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262 Cards in this Set
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[Phamacokinetics] |
a range of plasma concentrations between a minimal effective concentration (MEC) and a minimal toxic concentration (MTC). |
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[Phamacokinetics]
Define MEC |
minimum effective concentration
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[Phamacokinetics]
Define MTC |
minimum toxic concentration
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[Phamacokinetics]
Define therapeutic drug monitoring |
Useful for: narrow therapeutic window drugs to ensure therapeutic effect & avoid toxicity |
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[Phamacokinetics] |
Most important factors in dosing:
–Half–life –Clearance –Volume of distribution |
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[Phamacokinetics]
Explain the concept of half–life |
Half–life = time required for 50% completion of a process
–index of: time–course for drug–elimination & drug–accumulation |
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[Phamacokinetics]
Describe the relationship between half–life & first–order processes |
rate of elimination is directly PROPORTIONAL to drug CONCENTRATION
– %drug / minute |
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[Phamacokinetics]
Describe the relationship between half–life & zero–order processes |
constant amount of drug is eliminated per unit of time regardless of drug concentration
– 10 mL / minute |
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[Phamacokinetics]
How many half–lives does it take to complete a process? |
~5
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[Phamacokinetics]
Recall the maximum clearance rates for a drug eliminated by hepatic clearance, renal tubular secretion, & glomerular |
Liver blood flow (1500mL/min)
Renal blood flow (660mL/min) Glomerular filtration rate (120–130mL/min) |
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[Phamacokinetics]
Factors Affecting Drug Half–Life |
aging (decr. muscle mass, decr. distribution)
obesity (increase adipose mass, increase distribution) Pathologic fluid (increase distribution) |
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[Phamacokinetics]
Explain the concept of clearance & its relationship to drug dose & steady–state drug plasma concentration |
–apparent volume of fluid completely cleared of drug per unit of time (by metabolism and/or excretion)
–it’s an index of how well a drug is removed irreversibly from circulation –quantitative measure of rate of removal of a substance from the body CLsystemic = Renal + Liver + other |
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[Phamacokinetics]
What can change a drugs clearance? |
P450 induction (increase CL)
P450 inhibition (decrease CL) Cardiac failure (decrease CL) Hepatic failure (decrease CL) Renal failure (decrease CL) |
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[Phamacokinetics]
Explain the concept of a loading dose |
a loading dose is the amount/concentration/dose of a drug that will force the drug into the tissues, quickly bringing the Vd into the therapeutic range.
Doseloading = Css * Vd Doseloading = [Css * Vd ] / Foral |
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[Phamacokinetics]
Explain the relationship between half–life, volume of distribution and clearance. Employ these relationships to predict the pharmacokinetics of a drug. |
t 1/2 = [ 0.693 * Vd ] / CL
(t1/2) is directly related to (VD) (t1/2) is inversely related to clearance (CL) (t1/2) is dependent on VD and CL |
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[Phamacokinetics]
Given the appropriate data, calculate a new dose or a new dose interval in an individual with decreasing renal or hepatic function. |
New Dose = [CLdiseased / CLnormal] * Maint. Dose
New Dose Interval = |
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[Phamacokinetics]
Discuss First–Order Kinetics |
constant fraction of drug in the body is eliminated per unit of time
–rate of elimination by metabolism or renal excretion is proportional to plasma drug concentration –*half life, clearance, and volume of distribution are independent of dose, and clearance rate for any drug is constant |
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[Phamacokinetics]
Discuss Zero–Order Kinetics |
–elimination rate is independent of drug concentration and constant per unit time
–a constant amount of drug is eliminated per unit time –implies the clearance mechanism(s) is saturated or capacity limited (metabolism by enzymes or transporter |
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[Phamacokinetics]
Explain what is meant by dose‑dependent kinetics and explain the clinical implications. Name three drugs eliminated by dose–dependent kinetics. |
Drug elimination is first order (fixed percentage of drug removed per unit time) at low concentrations; however, at high concentrations, enzymes for breaking down drug are saturated, and elimination becomes zero order (constant amount of drug removed per unit time)
–Clinical implications: A small increase in dosage can cause adverse effects. –Phenytoin, Ethanol (reaches saturation quickly), aspirin |
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[Intro to Viruses]
What are the basic structural organization of human viruses? |
– DNA or RNA genome (ss or ds)
– surrounding capsid composed of protein capsomeres – naked or w lipid envelope – shape: icosahedral, helical, complex |
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[Intro to Viruses]
Describe some of the general characteristics of viruses (general, extra) |
– infrequently fatal
– majority of infections are asymptomatic – obligate intracellular parasites – no synthetic machinery – only one type of genomic nucleic acid – Not alive, complex mobile genetic elements |
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[Intro to Viruses]
List Common DNA viruses |
HBV – Hepatitis B
HPV – human papilloma virus Parvovirus B19 Adenovirus Herpesviridae Polyomaviruses |
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[Intro to Viruses]
List common RNA viruses |
Influenza
RSV Parainfluenza Hepatitis A, C, D, E Enteroviruses Encephalitis viruses Measles, Mumps, Rubella Norwalk, Rotavirus Virtually Everything else :P |
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[Cultural Awareness]
Identify populations at risk for certain disease processes & cultural barriers |
Cancer screening & management Cardiovascular disease, diabetes, HIV infection/aids, Immunizations, Infant Mortality, Mental Health, Hepatitis, Syphilis, TB
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[Cultural Awareness]
Describe the six focus areas in which racial & ethnic minorities experience serious disparities in health access & outcomes |
Cancer screening & management
Cardiovascular Disease Diabetes HIV infection / Aids Immunizations |
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[Cultural Awareness]
Describe how cultural beliefs & behaviors can affect assessment of the patient & adherence to your treatment plan |
Communication
family relationships diet & nutrition health beliefs & practices |
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[Intro to Viruses]
Describe the classifications of viruses |
By Nucleic Acid: RNA/DNA, segmented or non–segmented, linear or circular, SS or DS, +/– sense mRNA,
envelope capsid replication strategy |
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[Intro to Viruses]
Describe the nature of viral replication |
–Attachment – viral attachment proteins connect w cellular receptors
–penetration/uncoating – retraction of receptors, capsid digestion –biosynthesis – cellular synthetic processes redirected, become viral specific –maturation – viral components assembled –release – virus extracellular |
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[Intro to Viruses]
Mechanisms of viral pathogenesis, including alternatives to cell distruction |
–cell destruction – lytic, inhibition of host DNA, RNA &/or protein synthesis; immune–mediated tissue damage
–transformation – cell transformation to oncogenic > cell division rate increases –latent or persistent – ocult, virus becomes dormant, can later become re–activated –cell fusion – to form multinucleated cells –latent infection – chronic carrier, latent, or slow virus |
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[Intro to Viruses]
Epidemiological considerations with respect to the transmission & dissemination of viral diseases |
Transmission, age, gender, ethnic background, country of origin, travel history, occupation, season, underlying medical conditions.
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[Intro to Viruses]
the role of the immune system in viral disease symptomatology & recovery from infection |
antigenic variation, some viruses encode receptors for various mediators of Immunity thus blocking their ability to interact with receptors on the virus, some viruses reduce expression of class I MHC proteins thus reducing ability of cytotoxic T–cells to kill the virus–infected cells, direct cell–to–cell propagation & attenuated virus
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[Fungal] |
over 100,000 species pathogenic
~175 cause disease in man ~30 common |
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[Fungal] |
lives on dead or decomposing matter, soil dwellers
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[Fungal] |
Fungi vs. Bacteria cell type - Eukaryotic vs. prokaryote Cell interactions - uni/multicellular, able to differentiate vs. unicellular Membrane - ergosterol, no cholesterol vs. no sterols Cell Wall - peptidomanna, glycan, chitin, cellulose, chitosan vs. peptidoglycan, teichoic acid, lipopolysaccharide Metabolism - heterotrophic only vs auto or heterotrophic Oxygen Requirements - aerobic, anaerobic, facultative vs aerobic only Reproduction - asexual (conidia), sexual (spores) vs asexual(fision) |
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[Fungal]
Describe the differences between molds, yeasts, & dimorphisms |
molds: multicellular, long–tubelike extensions of the cell wall, grow naturally in soil environments @ 25 deg–C |
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[Fungal] |
crosswalls separating nuclei in a tube–like chain of fungi
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[Fungal]
Describe fungal pathogenesis {think definition, not process} |
basic mechanism of fungal pathogenicity is the ability to adapt to tissue environment & temperature (body & fever range) & withstand the lytic activity of host cellular defenses
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[Fungal]
Describe the fungal characteristics that pertain to Adherence |
some fungal species, particularly yeasts are able to colonized the mucosal surfaces of the oral, GI, & female genital tract
species of Candida that adhere best to epithelial cells are most often isolated from infections – fungal "adhesins" |
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[Fungal]
Describe the fungal characteristics that pertain to Invasion |
generally, non–invasive.
some proteases, lipases, ketatinases facilitate colonization, tissue invasion |
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[Fungal]
Describe the fungal characteristics that pertain to Resistance to phagocytosis |
Most fungi are extremely susceptible to phagocytic killing. Pathogenic strains can often be shown to have increased anti–phagocytic properties
Histoplasma capsulatum in yeast form can multiply within macrophages |
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[Fungal]
Describe the fungal characteristics that pertain to Tissue Injury |
No exotoxins, endotoxins. Fungal metabolic products do not injure tissues directly. Tissue injury is most often a result of inflammation & immune responses to fungal presence
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[Fungal]
Describe the important methods available to aid in the diagnosis of fungal infections |
KOH digestion & microscopy
10% KOH Wood's lamp culture, visualization, carbohydrate assimilation test, Ag/Ab detection, PCR |
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[Fungal]
Clinical classification of medically relevant fungi |
Superficial – infections of the dead, superficial areas of the skin or hair shaft, no cellular response, cosmetic problems only
Cutaneous – living tissue is not invaded, organisms colonize the keratinized stratum corneum b/c of their keratinolytic ability > disease results from the host reaction to fungi metabolic products subcutaneous – usually requires implantation, adaptation of organisms to tissue environment requires relatively long periods of time systemic – agents that are inherently virulent and cause disease in healthy humans (acquired via respiratory tract) > requires significant exposure to fungal spores opportunistic – in patients with impaired host defenses or alterations in normal bacterial flora |
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[Parasites]
Define Definitive Host |
host in which the parasite reaches sexual maturity
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[Parasites]
Define Intermediate Host |
host in which asexual reproduction or larval development takes place
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[Parasites]
Define Vector |
transmitting agent, usually arthropod
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[Parasites]
Explain the difference between trophozoite & a cyst |
Trophozoite – metabolically active & motile stage of many protozoan parasites
Cyst – generally smaller & has an outer protective layer to enhance survival in the environment |
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[Parasites]
World–wide, how prevalent are infections caused by parasites |
Toxoplasmosis = 1–2 billion
Ascariasis = 1 billion Malaria = 200–300 million Schistosomiasis = 200–300 million Giardiasis = 200 million Trypanosomiasis = 15–20 millions |
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[Parasites]
Describe the probable roles of IgE antibody & eosinophils in combating parasitic infections |
IgE coats the parasite
Eosinophils will target, attack, & eat the parasite |
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[Parasites]
Describe clinical presentation & basic characteristics of Giardia infection |
–most common cause of parasitic gastroenteritis
–infection from ingestion of cysts –average incubation period of 10 days –attaches to intestinal mucosa & causes shortening of the villi, inflammation of crypts & lamina propria – diarrhea due to malabsorption –immune response –treatment – metronidazole |
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[Parasites]
Case Study! |
–Your patient is a 5–year–old female accompanied by her mother.
–The chief complaint is nausea, vomiting, and foul–smelling diarrhea for several days. –The mother states that the watery stool looks greasy. The child has had little appetite. –The patient attends a pre–school this year, and had been in day care since she was 2–years–old. –Physical exam reveals moderate epigastric tenderness. The child is slightly below normal weight. |
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[DS – Intro to Antimicrobial Pharm]
Describe bacteriostatic |
inhibits/stops growth & reproduction of bacteria but do not kill them
works with the immune system to remove organisms from the body *tetracycline |
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[DS – Intro to Antimicrobial Pharm]
Describe bactericidal |
kill bacteria
– interference w a process essential for life –useful with endocarditis, meningitis, & neutropenic cancer patients *PCN |
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[DS – Intro to Antimicrobial Pharm]
Describe Time–dependent killing |
killing effect is directly proportional to the amount of time the drug concentration at the site of infection is above the MIC of the organism
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[DS – Intro to Antimicrobial Pharm]
Define MIC |
minimum inhibitory concentration
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[DS – Intro to Antimicrobial Pharm]
Are beta–lactam antibiotics time or concentration dependent? |
time–dependent killers
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[DS – Intro to Antimicrobial Pharm]
Describe concentration dependent antibiotics |
bacterial kill increases with increasing levels of the drug
concentration is not important Aminoglycosides & fluoroquinlones |
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[DS – Intro to Antimicrobial Pharm]
Describe selective toxicity |
adversely affect only type of cell & spare normal human cells
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[DS – Intro to Antimicrobial Pharm]
What are the 5 MoA of antibiotics |
1. inhibition of cell wall synthesis
2. Disruption of cell membrane function 3. Inhibitors of protein synthesis 4. Inhibition of Nucleic Acid synthesis 5. Inhibition of synthesis of Essential Metabolites |
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[DS – Intro to Antimicrobial Pharm]
What antibiotics inhibit cell wall synthesis Names & targets |
b–lactam – targets TG
Vancomycin – targets TP Bacitracin – stop dephosphorylation of bactoprenol Cycloserine – stop the addition of d–ala fosfomycin – inhibit nam |
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[DS – Intro to Antimicrobial Pharm]
Beta–lactam antibiotics: names |
PCN
Cephalosporins Carbapenem Monobactams |
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[DS – Intro to Antimicrobial Pharm]
List the types of PCN |
Natural PCN – PCN G
Extended–Spectrum PCN – amoxicillin |
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[DS – Intro to Antimicrobial Pharm]
List the generations & specific names of the Cephalosporins |
1 – cephalexin
2 – cefoxitin 3 – ceftriaxone 4 – cefepime |
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[DS – Intro to Antimicrobial Pharm]
What are the benefits of the higher generation cephalosporins |
– increased ability to cross the BBB
– increased resistance to b–lactamases – increased activity vs. gram negative |
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[DS – Intro to Antimicrobial Pharm]
Carbapenem: names |
Imipenem
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[DS – Intro to Antimicrobial Pharm]
Monobactams: names |
Aztreonam
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[DS – Intro to Antimicrobial Pharm]
Describe the Beta–lactam ring, uses, makeup, & limits |
–consists of b–lactam bonds
–can be cleaved by b–lactamases – inhibits PBPs inducing cell wall bursting |
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[DS – Intro to Antimicrobial Pharm]
Names of antibiotics that disrupt cell membrane function |
–Cidal & concentration–dependent
Amphotericin Ketoconazole Polymyxin Daptomycin Amy Keeps Pooping D***it |
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[DS – Intro to Antimicrobial Pharm]
Target & Names of the antibiotics that inhibit the synthesis of essential metabolites |
Target: mostly folic acid
Trimethoprim sulfonamides > sulfamethoxazole |
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[DS – Intro to Antimicrobial Pharm]
Target & names of antibiotics that affect nucleic acid metabolism |
Bactericidal – * Fluoroquinolones – Ciproflaxin RNA Polymerase * Rifampin |
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[DS – Intro to Antimicrobial Pharm]
Names of antibiotics that inhibit bacterial protein synthesis |
Aminoglycosides – Gentamycin ******
Tetracyclines – Doxycyclin Macrolides – Erythromycin Chloramphenicol Clindamycin Mupirocin Streptogramins |
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[DS – Intro to Antimicrobial Pharm]
Attributes of antibiotics that inhibit bacterial protein synthesis |
Bacteriostatic (except AG=cidal)
target 30s/50s |
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[DS – Intro to Antimicrobial Pharm]
resistance factors for antibiotics that inhibit bacterial protein synthesis |
Microbial Enzymes > AGs, alter enzyme, reduce binding
Ribosome protection > tetracyclines & Macrolides= compete for or alter binding site Efflux pumps > Macrolides & Tetracyclines Update reduced > Cephalosporins Natural Selection – |
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[DS – Intro to Antimicrobial Pharm]
Define PBPs |
peptidoglycan binding proteins
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[DS – Microbial Genetics & Drug Res]
Discuss the misuses of antibiotics |
–Given when they are not needed (according to CDC up to 50% of antimicrobial use in hospitals are inappropriate) (Outpatient prescriptions are often unnecessary particularly when treating URI)
–Continued when they are no longer necessary –Given at the wrong dosage –Wrong antibiotic is used to treat the infection –In many countries antibiotics can be purchased over the counter which leads to even more indiscriminate use – Antibiotic use and misuse has led to incr. in selective pressure |
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[DS – Microbial Genetics & Drug Res]
List the ways bacteria can resist antibiotics |
–Degrade or alter antibiotic (splitting of the Beta–Lactam ring) (Modify aminoglycosides)
–Efflux Pump (Tetracycline) (Macrolides) –Uptake reduced (Cephalosporins) –Overproduction of target metabolic bypass (Sulfonamides) (Timethoprim) – produces enzymes that breakdown the drug – Alteration of target (Penicillin binding proteins “transpeptidases”: Beta–Lactams) (50S ribosomal subunit modified so that it still functions but macrolide can no longer bind) (DNA gyrase and topoisomerase interferes with fluoroquinolones) – Pathogens develop resistance through natural selection (When bacteria are exposed to an antibiotic, more susceptible organisms will be killed leaving behind the more resistant bacteria to grow and multiply) |
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[DS – Microbial Genetics & Drug Res]
Explain Spontaneous Mutations |
Despite effective repair systems, mistakes in normal replication occur about 1 per 10^6 & 10^9 cells
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[DS – Microbial Genetics & Drug Res]
Explain Induced Mutations |
caused by mutagens
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[DS – Microbial Genetics & Drug Res]
Explain Mutations resulting in antibiotic resistance |
May arise prior to or in the absence of selective pressure; most antibiotic resistance occurs by point mutations
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[DS – Microbial Genetics & Drug Res]
Explain point mutations: |
substitution, deletion, or change of nucleotide base sequence
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[DS – Microbial Genetics & Drug Res]
List three methods of intracellular DNA transfer |
Transformation
Transduction Conjugation |
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[DS – Microbial Genetics & Drug Res]
Explain Transformation |
direct uptake & incorporation of exogenous genetic material (exogenous DNA) from its surrounding & taken up through the cell membranes
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[DS – Microbial Genetics & Drug Res]
Explain Transduction |
transfer of genetic material from one bacterium to another by means of a bacteriophage (virus)
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[DS – Microbial Genetics & Drug Res]
Explain Conjugation ******** |
transfer of DNA between bacterial cells by direct cell to cell contact (sex pilus)
F+ to F– only = unidirectional |
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[DS – Microbial Genetics & Drug Res]
Explain the importance of R–plasmids |
Conjugative Resistance R–plasmids
found in many gram–negative bacteria Contain the "F" factor (replication & transfer Gene) Contains resistant genes often coding for multiple resistances |
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[DS – Microbial Genetics & Drug Res]
Explain Transposons |
Mobile Genetic Elements
–can move from place to place on the chromosomes & into/out of the plasmids –carry both insertion sequences plus other genes often those coding for resistances –if transposons insert into a functional gene, it will be destroyed = cell death transposons are biological mutagens |
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[Drug Metabolism]
4. Discuss the major pathways of Drug metabolism: Phase I only |
–add group to molecule (OH, SH, COOH, NH2) – more water soluble |
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[Drug Metabolism]
4. Discuss the major pathways of Drug metabolism: Phase II only |
–conjugation: endogenous substrate added to the drug by acetylation, sulfonation, or glucuronidation
–usually forms a highly polar, inactive metabolite that is excreted via kidneys –Phase 1 addition prep's the molecule for Phase 2 addition – large change in structure, biological activity, LS, etc |
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[Drug Metabolism]
5. Recall the basic types of Phase I metabolism |
Oxidations
Reductions Hydrolysis goal: add or change the molecule to make it more polar thus less LS & more water–soluble |
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[Drug Metabolism]
6. What are the top three CYP450s involved in drug metabolism in humans? |
CYP3A4
CYP2d6 CYP2c9 |
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[Drug Metabolism]
6. What food product inhibits intestinal CYP3A4 |
Grapefruit juice
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[Drug Metabolism]
6. Which transporter works in cooperation with CYP450s to limit systemic exposure to drugs |
P–glycoproteins
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[Drug Metabolism]
7. Recall the different types of Phase II metabolisms & discuss its role in drug elimination & excretion |
Glucuronidation, Acetylation, Sulfation
– attaches an endogenous substrate that usually increases the polarity, inactivates it, and makes it less LS |
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[Drug Metabolism]
8. Predict potential effects of a drug acting as an inducer or inhibitor of an enzyme that is responsible for the metabolism of another drug. |
Induction: cause an increase in the expression of an enzyme, increasing the speed at which a SPECIFIC drug is metabolized and removed from the body.
Inhibitor: cause the suppression of the enzymes that metabolize a SPECIFIC drug, increasing the time the drug stays in the body. |
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[Drug Metabolism]
consequences of drug metabolism |
1. less lipid soluble, now kidney can excrete it
2. less stored in fat 3. more water soluble 4. more ionized at physiological pH 5. less bound to plasma proteins 6. less able to penetrate cell membranes 7. more readily excreted in urine by the kidneys |
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[Drug Metabolism]
general characteristics of drug metabolites |
1. more water soluble
2. more easily excreted by kidneys 3. frequently inactivates a drug (inactivated by liver) 4. metabolism MAY activate a drug (bioactivation) 5. Prodrug concept à prodrug (precursor) is not active, metabolite is active may have no, <, =, or > pharmacological activity than parent drug can sometimes be toxic |
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[Drug Metabolism]
Explain the functional importance of drug metabolism as it relates to the elimination and excretion of drugs |
1. Biotransformation makes drugs more lipid soluble, more water soluble, more ionized, less bound to plasma proteins, etc (see above). This allows the metabolites to be more easily eliminated and excreted through the kidneys.
2. Significance of metabolism: Termination of a drug's pharmacological effect(s) & enhancement of its excretion. This allows intermediates to become polar, non–toxic, metabolites which can then be excreted. |
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[Drug Metabolism]
Discuss the role of metabolism in acetaminophen toxicity |
Metabolism allows acetaminophen to be turned into non–toxic metabolites. The major pathway (95%, phase 2) uses glucoronidation & sulfation to create inactive, non–toxic metabolites, which can then be excreted in the urine. The minor pathway (5%, phase creates reactive toxic intermediates, but these can be neutralized into non–toxic metabolites through glutathione conjugation.
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[Drug Metabolism]
Describe the implications of an intermediary drug metabolite being more reactive than the parent compound |
1. the reactive toxic intermediates are actually more reactive than the parent compound (acetaminophen) so the MUST be converted to non–toxic metabolites in order for them to be excreted
2. glutathione conjugation converts the toxic metabolites to the non–toxic form 3. happens when there is more drug present than the metabolic enzymes can handle 4. enzymes become saturated in the major pathway (phase 2) and so excess drug is metabolized by the minor pathway (CYP450 enzyme) 5. in this case the glutathione becomes depleted à drug cannot be converted to non–toxic metabolite so the toxic metabolic becomes reactive à hepatotoxicity cellular necrosis |
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[Drug Metabolism]
Discuss Phase I of drug metabolism |
1. adds hydroxyl (OH) or some other group (SH, COOH, NH2)
2. more polar means more H2O soluble 3. if polar enough, may be excreted 4. many phase I products not eliminated rapidly 5. metabolites may be inactive 6. over ½ of all drugs are metabolized by a group of P450 enzymes 7. usually prepares a molecule for phase II 8. usually produces minor changes in chemical structure, LS, and biological activity |
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[Drug Metabolism]
Discuss Phase II of drug metabolism |
1. conjugation an adds "something" to the drug; big water soluble drugs
2. glucuronic acid, sulfate, glutathione, acetyl groups 3. usually forms a highly polar, inactive metabolite that is renal excreted 4. Phase I metabolite may be needed as a substrate for phase II metabolism 5. Glucuronidation – hooks glucuronite groups; most important 6. Acetylation 7. Glutathione conjugation 8. Glycine conjugation 9. Methylation 10. produce large changes in structure, biological activity and LS (big decreases) |
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[Intro to Metabolism]
2. Describe the relationship between oxygen consumption & resting metabolic rate |
–the amount of oxygen intake can be used to estimate metabolic rate
–measurement of the amount of energy needed to maintain normal function –because energy prod. requires O2, oxygen consumption can be measured & used to estimate RMR/BMR higher intake = higher Metabolic Rate |
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[Intro to Metabolism]
List the 3 phases in aerobic respiration |
Phase 1: oxide fuels
Phase 2: Make ATP Phase 3: Use ATP |
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[Intro to Metabolism]
Describe Phase 1 of aerobic respirations |
turn everything into acetyl CoA
Oxidize acetyl CoA in the TCA fuels oxidized to CO2 NAD & FAD reduced to NADH / FADH2 |
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[Intro to Metabolism]
Describe Phase 2 of Aerobic Respiration |
Oxidative Phosphorylation
– make ATP through the electron transport chain – uses oxygen as the final electron acceptor – FADH2 & NADH are re–oxidized back to FAD / NAD |
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[Intro to Metabolism]
Describe Phase 3 of Aerobic Respiration |
Using ATP will generate ADP
cycle starts over |
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[Intro to Metabolism]
1. Cellular carriers of Energy |
ATP – Adenine Triphosphate
GTP – Guanine Triphosphate CTP – Creatine Triphosphate UTP – Uridine triphosphate |
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[Intro to Metabolism]
Glycolysis Explain why the pathway exists & in which tissues it occurs |
Pathway: glucose ––> pyruvate + 2 ATP
Where: RBCs only use glucose for energy – (no mitochondria) Brain doesn't absorb lactate (unless forced) so will always use glucose & ketones – (if forced w extended fasting) |
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[Intro to Metabolism]
TCA Cycle Explain why the pathway exists & in which tissues it occurs |
(aerobic respiration phase 1)
pathway: acetyl CoA converted to CO2, H2O, ATP |
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[Intro to Metabolism]
Oxidative phosphorylation Explain why the pathway exists & in which tissues it occurs |
(aerobic respiration phase 2)
pathway: makes ATP through the electron transport chain, FADH2 & NADH donate electrons to the process – depends on oxygen Where: inside the mitochondria |
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[Intro to Metabolism]
Fatty Acid synthesis Explain why the pathway exists & in which tissues it occurs |
pathway: acetyl CoA –––> Fatty acids
– NADPH oxidized to NADP – pentose phosphate pathway reduces NADP to NADPH Where: Liver |
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[Intro to Metabolism]
Triglyceride synthesis Explain why the pathway exists & in which tissues it occurs |
pathway: fatty acids ––> triglycerides
where: made in the liver, transported to the adipose via lipoproteins – Dietary triglycerides are transported via chylomicrons |
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[Intro to Metabolism]
Lipolysis Explain why the pathway exists & in which tissues it occurs |
pathway: triacylglycerols broken down into fatty acids & glycerols
– glycerol goes right into gluconeogenesis Where: adipose tissues |
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[Intro to Metabolism]
Beta–oxidation Explain why the pathway exists & in which tissues it occurs |
pathway: fatty acids (oxidized) ––> acetyl CoA
– NADH & FADH2 are generated where: muscle, liver, & "other tissues" |
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[Intro to Metabolism]
Gluconeogenesis Explain why the pathway exists & in which tissues it occurs |
pathway: converting lactate, certain amino acids, or glycerol into glucose
– glycerol comes straight from lypolysis where: – liver (during fasting state) – kidneys (slight) |
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[Intro to Metabolism]
6. Explain the difference between aerobic & anaerobic metabolism |
Aerobic metabolism: oxygen is available as the final electron acceptor
– acetyl CoA is used in the TCA cycle to produce ATP, CO2, H2O Anaerobic metabolism: occurs where no O2 available. Pyruvate is converted to lactate – cannot generate acetyl CoA, thus no TCA (no oxidative phosphorylation) – primary metabolism of RBCs |
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|
[Intro to Metabolism]
6. Describe the uses of lactate in the fed & fasted states |
Fasting: lactate is the product of glycolysis in RBC's & exercising muscles
Fed: RBCs primary metabolism is glycolysis whose result is lactate. |
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|
[Intro to Metabolism]
7. Indicate the metabolic process that will provide the cell with the energy during Fed & Fasted states. Red Blood Cells |
Fed: glycolysis
Fasted: glycolysis still – only method available to RBCs |
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|
[Intro to Metabolism]
7. Indicate the metabolic process that will provide the cell with the energy during Fed & Fasted states. Adipose Cells |
Fed: glycolysis
Fasted: lipolysis |
|
|
[Intro to Metabolism] |
Fed: glycolysis, TCA, Oxydative Phosphorylation
Fasted: if extended: ketogenesis + whatever stores of glucose can be produced |
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|
[Intro to Metabolism]
7. Indicate the metabolic process that will provide the cell with the energy during Fed & Fasted states. Muscle Cells |
Fed: glycolysis (glucose = lactate)
Fasted: glycogenolysis + ketones |
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|
[Intro to Metabolism]
7. Indicate the metabolic process that will provide the cell with the energy during Fed & Fasted states. Liver Cells |
Fed: glycolysis
Fasted: B–oxidation, Amino Acids |
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[Intro to Metabolism]
8. Explain how the liver works with the other systems to maintain homeostatic blood glucose during a prolonged fast. |
– continues to convert fatty acids to ketone bodies
– since the brain continues to use a limited amount of glucose, the liver needs to produce less glucose per hour during prolonged fasting than during shorter periods of fasting. – because the stores of glycogen in the liver are depleted by ~30 hours of fasting, gluconeogenesis is the only process by which the liver can supply glucose to the blood |
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[Intro to Metabolism]
8. Explain how the Adipose Tissue works with the other systems to maintain homeostatic blood glucose during a prolonged fast. |
– as blood insulin decreases or blood glucagon increases, adipose triacylglycerols are mobilized by lipolysis
– most fatty acids cannot provide carbon for gluconeogenesis ––> fatty acids serve as a fuel for muscle, kidney, & most other tissues and are oxidized to acetyl CoA & subsequently to CO2, H2O in the TCA cycle – supplies the blood with its major source of fuel via the glycerol portion of the triglyceride |
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[Intro to Metabolism]
8. Explain how the RBCs works with the other systems to maintain homeostatic blood glucose during a prolonged fast. |
transfer lactate to the blood so that it can be reconverted back to glucose
|
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[Intro to Metabolism]
8. Explain how the Muscle works with the other systems to maintain homeostatic blood glucose during a prolonged fast. |
– breakdown proteins to amino acids = transferred back to the liver to produce glucose
– acetyl CoA used in TCA cycle to generate ATP, CO2, H2O – muscle use of ketones decreases – brain use of ketones increases – brain use of glucose decreases – liver gluconeogenesis decreases – muscle protein degradation decreases – liver production of urea decreases |
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[DS – Metabolism]
1. What metabolic processes is insulin going to stimulate? |
Insulin: increases the breakdown of glucose when blood glucose levels are high
Stimulates: glycolysis, TCA cycle, Oxidative Phosphorylation, Triglyceride Synthesis, Glycogenesis, Fatty Acid Synthesis |
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[DS – Metabolism]
1. What metabolic processes is glucagon going to stimulate? |
Glucagon: increases during the fasted state, signals the liver to utilize shared carbohydrates to release glucose into circulation. Signals adipose to degrade triacylglycerols into fatty acids(energy via b–oxydation) & glycerol(gluconeogenesis)
Stimulates: TCA Cycle, Oxidative Phosphorylation, Lipolysis, Beta–oxidation, gluconeogenesis, glycogenolysis |
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[DS – Metabolism]
2. Name the primary regulator of insulin |
Pancreas in response to a high–carbohydrate meal / serum glucose concentration
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[DS – Metabolism]
2. Describe the mechanism through which the release of insulin occurs |
–insulin is rapidly removed from circulation & degraded by the liver, so blood insulin levels decrease rapidly once the rate of secretion slows.
–neural signals from ANS help to coordinate insulin release with the secretory signals initiated by the ingestion of fuels – certain amino acids can stimulate insulin secretion – gut hormones in response to food intake can aid in onset of insulin release –epinephrine decreases the release of insulin |
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[DS – Metabolism]
2. Name the primary regulator of glucagon |
suppressed by insulin & glucose
|
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[DS – Metabolism]
2. Describe the mechanism through which the release of glucagon occurs |
– certain hormones stimulate glucagon secretion (cortisol & epinephrine)
– many amino acids also stimulate glucagon release |
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[DS – Metabolism]
4. Describe the effects of epinephrine on energy metabolism [big picture] |
–mobilize fuels during acute stress
–stimulate glucose production from glycogen |
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[DS – Metabolism]
4. Describe the effects of cortisol on energy metabolism [big picture] |
– provides for changing requirements over the long term
–stimulates glucagon secretion –stimulates amino acid mobilization from muscle protein –stimulates gluconeogensis –stimulates fatty acid release from adipose tissues |
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[DS – Metabolism]
5. What class of receptor/signal transduction pathway does Glucagon exert its effect. |
* binds to GPCRs to stimulate synthesis of cAMP
–activates glucose production from glycogen in the liver but not in the skeletal muscles –glucagon–stimulated phosphorylation of enzymes simultaneously activates gl;ycogen degradation, inhibits glycogen synthesis, & inhibits glycolysis in the liver |
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[DS – Metabolism]
5. What class of receptor/signal transduction pathway does Insulin exert its effect. |
* uses tyrosine–kinase receptors for signal transduction
–reverses glucagon–stimulated phosphorylation –stimulates the phosphorylation of several enzymes –induces & represses the synthesis of specific enzymes –acts as a growth factor & has general stimulatory effects on protein synthesis –stimulates glucose & amino acid transport into cells |
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[DS – Metabolism]
5. What class of receptor/signal transduction pathway does Cortisol exert its effect. |
* bind intracellular receptors or binding proteins
– move to the nucleus & interact with chromatin – change the rate of gene transcription on the target cell –stress hormone |
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[DS – Metabolism]
5. What class of receptor/signal transduction pathway does NE/Epi exert its effect. |
* act as neurotransmitter or hormone
– bind to adrenergic receptors – work through the cAMP system (GPCRs) |
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[DS – Metabolism]
6. Which hormone would be secreted during: An Overnight Fast |
Decreased insulin
increased glucagon |
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[DS – Metabolism]
6. Which hormone would be secreted during: Prolonged Starvation |
Decreased insulin
increased glucagon |
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[DS – Metabolism]
6. Which hormone would be secreted during: Exercise |
increased glucagon
|
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[DS – Metabolism]
6. Which hormone would be secreted during: Surgery, trauma, or severe infection |
increased Cortisol
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[DS – Metabolism] |
increased insulin
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[DS – Metabolism]
6. Which hormone would be secreted during: A protein rich meal |
increased insulin
|
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[DS – Metabolism]
6. Which hormone would be secreted during: a "fight or flight" situation |
epinephrine
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[Intro to Metabolism]
What is the main anabolic hormone? |
Insulin
|
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[Intro to Metabolism]
Which is considered the "fasted state" hormone? |
Glucagon
|
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[Intro to Metabolism]
How many days (about) before the brain begins to utilize Ketones & whatever glucose is available? |
~4 days
|
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[Intro to Metabolism]
When will the liver produce Ketones? |
only when fasted & only when there is excess acetyl CoA
|
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[Intro to Metabolism]
This is an important source of Amino Acids during the fasted state |
Skeletal Muscle
|
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[Intro to Metabolism]
What systems can export glucose into the blood stream? |
Liver [& kidney]
|
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[Intro to Metabolism]
The pathway that reduces NADP back to NADPH |
Pentose Phosphate Pathway
|
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[Intro to Metabolism]
Are important for energy storage & the transport of dietary fat |
Triglycerides
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[Intro to Metabolism]
What tissues can make glycogen? |
liver
muscles * all tissues in very small quantities |
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[Intro to Metabolism]
What tissues can make fatty acids |
Liver
* a little in the adipose tissue |
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[Intro to Metabolism]
What tissues are only capable of using glucose |
Red Blood Cells
Brain (until starvation, then Ketones + glucose) |
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[Intro to Metabolism]
Oxidative phosphorylation requires these: |
Mitochondria & Oxygen
|
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[Intro to Metabolism]
The end result of metabolism without oxygen |
Lactate
|
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[Intro to Metabolism]
Glucose can be metabolized into: |
glucose–6–p
|
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[Intro to Metabolism]
Glucose–6–p can be metabolized into: |
Glucose
Glycogen (glycogenesis) Pyruvate (glycolysis) Reduces NADPH via PPP |
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[Intro to Metabolism]
What is the function of the pentose phosphate pathway |
recycle NADPH
|
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[Intro to Metabolism]
Glycogen can be metabolized into: |
glucose–6–p (glycogenolysis)
|
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[Intro to Metabolism]
Pyruvate can be metabolized into: |
Glucose–6–p (gluconeogenesis)
Lactate Acetyl CoA |
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|
[Intro to Metabolism]
Lactate can be metabolized into: |
Pyruvate
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[Intro to Metabolism]
Amino Acids can be metabolized into: |
Pyruvate
Acetyl CoA |
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[Intro to Metabolism]
Ethanol can be metabolized into: |
Acetyl CoA
|
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[Intro to Metabolism]
Triacylglycerols can be metabolized into: |
Fatty Acids [lipolysis] (+ glycerols)
|
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|
[Intro to Metabolism]
Fatty Acids can be metabolized into: |
Triacylglycerols (synthesis w glycerol)
Acetyl CoA (B–Oxidation) |
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[Intro to Metabolism]
Ketones can be metabolized into: |
Acetyl CoA
|
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[Intro to Metabolism]
Acetyl CoA can be metabolized into: |
Fatty Acids (Fatty Acid Synthesis)
Ketones utilized by TCA cycle to Oxidative phosphorylation |
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|
[Intro to Metabolism]
Describe RMR |
– Resting Metabolic Rate
– measurement of the amount of energy needed to maintain normal function – energy production requires Oxygen, thus Oxygen can be measured to calculate RMR/BMR |
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[Intro to Metabolism]
Define Digestion |
breaking food down into absorbable components
|
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[Intro to Metabolism]
Define Absorption |
transfer of digested components from the gut to the blood
|
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[Intro to Metabolism]
Define Metabolism |
What happens after the molecule has been absorbed
|
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[DS – Byproducts of Metabolism]
Describe the benefits of lactate and ketone production |
lactate can be used for energy or in gluconeogenesis. Ketones can be used as a source of fuel and is a normal production by the liver.
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[DS – Byproducts of Metabolism]
Recall that amino acid catabolism generates ammonia and name the process through which the ammonia is detoxified and eliminated. Name the organ in which this occurs |
the ammonia is turned into urea in a process called the urea cycle which occurs primarily in the liver
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[DS – Byproducts of Metabolism]
Interpret BUN lab results |
urea in the blood is measured by blood urea nitrogen (BUN)
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[DS – Byproducts of Metabolism]
Describe the importance of the glutathione peroxidase system in neutralizing reactive oxygen species including the role of NADPH and the pentose phosphate pathway |
it neutralizes ROS by acting as a reducing agent in a process catalyzed by glutathione peroxidase. NADPH is an electron donor used to regenerate reduced glutathione which can then neutralize another molecule of peroxide. Pentose phosphate pathway is the ONLY pathway that can produce NADPH in red blood cells.
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[DS – Byproducts of Metabolism]
Define the term methemoglobin and explain the roles of the glutathione peroxidase system and methemoglobin reductase in preventing it from forming and regenerating ferrous hemoglobin |
Methemoglobin is when the iron in heme is oxidized from its ferrous (Fe2+) to its ferric state (Fe3+). Methemoglobin reductase uses NADH to re–reduce the heme iron back into the ferrous state.
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[DS – Byproducts of Metabolism]
Explain how bilirubin is eliminated and interpret bilirubin lab results |
Bilirubin will travel to the liver on albumin and once it's there, the liver will convert it to bilirubin diglucuronide via an enzyme called glucuronyl transferase. It will then be excreted in the bile. Bilirubin diglucuronide is called conjugated bilirubin because it has been conjugated to something else. Indirect bilirubin is not conjugated and if there is a problem with the bile duct then the excess bilirubin will go into the blood.
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[DS – Byproducts of Metabolism]
Alanine and aspartate aminotransferase (ALT and AST) |
Enzymes that are important for amino acid and nitrogen metabolism. Present at high concentrations in the liver.
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[DS – Byproducts of Metabolism]
Alkaline phosphatase |
disorders affecting the bile duct can result in elevated serum levels of this enzyme
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[DS – Byproducts of Metabolism]
Bilirubin (direct and indirect) |
if a bile duct is blocked then you will find bilirubin in the blood and indirect bilirubin would be elevated if you have a genetic defect in glucuronyl transferase or if the liver is damaged
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[DS – Byproducts of Metabolism]
Albumin |
albumin is produced by the liver, it will often be present at reduced amounts in patients with suboptimal liver function
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[Intro to Bacteria I & II]
Nucleoid |
Bacterial chromosome of coiled DNA (~2000–4000 genes)
|
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[Intro to Bacteria I & II]
Plasmid |
Smaller circle of DNA
Carries genes for antibiotic resistance, toxin production, etc. ~5–100 genes |
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[Intro to Bacteria I & II]
Cytoplasm |
PACKED with ribosomes (most: polysomes)
Ribosomes (50S and 30S) are sites for some antibiotics Also has Inclusion Bodies (storage granules and gas vacuoles) |
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[Intro to Bacteria I & II]
Cytoplasmic Membrane |
Osmotic barrier
Specific transport (nutrients) generates ATP through respiration Senses environmental changes |
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[Intro to Bacteria I & II]
Cell Wall |
Peptidoglycan (aka murien)
Site for lysozyme (tears) Synthesis is site for many antibiotics Strength and shape to the cell |
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[Intro to Bacteria I & II]
Outer Membrane |
Gram Negative ONLY
Contain Porins (entry of nutrient molecules) Lipoprotein (anchors outer membrane to cell wall) Composed of Lipopolysaccharides (specific O–side chain, core polysaccharide) |
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[Intro to Bacteria I & II]
Periplasmic Space |
Space between outer and inner membrane
Gel contains loose network of murien ("cell wall") Hydrolytic and degradative enzymes Other enzymes involved in peptidoglycan synthesis, nullification of toxins, etc. |
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[Intro to Bacteria I & II]
Cell Envelope |
Entire outer complex (cell wall, inner and outer membranes)
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[Intro to Bacteria I & II]
Bacterial Capsule |
aka Glycocalyx
Composed of polysaccharides Viscous, fibrous matrix Antiphagocytic *Encapsulated bacteria = smooth, nonencapsulated = rough |
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[Intro to Bacteria I & II]
Pili (fimbriae) |
Responsible for attachment to specific cell types (e.g. Streptococcus to throat cells)
Used in sexual genetic transfer |
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[Intro to Bacteria I & II]
Flagella |
Motility via proton motive force
Long helical filament, flexible hook, basal body Spins counterclockwise (straight); clockwise (tumbles) |
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[Intro to Bacteria I & II]
Spores |
Metabolically inactive bacteria
Survive literally almost everything |
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[Intro to Bacteria I & II]
Gram + |
Thick peptidoglycan layer over cell membrane
|
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[Intro to Bacteria I & II]
Gram – |
Outer membrane, thin peptodiglycan layer, inner membrane
|
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|
[Intro to Bacteria I & II]
Difference between prokaryotes and eukaryotes? |
Eukaryotes have membrane–bound organelles; prokaryotes do not
|
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[Intro to Bacteria I & II]
Main targets for antimicrobial activity |
Cytoplasm
Peptidoglycan cell wall |
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[Intro to Bacteria I & II]
Symbiosis |
An association between two organisms that live together
|
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[Intro to Bacteria I & II]
Mutualism |
Mutually beneficial association
|
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[Intro to Bacteria I & II]
Commensalism |
One organism benefits, but neither is harmed
|
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[Intro to Bacteria I & II]
Parasitism |
One organism benefits at the expense of the other
|
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[Intro to Bacteria I & II]
Actions of normal human flora |
–Occupy tissue receptors
–Antagonize other bacteria (bacteriocins) –Synthesize vitamins and growth factors (B complex, K, E) –Help assimilate ruffage from glycosidase production –metabolize cholesterol and bile acids –Stimulate proliferation of Gut–Associated Lymphoid Tissue (GALT) |
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[Intro to Bacteria I & II]
athogenicity |
Ability to inflict damage
|
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|
[Intro to Bacteria I & II]
Invasiveness |
–Colonization
–Ability to bypass or overcome host defenses –Production of extracellular substances that facilitate invasion |
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|
[Intro to Bacteria I & II]
Toxigenesis |
–Soluble
–Transported by blood and lymph –Cause cytotoxic effects at tissue sites |
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|
[Intro to Bacteria I & II]
Gram + Cocci |
–Staphylococcus
–Streptococcus |
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|
[Intro to Bacteria I & II]
Gram + Rods |
–Corynebacteria
–Bacillus –Listeria |
|
|
[Intro to Bacteria I & II]
Gram + Spiral |
None! HAHAHAHAHA
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|
[Intro to Bacteria I & II]
Gram – Spiral |
–Treponoma
–Borrelia |
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|
[Intro to Bacteria I & II]
Gram – Rods |
–Pseudomonas
–E. coli –Haemophilus –Bacteroides |
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|
[Intro to Bacteria I & II]
Gram – Cocci |
Neisseria
|
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|
[Intro to Bacteria I & II]
Acid Fast Organisms |
Mycobacteria
|
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|
[Intro to Bacteria I & II]
Intracellular (obligate parasites) |
–Chlamydia
–Rickettsia |
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|
[Intro to Bacteria I & II]
Wall–less |
–Mycoplasma
|
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[Intro to Bacteria I & II]
Bacterial Metabolism |
–HIGHLY efficient
–Building blocks synthesized in amounts proportional to the needs of making macromolecules –Toxic intermediates don't accumulate –Optimal levels of enzymes and cellular organelles are available –Unnecessary enzymes are not made –Cell senses and responds to environment –Cell grows at maximum growth rate allowed by environmental conditions |
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[Intro to Bacteria I & II]
How is Proton Motive Force (pmf) generated? |
Reducing power (ability to donate electrons) forces electrons to pass through Electron Transport Chain located in cytoplasmic membrane; protons are ejected, forming a concentration gradient of protons known as the proton motive force (pmf) (respiration)
Pmf is used for cellular work |
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[Intro to Bacteria I & II]
How is ATP generated? Substrate level phosphorylation |
A phosphorylated intermediate is converted to a high energy phosphate bond, which reacts with ADP to produce ATP
|
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|
[Intro to Bacteria I & II]
How is ATP generated? Chemiosmosis |
Pmf drives protons back into cell through ATPase generating ATP from ADP
|
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|
[Intro to Bacteria I & II]
What happens when reducing power is in short supply? |
ATP is hydrolyzed to ADP, expelling protons from the cell and creates pmf, driving electrons in opposite direction along ETC.
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|
[Intro to Bacteria I & II]
Nutrient energy mechanisms |
–Active transport
–Group translocation (phosphorylation)–most common –Facilitated diffusion (metabolism of nutrients)– less common |
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[Intro to Bacteria I & II]
Binary Fission |
–Cell grows to twice their size
–Divide by binary fusion –Begins at origin and proceeds in both directions –Takes ~40 mins at 37 degrees C –In culture doubling every 20 mins, DNA replication must initiate every 20 mins –Multifork replication used to accomplish this (already beginning second replication as first is completed) |
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[Intro to Bacteria I & II]
Phases of growth in bacteria |
–Lag: Senses the environment and makes enzymes necessary to start growth
–Exponential: (log) rapid growth occurs –Stationary: Growth halts as resources are used up from the environment –Death: (log) |
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[Intro to Bacteria I & II]
Nutrition Requirements |
–ALL cells are heterotrophic: need performed hydrocarbons like sugars in order to grow (gets from host)
–Some (ex E.coli) need only inorganic salts and a nitrogen source –Others (streptococcus) require more complex media (vitamins, amino acids, purines, etc.) –Others require VERY enriched medium––Fastidious |
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[Intro to Bacteria I & II]
Oxygen requirements Strict Anaerobes |
–Neisseria or Pseudomonas
–Respiration occurs via electron transport chain, with Oxygen as final e acceptor –Cytochrome oxidase enzyme |
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[Intro to Bacteria I & II]
Oxygen requirements Obligate anaerobes |
–Clostridium
–Only grow in absence of CO2 –Fermentation: terminal e acceptor is an organic metabolic intermediate –> organic acids (lactic acids) –Usually lack superoxide dismutase, catalase, Catalast, and peroxidase |
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|
[Intro to Bacteria I & II]
Oxygen requirements Facultative |
–E. coli (most pathogenic bacteria)
–Bacteria grow aerobically in presence of oxygen, anaerobically in absence |
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|
[Intro to Bacteria I & II]
Oxygen requirements Aerotolerant |
–tolerate oxygen, but grow fermentatively
|
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|
[Intro to Bacteria I & II]
Iron Uptake |
–Necessary for bacterial growth
–Free iron scarce in blood and tissue––bound –Bacteria create siderophores: iron chelating compounds |
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|
[Intro to Bacteria I & II]
Difference between fermentation and aerobic respiration |
Ferm: w/o O
Aerobic: w/ O |
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|
[Intro to Bacteria I & II]
Steps in Peptidoglycan synthesis |
1. Uridine diphosphate (UDP) carrier activates N–acetylmuranic acid (NAM) and N–acetylglucosame (NAG)
2. Pentapeptide added to UDP–NAM 3. UDP–NAM–PEP transfers to bactroprenol phosphate 4. UDP–NAG added to UDP–NAM–PEP (peptidoglycan monomer) 5. bactroprenol phosphate transports monomer through cell membrane 6. Autolysins break glycosidic bond b/w peptidoglycan and peptide cross–linkages of existing cell wall 7. Transglycosidase (TG) enzyme inserts and links monomers into new ppg 8. Transpeptidases (TP) reform peptide cross–links |
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|
[Intro to Bacteria I & II]
Fosfomycin |
Inhibits phosphoenopyruvate transferase; prevents formation of NAM
|
|
|
[Intro to Bacteria I & II]
Cycloserine |
Analogue of D–ala; blocks addition of dipeptide to UDP–NAM
|
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|
[Intro to Bacteria I & II]
Bacitracin |
Blocks dephosphorylation of bactroprenol phosphate (prevents transport of ppg monomer across cell membrane
|
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|
[Intro to Bacteria I & II]
Vancomycin: |
binds to peptides of ppg monomers and blocks (TG)
|
|
|
[Intro to Bacteria I & II]
Beta–lactams |
–Penicillins, Cephalosporins, Carbepenems
–bind to TP |
|
|
[Intro to Bacteria I & II]
Linezolid |
Blocks initiating complex (translation)
–30S inhibitors: –Tetracycline, Aminoglycosides –50S inhibitors: –Macrolides, Chloramphenicol |
|
|
[Intro to Bacteria I & II]
Fluoroquinolones |
Inhibits DNA gyrase or topoisomerase
|
|
|
[Intro to Bacteria I & II]
Metronidazole |
Disrupts DNA helical structure under anaerobic conditions
|
|
|
[Intro to Bacteria I & II]
Rifampin |
Binds to RNA polymerase
|
|
|
[Intro to Bacteria I & II]
Sulfonamides |
Blocks synthesis of dihydropteroic acid
|
|
|
[Intro to Bacteria I & II]
Trimethoprim |
Blocks synthesis of tetrahydrofolate
|
|
|
[Intro to Bacteria I & II]
Polymyxins |
Interact with with phospholipids
|
|
|
Name the 4 major dietary sources of fuel
|
Carbohydrates
Fats Proteins ? unknown, clarify |
|
|
Explain: Catabolism vs. Anabolism
|
Catabolism: breaking down for energy
Anabolism: constructing a molecule, requires |
|
|
Monosaccharides
|
Glucose
Galactose Fructose |
|
|
Disaccharides
|
Lactose
Maltose Sucrose |
|
|
Sucrose is made up of what saccharides
|
glucose + fructose
|
|
|
Maltose is made up of what saccharides
|
glucose + glucose
|
|
|
Lactose is made up of what saccharides
|
glucose + galactose
|
|
|
Polysaccharides
|
Cellulose
Hemicelluloses Pectin beta–glucans Fructans |
|
|
The portion of the reducing sugar that is oxidized in a cupric compound
|
Aldehyde group
|
|
|
What color will the glucose or galactose oxidase tests turn in the presence of a reducing sugar?
|
Blue
|
|
|
What is the difference between an unsaturated & polyunsaturated fatty acid?
|
1 double bond vs. >1 double bond
|
|
|
Results from partial hydrogenation of vegetable oils
|
trans
|
|
|
Most abundant double bond arrangement in fatty acids
|
CIS
|
|
|
used to make vegetable oils more solid at room temperature
|
hydrogenation
|
|
|
structure of triglycerides
|
3 fatty acids
one glycerol |
|
|
Importance of Triglycerides
|
energy storage
transport of dietary fats |
|
|
Three main body fuel stores
|
proteins |
