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MicroPath Final

MicroBiology and Pathophysiology

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 - 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 - 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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