever
Interferons Cytokine that causes fever
Kinin system Plasma protease
Leukotrienes Arachidonic acid metabolite
Lipoxins Arachidonic acid metabolite
Prostaglandins Arachidonic acid metabolite
Serotonin Vasoactive amine
Serum Protein Electrophoresis (SPEP) - How do you interpret its results? Albumin followed by other acute phase proteins and lastly Ig - 1 big spike is normal (albumin) - 1 big spike (albumin) with other smaller spikes in the middle means acute inflammation - 2 big spikes (albumin and Ig) with smaller spikes in between means ch
TNF-alpha Cytokine that causes fever
What 3 chemical mediators of inflammation cause fever? TNF-Alpha - IL-1 - IL-6
What 3 chemical mediators of inflammation cause leukocytosis? TNF-Alpha - IL-1 - CSFs increase the number of circulating immature neutrophils or "band"cells (LEFT SHIFT)
What 3 chemical mediators of inflammation cause pain? Bradykinin - PGE2 - Substance P
What do you think of a micro image where everything is teal except a couple random black dots?? Stained Yeast (Histoplasma) - Infections cause granuloma formation - GRANULOMATOUS INFLAMMATION
What do you think of a micro image with gram-negative cocci and cells with kidney-shaped nuclei? Acute inflammation - Weird nuclei are neutrophils!!
What is trichrome stain and when do you see it? Stains collagen BLUE - Seen in micro images of chronic inflammation with FIBROSIS
What type of cell is prevalent in purulent exudate? Neutrophils - look for the bilobed nuclei
bFGF Stimulates cell division and angiogenesis
Collagen Provides tensile strength to support epithelial cells and it surrounds connective tissue cells
EGF = TGF-Alpha Stimulates cell division for many cell types and angiogenesis - Binds to the epidermal growth factor receptor on the cell surface
Elastic fibers Provides tissue with recoil ability
Fibronectin Adhesive glycoprotein that binds other stuff together - Early stabilizer of wonds - Regulates cell migration (chemotactic for fibroblasts and macrophages)
Fibroplasia AKA Fibrosis - Process characterized by the proliferation of fibroblasts and consequent deposition of extracellular matrix (predominately collagen) by the fibroblasts
Granulation tissue Know this for histological images!! Repair tissue composed of activated fibroblasts and proliferating small blood vessels along with extracellular matrix and variable numbers of inflammatory cells
Heparan sulfate proteoglycan Helps tissue retain water
How long does it take the epithelium to reach normal thickness in a primary wound? Approximately 5 days or less
IL-8 Chemotactic to neutrophils - Stimulates angiogenesis - Produced by macrophages
Laminin Part of the basement membrane
Name 2 genetic defects that affect collagen Ehler-Danlos and Osteogenesis imperfecta
Organization IMPAIRED FUNCTION AFTER REPAIR - The reparative process characterized by fibrosis. It typically occurs in tissue that has been injured sufficiently to destroy the stromal framework and/or regenerative capacity of the parenchymal tissue
PDGF Stimulates production of IL-1 and bFGF - Chemotactis - Stimulates collagen synthesis
Proteoglycans Organizes ECM
Regeneration New growth or repair of tissues lost due to disease or injury
Resolution NORMAL FUNCTION AFTER REPAIR - The return of a tissue to its normal state following a pathologic condition such as inflammation - Typically characterized by the enzymatic digestion of an exudate followed by removal of the breakdown products
TGF-Beta Chemoattractive from fibroblasts - Stimulates collagen synthesis - Inhibits proliferation of some cell types ( leukocytes and most epithelial cell types)
Thrombospondin Involved in cell-cell and cell-matrix binding - Inhibits angiogenesis
Type IV collagen Part of the basement membrane
VEGF Stimulates: division of endothelial cells - angiogenesis - transcytosis
What 2 factors contribute to wound strength and what percent of normal is it during the first week following primary injury? Due to fibrin and repithelization - Strength is 5-10% of original
What 2 things characterize a 1 month old primary wound? Scant/Absent inflammation - Decreased vascularity
What 3 things characterize a 2-3 week old primary wound? Fibroplast proliferation - Collagen accumulation - Decreases inflammation
What does a primary wound look like after 1 year? A hypocellular hypovascular scar
What percent of normal is a primary wound after one month and what factor coorelates with the amount of strength? 15-20% of the original strength - Strength coorelates with the increase in collagen content
When do neutrophils appear after a primary wound? By day 2
When do neutrophils appear after a primary wound? Within 24 hrs they begin to infiltrate the margins
When do neutrophils leave and macrophages are the only ones left in a primary wound? By day 5
When does collagen begin to bridge a primary wound? By day 5
When does granulation tissue begin to invade a primary wound? By day 3
When is epithelial continuity restored after a primary wound? By day 2
Wound contraction Reduction in the size of the wound - Up to 70-80%
Congestion PASSIVE increased volume of blood in the vessels of a tissue
Congestive heart failure (CHF) Cardiac output is inadequate to meet the metabolic demands of the body
Contusion Bruise - A hemorrhage within tissue following rupture of small blood vessels by blunt force injury
Ecchymoses Large blotchy hemorrhages
Edema Accumulation of excess fluid in the interstitial space
Hemarthrosis Hemorrhage into joint space
Hematoma Accumulation of blood within a tissue or space
Hemopericardium Hemorrhage into pericardial sac
Hemoperitoneum Hemorrhage into peritoneal cavity
Hemophilia = "Easy bleeder"
Hemorrhage The escape of blood from the cardiovascular circuit
Hemothorax Hemorrhage into pleural cavity
Hyperemia ACTIVE increased volume of blood in the vessels of a tissue
Left-sided heart failure Results in pulmonary congestion and edema and reduced renal perfusion. Consequences of reduced renal perfusion: Impaired secretion of nitrogenous wastes (pre-renal azotemia) - activation of the renin-angiotensin-aldosterone system - retention of sodium an
Petechiae Minute (1-2 mm) hemorrhages
Purpura Medium-sized (up to about 1 cm) hemorrhages
Right-sided heart failure Results in systemic and portal venous congestion. Manifests as: edema - effusions within body cavities - impairment of organ function (especially the liver). Associated with: pulmonary hypertension - primary myocardial disease - diseases that cause left
Shock A state of inadequate perfusion characterized by a disproportion between the circulating blood volume and the volume of the circulating system that needs to be filled (in other words, there is an inadequate effective circulating blood volume)
Activated Partial Thromboplastin Time (aPTT) Assesses intrinsic and common pathways - Used to monitor heparin therapy
Alpha2-antiplasmin Primary inhibitor of plasmin
Annexin V Inhibits tissue factor
Anticoagulants Prostacyclin (PGI2) - Thrombomodulin - Tissue factor pathway inhibitor (TFPI)
Antithrombin Inhibits all serine proteases except factor 7a - Heparin binds to it and increases its activity
Aspirin An "anti-platelet" agent - Inhibits cyclo-oxygenase activity irreversibly - Prolongs bleeding time
Blood clot Gel-like matrix that includes: water - fibrin - other plasma proteins - platelets - WBCs - RBCs
Christmas disease/Hemophilia B Factor 9 deficiency
Classic hemophilia/Hemophilia A Factor 8 deficiency
Coagulation Clot formation - The goal is fibrinogen -> cross-linked fibrin
Does liver disease increasing bleeding or clotting? It causes increased bleeding even though it decreases production of both coagulation and anti-coagulation facts
Embolus Clot material that has relocated to a site distant from that at which it formed
Factor V Leiden People with this mutation get blood clots!! Most common hereditary thrombosis syndrome - Mutant form of factor V CANNOT be degraded by protein C and protein S (anti-coagulants that regulate the clotting cascade)
Fibrinolysis Clot dissolution - The goal is cross-linked fibrin -> fibrin degradation products - Mediated primarily by plasmin
Heparin Binds to antithrombin and increases its activity (inhibits serine proteases especially 2a and 10a)
Plasmin Primary mediator of fibrinolysis
Plasminogen activator inhibitor-1 (PAI-1) Converts fibrin to fibrinogen - Inhibits factors 5 and 8
Plasminogen activator inhibitor-1 (PAI-1) Inhibits tPA and uPA
Platelets Add mechanical strength to clots - membrane promotes activation of clotting factors - Granule contents mediate vasoconstriction and angiogenesis
Procoagulants Include von Willebrand factor (vWf)
Profibrinolytics Include tissue plasminogen activator (tPA)
Prostacyclin (PGI2) Vasodilator - Inhibits platelet aggregation
Proteins C and S Inactivate factor 5 and 7 - Enhance fibrinolysis
Proteins S and C Inactivate factors 5 and 8 - Enhance fibrinolysis
Prothrombin Time (PT)/International Normalized Ration (INR) Assesses extrinsic and common pathways - Used to monitor warfarin therapy
The 1 clotting cascade matrix protein Fibrinogen
The 1 clotting cascade transglutimase Factor 13 - Crosslinks soluble fibrin into insoluble fibrin strands
The 2 clotting cascade factors that are encoded on the X-chromosome Factors 8 and 9 (the one's associated with Classic Hemophilia and Christmas disease)
The 4 clotting cascade co-factors High molecular weight kininogen (HMWK) - 5 - 7 - Tissue factor
The 4 main regulators of fibrinolysis tPA - uPA - PAI-1 - Anti-plasmin
The 7 serine protease clotting factors Prekallikrein - 2 - 7 - 9 - 10 - 11 - 12
Thrombin Converts factor 13 to its active form so that it can cross-link fibrin
Thrombomodulin An endothelial receptor for thrombin - binding causes activation of protein C which cleaves factors 5a and 8a so they can not longer promote coagulation
Thrombophilia = Predisposed to thrombosis - Inherited or acquired
Thromboxane A2 (TXA2) Vasoconstrictor - Enhanced platelet aggregation
Thrombus A blood clot that remains at its site of formation
Tissue factor pathway inhibitor (TFPI) Anti-coagulant - Binds to factor 10a and inactivates the 8a:tissue factor complex
Tissue plasminogen activator (tPA) Anti-coagulant - Activates plasminogen to release plasmin
Urinary-type plasminogen activator (urokinase = uPA) Like tPA - Converts plasminogen to plasmin
Virchow's Triad The 3 factors that promote thrombus formation -Endothelial injury - Abnormal blood flow (either stasis or turbulence) - Blood hypercoagulability
Vitamin K dependent clotting factors Factors 2 - 7 - 9 - 10 and proteins C and S
von Willebrand factor (vWf) Promotes platelet adhesion by binding to their gp 1b receptors - Complexes with factor 8:C (a procoagulant factor) to prevent its degradation - synthesized by endothelial cells and stored platelet alpha granules - deficiency causes bleeding disorder
Warfarin Inhibits all Vit K-dependent clotting factors
What is the only acceptable anticoagulant for use in collection of blood for coagulation testing? Citrate - It chelates Ca2+
Which begins to act more quickly heparin or warfarin? Heparin b/c it inhibits prothrombin (factor 2) which has the longest half-life (3-4 days) - Heparin can increase the activity of antithrombin immediately
Which clotting factors have the longest and the shortest half-lives? Fibrinogen t1/2 is longest (3-4 days) - Factor 7 t1/2 is shortest (4-6 hours)
Which coagulation test should be used to monitor Heparin Tx? aPTT - intrinsic and common pathways
Which coagulation test should be used to monitor Warfarin (Coumadin) Tx? PT/INR - extrinsic and common pathways
Angelman syndrome Due to deletion of the maternal chromosome at the 15q11-13 locus. Symptoms: hyperactivity - inappropriate laughter - severe mental retardation
Cystic fibrosis Autosomal recessive
Down syndrome Chromosomal abnormality
Duchenne muscular dystrophy X-linked recessive
Fragile X syndrome X-linked recessive
Gaucher Disease Autosomal recessive
Genetic imprinting Imprinted allele in biologically inactive. Disease results if the non-imprinted allele is deleted or mutated.
Klinefelter syndrome Chromosomal abnormality
Mitochondrial disease Disease that can only be inherited from the mother
Multifactorial inheritance Diseases that result from multiple genes as well as the environment. Examples: hypertension - atherosclerosis - congenital anomalies - diabetes
Neurofibromatosis-1 Autosomal dominant
Phenylketonuria Autosomal recessive
Polycystic kidney disease Autosomal dominant
Prader-Willi syndrome Due to deletion of the paternal chromosome at the 15q11-13 locus. Symptoms: hypotonia - obesity - hypogonadism - mental retardation
Turner syndrome Chromosomal abnormality
A critical lack of protein results in… Kwashiorkor
An overall lack of calories results in… Marasmus
Beriberi B1 (Thiamine) deficiency. Often seen with alcoholism. Wet: High-output CGF and dilated cardiomyopathy (tachycardia and edema). Dry: Peripheral neuropathy with muscular atrophy and diminished sensations and reflexes.
Iron deficiency Caused by: Blood loss - inadequate dietary intake. Causes: Hypochromic microcytic anemia and developmental abnormalities in toddlers.
Kwashiorkor Total protein malnutrition with enough calories overall
Marasmus Total calorie malnutrition
Protein deficiency Causes Kwashikwor or Marasmus (depending on whether or not there is total calorie deficiency as well)
Selenium deficiency ASSOCIATED WITH CONGESTIVE CARDIOMYOPATHY. Usually seen in the context of unsupplemented TPN.
Thiamine deficiency Beriberi and Wernicke-Korsakoff Syndrome
Vitamin A deficiency Causes night blindness, xerophthalmia and Bitot's spots. Stored in the liver where RESERVES ARE SUFFICIENT FOR MANY MONTHS OF DEPRIVATION.
Vitamin C deficiency Scurvy
Vitamin E deficiency Associated with diseases that cause fat malabsorption. Causes: Neurologic damage (degeneration of the posterior column) - pigmented retinopathy - skeletal muscle disease
Wernicke-Korsakoff syndrome CNS effects of thiamine (vitamin B1) deficiency
What causes necrosis of the mamillary bodies? Thiamine (vitamin B1) deficiency - Wernicke-Korsakoff syndrome
What characterizes "dry" Beriberi? Peripheral neuropathy
What characterizes "wet" Beriberi? Cardiomyopathy and high-output CHF
What vitamin deficiency does keratomalacia result from? Vitamin A
What vitamin maintains ferrous iron in the reduced state? Vitamin C
Zinc deficiency CAUSES A RASH ESPECIALLY IN INFANTS!!! May be seen in the context of unsupplemented TPN. Autosomal recessive condition involving metal ion transport (acrodermatitis enteropathica).
Alpha-fetoprotein (AFP) Tumor marker for liver and germ cell cancers
Bevacizumab (Avastin) Humanized antibody directed against VEGF
CA 125 Tumor marker for ovarian cancer
Carcinoembryonic antigen (CEA) Tumor marker for GI and breast cancers
Cetuximab (Erbitux) Monoclonal antibody directed against the extracellular domain of EGFR
Familial breast cancer Mutations in BRCA-1 and BRCA-2 genes
Familial polyposis APC mutation
Hereditary Nonpolyposis Colorectal Cancer (HNPCC) DNA mismatch repair gene defects
hMSH2 DNA mismatch repair gene that is mutated in HNPCC
Human chorionic gonadotropin (hCG) Tumor marker for trophoblastic and germ cell tumors
Imatinib mesylate (Gleevec) Tyrosine kinase inhibitor that targets bcr-abl
Methods to detect minimal residual cancer cells Histologic or cytologic study of tissues or fluids - Flow cytometry - FISH - Molecular studies (PCR) - Tumor markers
Most common cancers in men Lung -> Prostate -> Colon
Most common cancers in women Lung -> Breast -> Colon
Prostate-specific antigen (PSA) Tumor marker for prostate cancer
Tumor suppressor genes - mutator type Genes that function in DNA repair or regulation of apoptosis
What is the 2 hit hypothesis? 1 allele has germline mutation, and 2nd allele is mutated through somatic mutation
What's the result of mutator gene mutation? Leads to loss of genomic stability and more mutations
What's the result of tumor suppressor gene mutation? Leads to activation of cell cycle, despite possible DNA damage, passing defects on to progeny
Xeroderma pigmentosum Mutation in genes involved in nucleotide excision repair of pyrimidine-pyrimidine dimers caused by ultraviolet damage
Aflatoxin B1 Exposure increases risk of hepatocellular carcinoma
Diffuse interstitial fibrosis especially in lower and peripheral lung is indicative of… Asbestosis
Insulation Construction and Demolition and Shipbuilders associated with… Asbestosis
I've been working in a ship yard and smoking like a chimney. I may be at risk for…. Asbestosis. Diffuse interstital fibrosis. 87x relative risk of lung cancer vs. no exposure and no smoking.
What kind exposure causes globus pallidus necrosis? Carbon monoxide poisoning!!
What does Tylenol toxicity cause and how long between OD and effect? Centrolobular hepatic necrosis 3-5 days later
What type of lesion is associated with hypersensitivty pneumonitis? Chronic exposure causes granulomatous interstitial pneumonia with interstitial fibrosis
What are the two enzymes that are inhibited by lead and what are the effects of their inhibiton? d-ala dehydrase (causes a buildup of d-ala) and ferrochetalase (causes a buildup of porphyrins in the blood and these are toxic to the liver)
Form of mercury that is absorbed by the respiratory system and affects the brain Elemental Hg
Aflatoxin B1 From Aspergillus flavus (mold) often in warm moist peanuts or grains. Broken down by mixed function oxidases in the liver. Results in epoxides that can covalently bind to DNA. If cell division occurs before the DNA can be repaired, carcinogenesis may o
What enzyme is depleted in Tylenol toxicity? Glutathione
Overall, what is the product that lead inhibits the synthesis of? Heme
Themophilic actinomycetes - True molds - Animal antigens … associated with… Hypersensitivty pneumonitis = Extrinsic allergic alveolitis
Form of mercury that is absorbed by the GI tract and skin and affects the kidney Inorganic Hg
What are the effects of lead toxicity in children vs. those in adults? Kids get brain damage (acute changes include edema and vasculopathy both chronic changes are often subtle). Adults get peripheral neuropathy (demyelinization and axonal degeneration) often causing drop foot.
What would cause drop foot in an adult? Lead toxicity
What could causes a combination of (1) anemia (2) kidney tubular necrosis and interstitial nephritis and (3) abdominal pain? Lead toxicity but more likely to see the peripheral neuropathy and brain effects on exam
What cell type plays a large role in the effects of asbestosis? Macrophages. They secrete growth factor (IL-1) -> fibroblast proliferation and lysosomal enzymes and free radicals -> tissue injury. Both ultimately cause fibrosis.
Pneumoconioses Non-neoplastic lung diseases due to inhalation of dust particules. Generally restricted to inorganic dusts.
Form of mercury that is absorbed by the GI tract and skin and affects the brain Organic Hg
Collagenous nodules in upper lung is indicative of… Silicosis
Miners Stonecutters and Sandblasting associated with… Silicosis
Unique characteristic amongst tumor suppressors? Defect in DNA repair and apoptosis. Dominant negative (p53 forms dimers) effect.
What is a key difference in the cellular changes due to cancer promoter vs. cancer initiators? In contrast to the effects of initiators the changes resulting from promoters do not affect DNA and are reversible
Created by: megankirch