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292 Cards in this Set
- Front
- Back
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Name the basic amino acids.
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Arginine, histidine and lysine
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Name the acidic amino acids.
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Aspartic acid and glutamic acid
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Name the essential amino acids.
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Histidine, leucine, isoleucine, lysine, methionine, phenylalanine, valine
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List the prion diseases.
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Bovine spongiform encephalopathy, creutzfeldt-jacob diseasae, scrapie, deer-elk wasting disease and kuru
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What stabilizes the relaxed conformer of hemoglobin?
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Carbon monoxide - makes it harder for hemoglobin to release oxygen
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What stabilizes the taut conformer of hemoglobin?
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2,3-BPG - makes it harder for oxygen to bind oxygen (encourages hemoglobin to release oxygen where it is needed - shifts dissociation curve to the right)
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What is scurvy?
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Vitamin C deficiency - prolyl hydroxylase needes vitamin c to convert proline to hydroxyproline and lysine to hydroxylysine.
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Michaelis-Menton equation
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Vo = k2[ES]
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Vmax?
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Vmax = k2[E]t
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Key parts of Lineweaver-Burke plot
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y-axis = 1/Vo, x-axis = 1/[S], y-intercept = 1/Vmax, x-intercept = -1/Km
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How do competitive inhibitors change the plot?
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increase Km, no change on Vmax
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How do non-competitive inhibitors change the plot?
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decrease Vmax, no change on Km
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How do competitive inhibitors rotate the L-B plot?
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rotate up and left around the Y-intercept
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How do non-competitive inhibitors rotate the L-B plot?
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rotate up and left around X-intercept
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What tissues are GLUT4 receptors found in?
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muscle and adpiose (insulin dependent)
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Normal blood glucose level.
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80mg/dL (5mM)
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Steps of glycolysis.
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Glucose, G6P, F6P, F1,6bisP, GA3P, 1,3bPG, 3PG, 2PG, PEP, Pyruvate
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Irreversible (regulatory) steps in glycolysis.
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Hexokinase, Phosphofructokinase, Pyruvatekinase (encouraged by insulin, discouraged by glucagon)
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Extra step in gluconeogenesis.
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pyruvate => oxaloacetate => PEP
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Steps of glycogenesis
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G6P, G1P, UDP-G, Glycogen (a1-4 bonds make chain, a1-6 bonds make branches)
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Main steps of pentose phosphate pathway.
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G6P => Ribose5P and Erythrose4P
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Steps in beta oxidation.
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Fatty acyl CoA, Enoyl CoA, 3-hydroxyacyl CoA, 3-ketoacyl CoA, Fatty Acyl CoA + acetyl CoA (goes until 2 acetyl CoAs)
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How many ATP from 16 carbon fatty acid?
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131 (FADH2, NADH and acetyl CoA goes through TCA)
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Where do the 131 ATP come from?
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Every two carbons = 1 FADH2 and 1 NADH (5 ATP) and 1 acetyl CoA (12 ATP) = 17 ATP per 2 carbons
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Steps in TCA cycle.
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Acetyl CoA, Citrate, Isocitrate, a-Ketoglutarate, Succinyl CoA, Succinate, Fumarate, Malate, Oxaloacetate, Repeat (12 ATP per Acetyl CoA)
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What are the ketone bodies?
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acetoacetate, acetone, D3Hydroxybutyrate
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What tissues can use ketone bodies?
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brain and muscles
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What does ALT do?
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Alanine + a-ketoglutarate <-> Glutamate + Pyruvate
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What does AST do?
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Aspartate + a-ketoblugarate <-> Glutamate + oxaloacetate
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Coenzyme for AST and ALT?
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pyridoxyl phosphate
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Allosteric inhibitory of glutamate dehydrogenase?
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GTP (when energy is low, amin acid degradation is increased)
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Defects in the conversion of methionine to Cys cause?
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met => homocysteine => cys (requires VitB6) causes homocystineuria -
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What is the rate limiting step in the urea cycle?
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attachment of amonia (from amino acids) to phosphate via carbamoyl phosphate (uses biotin)
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Symptoms of phenylketonuria?
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defect in phenylalanine hydroxylase, elevated Phe, hypopigmentation, mental retardation and mousy odor (phenylpyruvic acid)
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Symptoms of maple syrup urine disease?
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error in catabolsim of branched chain amino acids, build-up of amino acids and alpha-ketoacids, neurological symptoms
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What are the purines?
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adenine and guanine
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What are the pyrimidines?
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cytosine, thymine and uracil
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What is the role of dihydrofolate reductase?
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convert DHF to THF
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Deficiency in Adesonine deaminase causes?
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SCID, build up of dATP, inhibitis ribonucleotide reductase, decreased lymphocyte production
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What does xanthine oxidase do?
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converts hypoxanthine => xanthine => uric acid (allopurinol targets this to treat gout)
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Symptoms of Lesch Nyhan syndrome?
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100% loss of HGPRT activity (needed to salvage purines)
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What is the only importatn pyrimidine salvage?
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thymidine - salvaged from free thymine and dRP, needs thymidine phosphorylase and thymidine kinase, inhibiting may be useful in cancer therapy (gancyclovir and zidovudine are analogs that thymidine kinase can use)
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Requirements for DNA polymerase to work.
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dNTPs, DNA template, Zn, Mg, primer (RNA or DNA with a free 3'-OH end)
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Job of DNA Polymerase I
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removes, replaces RNA primer, DNA repair, (YES proofreading, YES repair) synthesis on lagging strand
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Job of DNA polymerase III
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DNA replication, leading strand (YES proofreading, NO repair)
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Job of DNA helicase
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unzips annealed nucleotides
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Job of DNA ligase
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complete strand synthesis (phosphage linkage)
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How is condensed DNA produced?
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methylation
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When does telomerase stop?
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when RAP1 proteins bind
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What is a transition?
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A to G / T to C
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What is a transversion?
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A to T / G to C
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Deaminatino of cytosine forms?
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uracil - can result on a G-C pair being converted to A-T
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Job of RNA polymerase I
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produce rRNA
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Job of RNA polymerase II
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produce mRNA
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Job of RNA polymerase III
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produce tRNA and 5s rRNA
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Job of RNA mito
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produce mitochondrial RNAs
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What is a ribozyme?
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enzyme caused by folding of RNA molecule - Peptidyl transferase - primary enzymatic functino of the ribosome
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secondary structure of tRNA
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cloverleaf
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tertiary structure of tRNA
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leg of lamb
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Steps in mRNA formation.
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transcription, 5' cap, poly-A tail, excision of introns, splicing to add different tails
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What is the start codon?
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AUG - codes methionine
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Wobble base pairs for G anticodon?
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C or U
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Wobble base pairs for U anticodon?
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A or G
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Wobble base pairs for I anticodon?
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A, C or U
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Example of insulin as secretory protein.
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Insulin maked as preproinsulin - cleaved in ER to proinsulin - cleaved in golgi to insulin + c-peptide - secreted
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How are misfolded proteins handled?
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attached to ubiquitin and sent to proteasome
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What causes cystic fibrosis?
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incorrectly folded CFTR protein (has many B-sheets that lead to misfoldign) - improper regulation of ocmponents of sweat and mucus
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What is inactive X chromosome covered with?
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XIST gene transcript
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Where is the basal promoter located?
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40bp upstream of start site (contains tata box)
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Where is the upstream promoter located?
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200bp upstream - many transcription factors - turn gene on
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What are siRNA?
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small interfering RNA - dsRNA is cleaved by DICER into siRNA, siRNA binds to protein complex to form RISC, allows RISC to seek out complementary mRNA and destroy it
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Negative feedback example?
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increase in arterial pressure, stimulates stretch receptors, stimulates afferent autonomic nerves, stimulates autonomic efferent nerves, INHIBITS increase in arterial pressure
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Positive feedback example?
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pituitary gland secretes LH, LH stimulates ovary, ovary secretes estradiol, estradiol stimulates pituitary
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Total body water?
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60% of body weight
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ECF?
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1/3 of TBW (plasma + ISF)
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ICF
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2/3 of TBW (total - ISF - plasma)
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Plasma?
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1/4 of ECF
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What separates plasma from ISF?
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blood vessel wall
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What separates the ECF from the ICF?
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cell membrane
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Mostly intracellular ions?
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potassium
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Mostly extracellular ions?
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sodium, calcium
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Excretion formula to determine ECF
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Volume(ECF) = [(Amount Injected) - (Amount Excreted)] / (Concentration) ALWAYS CONVERT TO mg/L FIRST
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Define osmoles
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number of mols of a chemical compound that contribute to a solution's osmotic pressure ex: 1 mol/L of NaCL = 2 osmol/L (1 for Na and 1 for Cl)
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Define osmolarity
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the measure of solute concentration: number of osmoles of solute / Liter of solution
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Define molar equivalent
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the amount of substance that will react with one mole of electrons in a redox reaction
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Rank molecules from high to low permeability
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O2, H2O, Urea, Glucose, K+, Na+
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Endogenous ligand
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produced within the bodiy
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Exogenous ligand
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produced outside the body (ex: drug)
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Ligand with high specifity
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only binds to one receptor
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Ligand with high promiscuity
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binds to many receptors
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Synaptic signaling facts
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short distance, fast onset, high precision, can be delivered from far soma, FedEx
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Paracrine signaling facts
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short distance, fast onset, not as selective as synaptic, Loudspeaker
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Endocrine signaling facts
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long distance, slow onset, very non-specific, radio broadcast
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Autocrine signaling facts
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single cell gets weak autocrine signal, aplifies the signal, listserv
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Ionotropic receptor
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open or close when directly bound by a ligand (the receptor IS the pore)
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Metabotropic receptor
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indirectly linked to ion channels through coupling (G protein)
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Receptor sequestration
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pull receptor back into an endosome
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Receptor down-regulation
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pull receptor back into a lysosome
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Receptor inactivation
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remove a phosphate
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Steps of the 2nd messenger cascade
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Activate G protein, activate adenylyl cyclase, produce cAMP, activate Protein kinase A
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Activation of phospholipase C causes?
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cleavage of PIP2 into DAG and IP3, DAG activates protein kinase C, IP3 releases Ca2+ from ER
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Job of phosphodiesterase?
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degrades cAMP into AMP
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Job of protein phosphatase?
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remove phosphate from active PKA
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Job of Calmodulin?
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Ca2+ activates it and it activates protein kinases
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What does tyrosine kinase respond to?
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insulin, EGF and PDGF
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What does serine kinase respond to?
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TGF-b
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Job of mitogen-activated protein kinases (MAPKs)?
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activate Ras protiens (Ras proteins activate MAP kinase-kinase-kinase)
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Characteristics of gap junctions
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direct between cells, connexons, pass electrical current, ATP and second messengers, fast, bidirectional
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Characteristics of chemical synapse
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slow, unidirectional, action potential + neurotransmitter release
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Job of synapsin
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binds vesicles together as they more from endosome toward cell membrane
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Job of SNARE complex
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composed of synatobrevin, syntaxin and SNAP-25 - anchors vesicle to cell membrane
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Job of synaptotagmin
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when Ca2+ enters the cell, it binds to synaptotagmin and causes the vesicle membrane to fuse with the cell membrane
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Job of clathrin
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vesicles that are formed by membrane invagination are coated with clathrin and sent back to the endosome
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5 criteria to classify a neurotransmitter
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persent in the nerve terminal, released by electrical stimulation of neuron, specific receptors exist, direct application of substance mimics neuronal stimulation, there is a mechanism for terminating the action
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Otto Loewi experiment
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heart solution
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time constant =
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(resistance)(capacitance)
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size of time constant
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small = fast, large = slow
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nernst equation
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Ex = 26.73 ln [K+ out] / [K+in]
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Nernst potential for Na?
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67
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Nernst potential for K?
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-98
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Nernst potential for Cl-?
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-90
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Driving force = ?
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Em - Ex (x=ion)
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time constant again =
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(membrane resistance) x (membrane capacitance)
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How is the sign of a post synaptic potential determined?
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positive ion flowing in = positive, negative ion flowing in or positive ion flowing out = negative
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Absolute refractory period?
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time from beginning of depolarization to return to polarized (everything before relative refractory period)
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Relative refractory period?
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sodium channels begin to reactivate - NaKATPase brings back to resting potential
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Length constant?
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(membrane resistance) / (cytoplasmic resistance)
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size of length constant?
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small = fast, large = slow
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Increased axon diameter?
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increased velocity
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Increased myelination?
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increased velocity
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Isotonic contraction
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muscle contraction under a load (apply load, measure velocity of shortening muscle, repeat)
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Isometric contraction
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muscle does not change length (set muscle length, measure force, set new length, measure new force, repeat)
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total tension = ?
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passive tension + active tension
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lengthening contraction
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muscle length is increased while the muscle is contracting (quadriceps while going down stairs)
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Torque = ?
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force x distance
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define tetanus
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frequency summation
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purpose of t-tubules?
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propagate action potential into muscle
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haplotype
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snps that are close together (over 10 million have been identified)
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hemizygous
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used to describe males with a mutation in x chromosome (or females with loss of one x chromosomal locus)
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heterogeneity
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when a phenotype is caused by multiple alleles or loci
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uniparental disomy
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when an individual receives two copies of a chromosome from one parent and none from the other
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autosomal recessive pedigree pattern
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75:25 phenotype
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autosomal dominant pedigree pattern
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50:50 inheritance pattern (from heterozygous parent)
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x linked pedigree pattern
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absence of father-son inheritances - all daughters of affected male are carriers
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mitochondrial inheritance
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maternal inheritance - affects all children from affected mother - mitochondrial functions affected only
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equations for gene frequency
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p = frequency of allele A, q = frequency of allele a, p+q=1, p^2 + 2pq + q^2 = 1, p^2 = AA frequency, 2pq = Aa frequency, p^2 = aa frequency
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isochromosome
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formed when the centromere divides horizontally rather than vertically
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polyploidy vs aneuploidy
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polyploid = multiple copies of ALL chromosomes, aneuploid = multiple copies of a particular chromosome
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robertsonian translocation
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when the long arms of two acrocentric chromosomes join together
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philadelphia chromosome
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t(9;22)(q34;q11)
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types of down syndrome
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47,XX,+21 46,XX,rob(14;21)(q10;q10),+21 Mosaic 21q211 and partial
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trisomy 18
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edwards syndrome, clenched hands, crossed legs, feet with rounded bottom, interferes with normal development
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trisomy 13
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patau syndrome, cleft lip, clenched hands, close set eyes, severe mental retardation
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cri du chat syndrome
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deletion of part of chromosome 5, high pitched cry like a cat, downward slanted eyes, low birth weight
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22q11.2 deletion syndrome
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DiGeorge syndrome - thymic hypoplasia with diminished T-cell immunity and parathyroid hypoplasia with hypocalcemia
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Klinefelter syndrome
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XXY, male hypogonadism, large breasts, cells have barr body = results from random x inactivation
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47, XYY syndrome
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no major physical abnormalities, possible slow learning/speech development
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Turner syndrome
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45XO, hypogonadism in females, some are mosaic
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Trisomy X
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XXX, x inactivation in females will cause most to be asymptomatic
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Multifactorial disorder
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genes + environment + other factors
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concordance
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rate of both twins showing a particular phenotype
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heritability
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(variance in DZ - Variance in MZ) / (Variance in DZ)
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Causes of congenitial abnormalities
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50% = complex inheritance, 25% = chromosomal imbalance, 20% = single-gene mutation, 5% = environmental teratogen
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Noninvasive prenatal testing
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prenatal risk assessment screening, obstetrical ultrasonography
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Invasive prenatal testing
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amniocentesis, chroionic villus sampling
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genetic intervention strategies
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gene transfer, siRNA, mutant protein trapping, protein/enzyme replacement
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southern blot
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DNA - hybridized with probes
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northern blot
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RNA
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western blot
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protein
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Blot Acronym
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SNoW DRoP
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Marfan Syndrome
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basic defect in connective tissue. All symptoms stem from mutation in fibrillin, defect in fibrillin 1, dominant trait
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Ehlers-Danlos syndrome
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extremely loose joints, hyperelastic skin, easy bruising, defect in collagen synthesis, dominant
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Familial Hypercholesterolemia
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high cholesterol levels, mutations of LDL receptor gene, heterozygous - respons to therapy, homozygous - needs other treatments
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Phenylketonuria
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missing phenylalanine hydroxylase, autosomal recessive, chromosome 12
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cystic fibrosis
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mutatin in CFTR, recessive, chromosome 7
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Neurofibromatosis
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excessive production of neural crest cells - leads to melanocytes, autosomal dominant
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sickle cell disease
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autosomal recessive, chromosome 11
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changes in reversible cell injury
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cell swelling, vacuole formation, decreased function of NaKATPase, fatty change, blebbing, swelling of mitochondria, clumping of chromatin, dilation of ER, increased pallor, increased turgor, increased weight
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changes in irreversible injury
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mitochondrial damage, severe membrane damage, massive calcium influx, pyknosis, karyorrhexis, karyolysis, rupture of lysosomes
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ATP depletion causes:
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Na-K pump failure, Na-Ca pump failure, cell swelling
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Loss of calcium homeostasis causes:
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massive calcium influx
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What are the reactive oxygen species?
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hydrogen peroxide, superoxide anion, hydroxyl radicals
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enzymes that remove ROS
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superoxide dismutase, glutathione peroxidase and catalase
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coagulative necrosis
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denaturation of cellular proteins. Tissue appears as solid mass, ghosted cell outline. Firm texture. Affects solid organs: heart, intestine, kidney, liver. Characteristic of ischemic injury
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liquifactive necrosis
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tissue digestion by phagocytes and hydrolytic enzymes. In the CNS, infarction results in liquifactive necrosis. Cavity filled with clear watery fluid. Hypoxic cell death of brain cell.
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Dry gangrenous necrosis
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widespread coagulative necrosis with NO infection
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Wet gangrenous necrosis
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widespread coagulative necrosis WITH infection
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Caseous necrosis
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combination of coagulative and liquifactive necrosis. Found in tuberculosis infection and fungal infection. Associated with granuloma formation - tissue architecture is COMPLETELY destroyed
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fatty necrosis
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typically occurs as a result of a release of pancreatic lipase - when mixed with calcium, it causes fat saponification
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fibrinoid
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occurs in the blood vessel, associated with immunological injury
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what happens during apoptosis?
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protein cleavage by Caspases, genetic activation, only affects single cells, no inflammatory response
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what does bcl-2 do?
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inhibits apoptosis
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what does p52 do?
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stimulates apoptosis
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Pyknosis, karyorrhexis, karyolysis
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darkening, fragmentation, disappearance
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hyperplasia
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increase in the number of cells - increased rate of division
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metaplasia
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reversible replacement of one mature cell by another mature cell type which is better able to tolerate the stress
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dysplasia
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not a true adaptive change - abnormal proliferation characterized by changeds in size, shape and organization of cells - not cancer, but may progress to cancer
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vessel proteins involved in rolling
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e-selectin, p-selectin
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vessel proteins involved in tight binding
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ICAM-1
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vessel proteins involved in diapedesis
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PECAM-1
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vessel proteins involved in migration
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bacterial products, C5a, IL-8, LTB4
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transudate
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hypocellular, protein poor
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exudate
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cellular and protein ritch
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labile cell
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multiply constantly throughout life - epithelial cells
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stable cell
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only multiply when receiving external stimulus - muscle cells
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permanent cell
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do not have the ability to multiply - RBCs
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function of IL-1 and TNF
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mediate fever
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left shift
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leukocytosis - 15,000-20,000 cells/ml
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highESR
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increased erythrocyte sedimentation rate
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oxygen independent killing
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release of lysosomal hydrolases
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granuloma
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central area of macrophages, epitheloid cells and multinucleated cells - surrouned by lymphocytes and plasmal cells - outer rim = fibroblasts and connective tissue, very center can have caseous necrosis
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leukocyte adhesion deficiency
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nonfunctioning CD18 - unable to extravasate
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myeloperoxidase deficiency
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lack myeloperoxidase (still have NADPH oxidase) = poor respiratory burst
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chronic granulomatous disease
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certain cells have difficulty forming ROS. Extremely defective respiratory burst
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macrophage activation
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differentiation of monocytes - express CD14 and CD11b
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innate immune system
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epithelial barriers, phagocytes, complement, NK cells (non-specific, non memory, fast, constant)
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adaptive immune system
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B-lymphocytes, antibodies, T-lymphocytes, effector T-cells (highly specific, has memory, slow, improves)
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primary lymphoid organs
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bone marrow and thymus
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secondary lymphoid organs
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spleen and lymph nodes
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good antigens
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large proteins (protein>carb>>>>lipid) (large>small)
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how phagocytes kill pathogens
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complement activation - CR1 on macrophage binds C3b on bacterium, endocytosis, phagolysosome formation
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C3a and C5a
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potent anaphylotoxins, allow proteins to extravasate, allows migration of monocytes and neutrophils from blood into tissue
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THF-a
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activates vascular endothelium and increases vascular permeability. Fever, mobilization of metabolites, shock (secreted locally or systemically)
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IL-1beta
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activates vascular endothelium, activates lymphocytes, local tissue destruction increases access of effector cells, fever, production of IL-6
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IL-1, IL-6, TNF-a effect on Liver
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acute phase protein release, mannose-binding lectin release, starts complement and opsonization
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IL-1, IL-6, TNF-a effect on Bone marrow
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neutrophil mobilization - phagocytosis
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IL-1, IL-6, TNF-a effect on hypothalamus
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increased body temperature, leads to decreased viral and bacterial replication
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IL-1, IL-6, TNF-a effect on fat/muscle
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protein and energy mobilization to generate increased body temp - decreased viral and bacterial replication
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Acute phase proteins
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c-reactive protein, fibrinogen, MBL, alpha1-antitrypsin, serum amyloid A
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C-reactive protein
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can activate the classical C' pathway (C4 -> C4a + C4b)
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Type I interferons
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inhibit viral replication and activate host-defense responses - induce resistance to viral replicaiton, increase expression of ligands for receptors on NK cells, activate NK cells to kill virus-infected cells
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MHC molecule
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present antigen after it has been processed - control T cell mediated immune responses - MHC class I binds to CD8 and TcR, MHC class II binds to CD4 and TcR
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CD8 T cell
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when it comes in contact with a virus infected cell that is expressing viral protein in its MHC, it will trigger death of tha tcell
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CD4 T cell (Th1)
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when it comes in contact with a macrophage that is presenting bacterial protein, it secretes cytokines and activates the macrophage. The activated macrophage secretes more cytokines and begins digesting its phagosomes.
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CD4 T cell (Th2)
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when it comes in contact with a B-cell expressing protein, it releases cytokines that activate the B cell into a plasma cell. The B cell releases its antibodies
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Regulatory T cell
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maintain tolerance to self-antigens and down-regulate autoimmune disease
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FcR
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cell surface receptors for the Fc regions of antibodies - found on phagocytes, APCs, mast cells and eosinophils - CRUCIAL for antibody mediated opsonization
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Avidity
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over strength of the combined binding sites (2x for IgG, 10x for IgM)
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VDJ recombinase
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catalyzes recombination of gene segments in B cells
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Affinity maturation
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affinity of antibodies for antigen increases with prolonged or repeated exposure to that antigen (occurs in germinal centers, B cells with the highest affinity have a selective advantage, only the best antibodies are produced)
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4 processes for antibody diversity
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multiple VDJ gene segments, multiple heavy and light chains, junctional diversity, somatic hypermutation
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how many possible combinations are there for antibodies?
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10^14
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features of IgG
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crosses placenta, neutralization
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features of IgM
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activation of complement
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features of IgA
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found in body secretions
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features of IgE
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sensitization of mast cells
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complement fixation
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when C3b is bound in conjunction with antibodies
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Live attenuated vaccines
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smallpox, measles, mumps, rubella
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Killed (whole organism) vaccines
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influenza, polio, rabies
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Subunit or recombinant vaccines
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Hep. A and b, H. influenza type b and S. pneumonia
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Toxoid vaccine
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tetanus, pertussis, diptheria
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passive immunization
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no new response, immediate protection, no memory, temporary, OCCURS NATURALLY WITH MATERNAL ANTIBODIES
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active immunization
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new immune response, delayed protection, memory, occurs naturally with infection
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benign tumor
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generally slow growing, remain localized, do not recur, do not become malignant
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malignant neoplasms
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anaplastic, rapidly growing, invasive, metastatic
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how to name a benign tumor
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add -oma at the end
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how to name malignant tumor of epithelium
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add -carcinoma
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how to name malignant tumors of mesenchymal origin
|
add - sarcoma at the end
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adenoma
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benign tumor of glandular epithelium
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polyploidy vs aneuploidy
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any growth that projects out from the surface of a mucosal epithelium
|
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papilloma
|
benign microscopic finger-like projections growing on any surface
|
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sarcoma
|
malignant tumor of connective tissue
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carcinoma
|
malignant tumor of the epithelial tissue
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teratoma
|
arise from gem cell layer - can differentiate into many forms
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choristoma
|
normal tissue, but present in an abnormal area
|
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hamartoma
|
normal tissue in the right area, but in abnormal quantity or arrangement
|
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pleomorphism
|
variability in size and shape of cells
|
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seeding
|
invasion of the body cavity - typical of ovarian cancer
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blood spread
|
veins are mostly penetrated, liver and lung are the common destinations, renal cell carcinoma, hepatocellular carcinoma
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lymphatic spread
|
more typical of carcinoma, follow lymphatic drainage, lung cancer to bronchial lymph node, breast cancer to axillary lymph node,
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sentinal node
|
first node in the line of drainage
|
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tumor invasion of ECM
|
detachment (loss of e-cadherin function), ECM degradation by proteases (MMPs, cathepsin D, uPA), attachment to novel EcM components, migration
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xeroderma pigmentosa
|
hyperpigmented skin lesion - autosomal recessive
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oncogenes
|
cause cancer when activated
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tumor suppressor genes
|
cause cancer when suppressed
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cachexia
|
loss of body fat/lean body mass, weakness, anemia, anorexia - caused by cytokines produced by tumor cells (TNF-a, IFN-gamma, IL-6) or by proteolysis inducing factor
|
|
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paraneoplastic syndrome
|
a disease or symptom that is the consequence of cancer but is not caused by the presence of cancer cells
|
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staging of cancer
|
used to evaluate the extent and the spread of the tumor - clinical, radiological or surgical examination - better than grading in clinically evaluating the tumor - based on size, extent of spread to LN and presence of metastasis, 0-IV
|
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grading of cancer
|
measure of how aggressive the tumors is - cytological examination - based on differention and number of mitosis, I-IV (higher - poorly differentiated, low = well differentiated)
|
|
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cytologic diagnosis
|
used for cancer of the cervix, uterus, lung, bladder, prostate and stomach
|
|
|
fine needle aspiration
|
used in palpable lesions - breast, thyroid, lymph nodes
|
|
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immunohistochemistry
|
confirms the tissue of origin of metastatic or poorly differentiated tumor - uses monoclonal antibodies
|
|
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PSA
|
marker for prostate cancer
|
|
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CEA
|
marker for GI cancer
|
|
|
a-feto protein
|
marker for hepatoceullular carcinoma
|
|
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Erb-2/HER2/Neu
|
receptor tyrosine kinase, inhibits apoptosis, gene amplificaiton of ErbB-2/HER2/Neu is found in breast cancer
|
|
|
Bcr-Abl
|
oncogene encoded on the philadelphia chromosome t(9;22), found in chronic myeloid leukemia, potent tyrosine kinase activity
|
|
|
Bcl-2
|
found in B-cell lymphoma, govern apoptosis (mitochondrial outer membrane permeability), caspase activity is no longer inhibited
|
|
|
Rb
|
retinoblastoma gene - deletions or mutations lead to retinoblastoma - eye cancer - cell cycle (G1-S) is no longer controlled
|
|
|
p53
|
endoes a transcription factor, mediates cell cycle, DNA repair, cell death, mutations or inactivations of p53 are found in 50% of all human cancers, p53 is a major suppressor that guards genome integrity
|
|
|
Wnt/B-catenin
|
wnt secretion results in the inactivation of APC, stabilization of b-catenin levels, transcription, and ultimately in "familial adenomatous polyposis)
|
|
|
HPV oncogenes
|
E6 - binds to and promotes degradation of p53 tumor suppressor. E7 binds to and inactivates Rb tumor suppressor
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