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MicroPath Final
MicroBiology and Pathophysiology
| Question | Answer |
|---|---|
| Neoplasm | group of cells with single progenitor and mutation(s) leading to growth advantage and proliferation |
| Oncology | study of cancer |
| Neoplasia | new growth |
| Malignant | neoplasm with invasive capability |
| Benign | neoplasm confined to a location |
| Cancer | crab |
| Carcinoma | epithelial origin - 80% cancers |
| Sarcoma | mesenchymal origin |
| Tissue name + oma | usually benign exceptions being lymphoma, thymoma, melanoma |
| Differentiation - resemblance to normal | |
| Anaplasia | “backward formation” – Pleomorphic - variable size and shape – Variable and bizarre nuclei – Loss of polarity / organizational pattern |
| Undifferentiated or anaplastic tumor cells | no longer resemble tissue of origin |
| Dysplasia | disorderly but non-neoplastic |
| Metastasis | Secondary implant of tumor discontinuous with primary tumor; Not all cancers have this ability; Sentinel lymph node |
| Dissemination via: | Seeding within body cavity (invasion of cavity) – Lymphatic spread (favored by carcinomas) – Hematogenous spread (sarcomas (venous)) |
| Epidemiology | incidence, geography, environment, age, hereditary, preneoplastic lesions |
| Classic model of carcinogenesis - 3 stages | 1. initiation 2. promotion 3. progression |
| Initiation | - rapid, un-repaired first mutation; irreversible |
| Promotion | - proliferation, then an “epigenetic” process (chemical but not genetic) affects gene expression, fosters development, ends with carcinogenesis; cell “transformed” to malignant |
| Progression (continued development after malignancy) | - acquisition of further mutations required for metastasis |
| What are the hallmarks of cancer? | Self-sufficient in growth signals (unregulated);Inhibitory signals ignored; Evasion of cell death; Limitless replicative potential; Angiogenesis; Ability to invade local tissues (and spread); Altered metabolic pathways;Immune system evasion |
| Carcinogenic agents | virus, radiation, chemicals |
| Grade/Staging | Grades - malignancy and Stage - of development |
| Grade - of malignancy | - of Malignancy - I-IV reflect increasing anaplasia |
| Stages of development | - of Development based on size of tumor, extent of lymph spread, metastases or not |
| TNM system | T1-4, NO-3, MO-1 |
| AJC method | 0- IV |
| Infectious Agents | Prions, Viruses, Bacteria, Fungi, Protozoa, Helminths (Ectoparasites) |
| Prions | abnormally folded proteins, BSE - bovine spongiform encephalopathy - |
| accumulation of prion protein causes | neural spongiform damage |
| Viruses | Intracellular parasites, DNA or RNA genome, surrounded by capsid; Transient or persistent (Chronic or latent); Can be tumor-causing |
| Bacterial shapes | Sphere, rod, spiral |
| Gram Staining | positive or negative (easier vs. harder to treat) |
| Bacterial factors | Obligate intracellular, facultative intracellular, or extracellular; Projections: Flagella, pili; Colonize skin and GI tract >3000 types in normal gut! Estimated 10 m - 1 b types; shapes, aerobic or anaerobic, gram staining, shapes- sphere, rod, spiral |
| Gram positive factors | one layer, thick, absent outer membrane, possible periplasmic space, petidoglycan, teichoic acid and lipotechoic acid, less lipid, no porin proteins, more penetrable permeability, less resistance to molecules |
| Gram negative factors | two layers, thin, outer membrane, periplasmic space, porin proteins, more lipid, less peptidoglycan, less permeability of molecules, lipopolysaccharide, peptodoglycan, lipoportei |
| Eukaryotic | have membrane bound organelles |
| Prokaryotic cells (inc. bacteria) | are much smaller and simpler, with no separate organelles |
| Fungi | Food!, Antibiotics, Fermentation; Thick walls and membranes; Yeast or Hyphae Superficial or Deep infxns; Endemic or Opportunistic |
| Protozoa | single-celled, replicate intra or extra- cellularly , major problem in developing countries |
| Protozoa causing diseases | Toxoplasmosis, malaria, giardia, amoebic dysentary, African sleeping sickness, cryptosporidium, trichomonas |
| Helminths | parasitic worms, complex life cycles, roundworms, tapeworms, flukes |
| Ectoparasites | insects, arachnids, live on or in skin |
| modes of identifying | staining, antibodies, molecular techniques |
| Major contributing Factors to emerging infectious diseases | human behavior, environmental changes, adaptive pathogens |
| Bioterrorism danger based on | transmissibility, mortality, ease of production, effectiveness of therapy |
| Categories of bioterrorism | A - high risk; anthrax, small pox B- moderate; salmonella, e.coli C- emerging threats |
| Transmission routes of entry (and protective factors) | skin - pricks, bites, wounds, burns , GI - fecal contaminated food or water; respiratory - inhaled microbes, Urogenital - urethra - BL-KD, Vaginal |
| protective factors of skin | - Keratin, pH, fatty acids |
| protective factors of GI tract | acid, mucus, enzymes, peptides, flora, IgA |
| protective factors of respiratory | hair, mucus, cilia, macrophages |
| protective factors of urogenital | tube length, urine flow |
| protective factors of vaginal | pH, flora, secretions |
| Infx, dz spread within the body through | direct invasion - secrete lytic enzymes(some ext. cellular bacteria, fungi, helminths) blood or lymph spread (viruses, most bacteria, some protozoa, all helminths) cell to cell (most viruses) |
| Every fluid or tissue that is normally secreted, excreted, or shed is used by microorganisms to leave the host for transmission | Skin, saliva, respiratory droplets, feces, blood, STIs, vertical transmissions |
| how do microorganisms cause disease? Viral mechanisms | directly enter host cells, replicate at host's expense, bind to specific cell types, cytopathic effects, evade immune system |
| cytopathic effects | prevent synthesis of critical molecules, induce apoptosis, trigger immune attack of affected cells, transform infected cells into benign or malignant tumor cells, |
| How do bacterial mechanisms cause dz? | adhere to host cells, enter cells (intra. cellular b.) or travel btw cells, produce toxins, evade immune system; injurious immune response - hypersensitivity( delayed immune reaction, antibody complex formation) |
| immune evasion techniques | antigenic variation(mutation, genetic shuffling, diverse serotypes, inactivating antibodies, resisting phagocytes,(resist binding of cells, inhibit or kill) suppressing adaptive responses |
| HSV 1, 2, VZV (3) | live in nerves, destroy infected cells - Herpes, Human Papilloma Virus, Varicella and Zoster |
| CMV (5) HHV 6, 7 | live in WBCs in blood, KD, glands; enlarge infected cells - cytomeglovirus and shingles chicken pox |
| EBV (4) HHV 8 | live in lymphoid tissue, infect T or B lymphocytes only - Kaposi syndrome |
| Gene | - hereditary factor that reacts with environment resulting in a trait |
| Allele | - variant of a gene (you inherit two alleles for each gene, one from each parent) |
| Trait - quantifiable characteristic eg eye color | quantifiable characteristic eg. eye color |
| Chromosome | - strand of DNA encoded with genes (humans have 22 pairs plus 2 sex chromosomes = 46) |
| Locus - location of a specific gene on a chromosome | location of a specific gene on a chromosome |
| Heterozygous (hybrid) | - alleles of a particular gene are non-identical |
| Homozygous | - alleles of a particular gene are identical |
| Autosomes | - “non-sexual” chromosomes |
| X- (and Y-) linked - | locus for gene is on sex chromosome |
| Dominant | - only one allele of a gene necessary to express the trait |
| Recessive | both alleles of a gene must be identical to express the trait |
| Genotype - | genetic constitution of an individual made up of alleles |
| Phenotype - | end result of genetic and environmental factors giving the clinical state of an individual |
| hereditary | derived from one's parents |
| congenital | present at birth ; Not always genetic, eg congenital syphilis Not all genetic disorders are congenital, eg Huntington’s disease |
| Important to know about genes | every cell has all genes, same DNA, 20-39,000 human genes, 99.5% idential in all humans, DNA organizes in chromosomes, chromosomes organized into genes, genes code for proteins mostly, DNA made up of base pairs |
| Base pairing - | adenine can form two hydrogen bonds with Thymine; Cytosine can form three hydrogen bonds with Guanine |
| DNA | 2 complementary strands, sequence of one determines the other - double helix |
| RNA | single stranded, may form secondary structures, participate in protein synthesis, 3 classes - messenger RNA, transfer RNA, ribosomal RNA |
| Genetic code | based on sequence of mRNA which is made up of nucleotides while proteins are made up of amino acids; must be specific relationship btw the nucleotide sequence and amino acid sequence, 3 N (a codon) for one amino acid |
| Essential amino acids | cannot be made by the body; must come from food - Nine: histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine |
| Nonessential amino acids | produced by the body; Alanine, asparagine, aspartic acid and glutamic acid |
| conditional amino acids | non usually essential except in times of illness & stress. Arginine, cysteine, glutamine, tyrosine, proline, serine, glycine, ornithine, |
| genetic mutations | permanent change, point mutation aka "missense" nonsense mutation, framshift, Trinucleotide repeat eg. Fragile X |
| other alterations | sequence and copy number variations (polymorphisms, SNPS & CNVs); epigenetics(methylation) non coding RNA ( regulatory ) |
| Genomic Imprinting | inherit only one working copy, depending on gene one is epigenetically silenced through the addition of methyl groups during egg or sperm formation - imprinting improperly can lead to 2 active/inactive copies - abnormals, cancer, etc. |
| Angelman Syndrome (AS) | Severe congenital mental retardation, unusual facial appearance, and muscular abnormalities ; Caused by abnormal function of a gene on chromosome 15; Maternal deletion |
| Prader- Willi Syndrome (PWS) | Obesity, low muscle tone, cognitive disabilities, and incomplete pubertal development; Loss of several genes on the chromosome 15; Paternal deletion |
| Mendel's Laws (Principles) | Segregation, Independent Assortment, Means - (The above principles include the simple assumption that one allele is dominant to another) |
| Segregation - M.law | gene pairs segregate (become alleles) when forming gametes (a parent will give only one copy to a child, a child is half and half of each parent) |
| Independent Assortment- M. law | genes for different traits assort independently of one another; |
| Means - M.law | Characteristic ratios of phenotypic classes, such as 3:1 |
| Single gene defects | autosomal recessive, autosomal dominant, X linked |
| AR inheritance: If both parents are carriers of the recessive allele for a disorder, all of their children will face the following odds of inheriting it: | AR: Autosomal Recessive Inheritance; 25% chance of having the disorder 50% chance of being a healthy carrier 25% chance of being healthy and not carrying the recessive allele at all |
| AR diseases - both parents carriers | Examples: sickle cell anemia, cystic fibrosis, albinism, beta-thalassemia |
| AR Inheritance: If one parent is a carrier and the other has a recessive disorder, their children will have the following odds of inheriting it: | 50% chance of being healthy carrier, 50% change of having disorder |
| Autosomal Dominant AD | disorders caused by dominant alleles, inheriting just one copy of D allele is enough to cause disorder, people who are heterozygous are not healthy carriers(Aa) they have disorders just like homozygous individuals (AA) |
| AD inheritance - if only one parent has a single copy of a dominant allele for a dominant disorder, their children will have the following odds of inheriting it | 50% inheriting disorder, 50% being entirely normal |
| AD diseases | Huntington, polydactyly, familial hypercholesterolemia, Marfan syndrome, achondroplasia dwarfism |
| X linked Disorders - recessive | Hemophilia, Duchenne muscular dystrophy, red green color blindness |
| Mutation induced disorders - Marfan, Ehler Danlos, Cystic Fibrosis, Familial hyperCHL, PKU, Galactosemia, TaySachs, Neimann Pick, hereditary tumors | Structural protein encoding genes, Receptor or channel encoding genes, enzyme encoding genes, lysosomal and glycogen storage dz, cell growth regulating genes |
| chromosomal disorders | Trisomy 21 - Down, Klinefelter Syndrome (XXY), Turner Syndrome (X) |
| Klinefelter Syndrome (XXY) | Sterility, testicular atrophy, gynecomastia |
| Trisomy 21 - Down Syndrome | Prenatal - nuchal thickening, distinct appearance, mental disorders, increased risks |
| Turner Syndrome (X) | Sterility, webbed neck, aortic coarctation |
| Dysostoses | aplasia, missing, extra, abnromal fusion |
| dysplasia | osteogenesis Imperfecta (brittle bones OI) Achondroplasia(dwarfism - inherited or spontaneous mutation, osteopetrosis - bones like stones |
| bones made of up | minerals and collagen |
| Acquired bone disorders | osteoporosis , Paget disease, Rickets, osteomalacia, hyperparathyroidism |
| Osteoporosis | loss of bone mass, can be regional(disuse), increased susceptibility to fracture, post menopausal - trabecular bone, compression fractures(vertebral collapse) senile or age related - cortical bone, fractures or weight baring bones - neck |
| causes of osteoporosis | primary - post menopausal, old age; secondary - endocrine disorders, GI disorders(absoprtion) drug exposures (steroids, chemicals, alcohol) |
| Paget disease | frenzied osteolysis , disordered rebuilding, resulting gain in bone mass - decreasing incidence, inflammatory response - may have viral trigger |
| RIckets and Osteomalacia | Vitamin D deficiency - children/deformity ; adults/under mineralization, fracture risk |
| PTH | regulates CA - activates osteoclasts, increased serum levels - entire skeleton affected, increased fracture risk, bone deformity, joint problems, reversible |
| Most common bone pathology of fractures | complete/incomplete, closed/compound; comminuted "pulverized" displaced |
| healing fracture | soft tissue callous, bony callous, remodeling |
| osteonecrosis | avascular necrosis - common in femoral head, knee shoulder ankle wrist - pn in joint first symptom, interruption in blood flow (infarction) due to trauma, inflammation, steroid use or unknown causes |
| osteomyelitis | bone and marrow inflammation caused by infection - common agents in include pyogenic or pus forming bacteria such as strep, e.coli, salmonella and TB, staph |
| osteoma | benign usually head and neck middle age, cosmetic or mechanical problems |
| osteoid osteoma and osteoblastoma | benign usually male - teens painful |
| osteosarcoma | malignant, rare, incidence peaks in teens and elderly |
| Osteochondroma | common, benign, long bones stop growing with rest of bone - early adult, teens |
| chondroma | benign, middle age, short tubular bones |
| chondrosarcoma | malignant, rare, usually in males +40 - painful |
| fibrous and fibroosseous tissue | fibrous cortical defects and nonossifying fibroma - development abnormalities, asymptomatic |
| fibrous dysplasia | benign - asymptomatic or deforming depending upon location |
| Ewing sarcoma | malignant, painful , tubular and flat bones |
| primitive neuroectodermal tumor | malignant, painful , tubular and flat bones |
| Giant cell tumor (GCT) | benign, aggressive, males and females 20-40, painful, often around knee |
| Metastases - any cancer can go to bone | most common bone malignancies |
| Joint disorders | osteoarthritis, RA, Juvenile RA, gout pseudogout, infectious arthritis, tumor |
| OA - aka degenerative joint disease (DJD) | articular cartilage underlying bone - primary due to age, secondary trauma, deformity dz, obesity |
| RA | systemic, inflammatory autoimmune - synovitis under cartilage underlying bone, 3x5 more females, genetic predisposition, usually symmetric affecting small joints, nodules, deformity, RA factor (Ab) immune complexes |
| Gout | acute arthritis due to uric acid crystal deposits 1% pop. more in males |
| Infectious arthritis | suppurative (septic) Lyme arthritis |
| Joint tumors and lesions | ganglion and synovial cysts - TGCT - |
| Soft tissue = not epithelial | bone, cartilage, CNS, blood, lymph |
| Tumors and tumor like lesions in soft tissue | adipose- liposarcoma, lipoma, fibrous tissue - fibrohistiocytic(dermal), skeletal mm - Rhabdomyosarcoma, Smooth mm - leiomyoma, synovium - synovial sarcoma |
| How do microorganisms cause disease? | bacterial mechanisms & injurious immune response (hypersensitivity - delayed reaction of immune system,; antibody complex formation. |
| Bacterial mechanism | adhere to host cells, enter cells or travel btw, produce toxins, evade immune system |
| Adverse drug reactions | |
| Heavy metal toxicity - symptoms of most common | lead exposure is absorped through LU or GI tract; organic is absorbed through skin - BONE, BLOOD, MARROW, NS, GI and KIDNEYS - targets; effects anemia to pain to peripheral neuropathy and encephalopathy |
| how are toxins excreted | Through excretory derivatives(polar water soluble ) bile, feces, serum, kidneys, urine |
| how and why is CO dangerous | result of incomplete combustion, safe in small amounts, displaces 02 from hemoglobin and binds to hemoglobin for long time, decreased 02 supply, can cause death |
| Xenobiotics - | exogenous chemicals that may be absorbed by the body through inhalation, ingestion, or skin contact |
| 2 phages of the Liver & reactions | Metabolizing reactions occur in 2 phages - I (hydrolysis, oxidation or reduction(cytochrome p450) and II - glucuronidation, sulfation, methylation, and conjugation with gulathione (GSH) |
| Endotoxins | end products of metabolism, bacterial endotoxins. |
| lipid soluble toxins are stored in | adipose tissue and contribute to increased toxic load with weight loss |
| Liver Detoxification pathway - Cytochrome 450 - catalyzes reactions that | are either detoxify xenobiotics or active them into active compounds that cause cellular damage if not removed or processed further (both product ROS) |
| ROS | reactive oxygen species capable of causing cellular damage |
| Liver Detoxification pathway- Cytochrome 450 | participates in metabolism of many common drugs such as acetaminophen, barbiturates, anticonvulsants, and alcohol; activity varies widely due to genetic and environmental factors - smoking fasting and alcohol use can effect activity |
| air pollutants can cause | increased airway reactivity, decreased lung function, inflammation of LU, infection, hypoxia, mortality |
| Lead toxic effects | hemolytic anemia, lead colic, kidney tubule inflammation, neuritis, encephalopathy, seizures, delayed development, intellectual impairment, lead lines |
| Toxic metals - Mercury | Inorganic - dental fillings, organic - fish - manifestation of toxicity depend on type and level of exposure, age and health of exposed person. |
| Signs of severe Mercury poisoning | tremors, inflammation of the gums, salivation excessive, psychiatric symptoms such as excitability, insomnia, and shyness (MAD HATTER) |
| Vitamins are | organic substances not synthesized by the body but necessary in the diet to prevent metabolic disorders |
| Deficiencies of any of the water soluble or fat soluble vitamins and trace elements necessary to a health diet cause | characteristics effects of "deficiency states" |
| Vit. A deficiency | night blindness, low immunity |
| Vit. D deficiency | Rickets in kids, osteomalacia in adults |
| Vit. E deficiency | hemolysis, vision and neurological problems |
| Vit. K deficiency | bleeding tendency |
| Vit. B1 - Thiamine | Beriberi ( nerves, heart, muscles) |
| Vit. B2 - Riboflavin | cheilosis, stomatitis, glossitis, dermatitis |
| Vit B3 - niacin | dementia, dermatitis, diarrhea |
| Vit B5- pantothenic acid | fats, hormones, cholesterol metabolism |
| Vit. B6 - pyridoxine p5p | anemia, inflammation, morning sickness |
| Vit B7 -biotin | alopecia, skin rash |
| Vit. B9 - folate | anemia, birth defects |
| Vit. B12 - cobalamin | anemia, neuropathies |
| VIt. C | scurvy |
Created by:
lauren1911
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