Microanatomy Test Answers – Flashcards
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| Diseases |
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| Problem: |
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| Duchenne Muscular Dystrophy |
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| Dystrophin defect; cannot link actin to plasma membrane well. Membrane becomes weak/permeable and extracellular crap floods cell, exploding it. |
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| Cystic Fibrosis |
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| Mutant CFTR unable to interact with actin to mediate opening/closing of Cl- channel. |
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| Wiskott-Aldrich Syndrome |
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| Actin nucleation and motility are defective. Eczema, thrombocytopenia (low platelet count) and immune deficiency. |
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| Shigella/Listeria bacteria |
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| bacteria hijack actin, increase infectivity |
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| Deafness |
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| Stereocilia degeneration |
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| Lissencephaly "smooth brain" |
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| Failure in neuronal migration due to dynein defect. Severe retardation, seizures, death by age 6 |
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| Polycystic kidney disease |
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| Excess proliferation of kidney cells leads to cyst formation |
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| Kartagener's syndrome |
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| Dynein defect. Reversed organs (situs inversus), respiratory infections, fertility problems. |
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| Alzheimer's disease |
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| Hyperphosphorylation of tau MAP protein; self-assembles to form tangles. |
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| Charco-Marie-Tooth disease |
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| Neurological disorder, defect of kinesin. Loss of muscle tissue and touch sensation |
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| Hypercholesterolemia |
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| Receptor-mediated endocytosis fails to draw LDL into cells. LDL and its cholesterol stay in blood plasma, elevating its concentration there. Premature atherosclerosis, heart attacks, xanthomas |
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| Bacterial toxin/virus/parasite invasion |
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| The toxic agent gets into the cell via Receptor-Mediated Endocytosis and is also resistant to lysosomal acidification/degredation. |
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| I-Cell Disease |
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| Phosphotransferase that tags Mannose-6-Phosphate onto lysosomal enzymes for direction into lysosome is defective. Enzymes never make it into lysosomes and are instead shunted into default constitutive secretion pathway. |
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| Gaucher’s Disease |
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| Lysosomal storage disease (lysosome enzyme defect) |
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| Tay-Sach’s Disease |
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| Lysosomal storage disease (lysosome enzyme defect) |
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| Fabry's Disease |
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| Lysosomal storage disease (lysosome enzyme defect) |
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| Pompe's Disease |
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| Lysosomal storage disease (lysosome enzyme defect) -> glycogen accumulation |
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| Zellweger syndrome |
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| No peroxisomes formed due to peroxin gene mutation. Typical PEX problems: accumulation of VLCFA and deficiency of plasmalogen (myelin component). Fatal in first year of life. |
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| X-linked Adrenoleukodystrophy |
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| Faulty protein transport into peroxisomes due to ABCD1 gene mutation in X chromosome. Typical PEX problems: accumulation of VLCFA and deficiency of plasmalogen (myelin component). Onset 5-12 yrs. Death 1-10 years after onset. Progressive neural deterioration and failure of adrenal glands to develop. |
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| Leber's Hereditary Optic Neuropathy |
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| Mutation in complex I in electron transport chain; leads to less effective mitochondria and reduced ATP synthesis. Also evidence that superoxide dismutase (SOD) impaired Causes build up of superoxide radicals Occurs in retinal ganglion cells resulting in blindness |
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| Leukemias |
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| Neoplasms in bone marrow of blood cell formation |
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| Aplastic anemia |
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| Bone marrow doesn't produce enough new cells to replenish mature blood cells |
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| Ehlers-Danlos |
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| Reticular fiber (Collagen III) synthesizing defect. Joint dislocations & skin deformations |
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| Marfan's Syndrome |
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| Fibrillin (part of elastin fiber) mutation. Tissues with lots of elastin are weak/malformed. Long limbs, weak aorta |
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| Scurvy |
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| Weak collagen, because of Vitamin C deficiency. Bleeding gums & bruising |
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| Paget's Disease of Bone |
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| More rapid osteoid production than mineralization |
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| Osteogenesis Imperfecta |
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| Abnormal collagen maturation in bone |
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| Osteomalacia |
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| Faulty mineralization |
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| Rickets |
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| Faulty mineralization (in children) |
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| Osteoporosis |
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| More bone resorption than formation; low bone density |
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| Osteoarthritis |
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| Deterioration of cartilage & bone |
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| Rheumatoid arthritis |
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| Deterioration of cartilage & bone |
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| Peroxisome structure |
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| -single lipid bilayer -small & spherical (.5-1um diameter) |
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| Peroxisome function |
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| -Beta oxidation of VERY long chain fatty acids -catalase degrades H2O2 buildup -Detox of alcohol (liver) & purines (kidney) -Biosynthesis of myelin, bile acids, cholesterol |
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| Peroxisome location |
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| all cells, but particularly liver & kidney |
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| Peroxisome replication |
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| fission or budding no endogenous DNA (proteins transported in via peroxins) |
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| Zellweger syndrome |
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| most severe peroxisome biogenesis disorder -can't form myelin --> fatal in first year |
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| X-linked adrenoleukodystrophy |
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| Most common peroxisomal disorder -Mutation in proteins that transport fatty acids in --> buildup of FAs --> death 1-10 yrs after onset |
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| Mitochondria structure |
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| ? 0.5-10?m ? Inner membrane (cristae e- transport) ? Outer membrane ? Intermembrane space (high H+) ? Matrix: mtDNA, ribosome, tRNA, TCA enzymes |
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| Mitochondria function |
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| ? ATP synthesis ? Ca homeostasis ? Regulation of apoptosis ? ? oxidation of fatty acids |
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| Mitochondria replication |
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| ? Binary fission replication |
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| Mitochondrial genetic defects |
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| ? Mt enzyme deficiency ? Mitochondrial DNA defects ? Autosomal DNA defects for mt proteins - Heteroplasmy is when mutated & normal mitochondria aren't evenly dispersed in development; so there may be problems with just one tissue |
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| Leber’s hereditary optic neuropathy |
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| loss of central vision, affects mostly males, optic nerve degeneration because not enough functional mito produce energy to maintain cells (heteroplasmy?) |
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| [image] |
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| peroxisome |
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| [image] |
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| mitochondria |
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| Steps of the electron transport chain |
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- (I) NADH dehydrogenase: H+>intermebrane, e->ubiquinone - (II) FADH2 dehydrogenase (succinate): FADH2>2H + FAD-+e-(ubiquinone) - (III) Cytochrome C reductase: H+ >intermembrane, e- (ubiquinone)>cytochrome c - (IV) Cytochrome c oxidase: H+ >intermembrane, e- used to reduce O2 to water - ATP synthase: H+ returns to matrix |
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| metaplasia |
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| Cell type conversion: o one type of cell replaced with another type, but organization maintained. Reversible |
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| Dysplasia |
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| Maturation abnormality o partial loss of organization, some increase in cell #; partially reversible |
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| Neoplasia |
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| Abnormal proliferation o increase in cell #, loss of control; irreversible |
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| Epithelial tissue |
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| -Lines free surfaces, both externally and internally (i.e. skin, sweat glands, GI, kidney tubules) -Supported by connective tissue -Serves as barriers -Cells tend to be tightly packed (look for high density of nuclei) with little ECM -Avascular -Tend to be polarized |
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| Connective tissue |
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| ex: bone, tendon, cartilage, blood -Provide structural support for many other types of tissue -Tend to have few cells (sparse density of nuclei) with lots of ECM -Fibroblasts are the most common type of ‘connective cell’ |
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| [image] |
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| connective tissue |
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| [image] |
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| contractile tissue |
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| [image] |
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| nervous tissue |
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| Contractile tissue |
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| -Specialized for rapid movement, responsive to electrical signals -Striated (cardiac, skeletal) vs. smooth muscle -Voluntary (skeletal) vs. involuntary (cardiac, smooth) -Many tubular structures (vasculature, GI tract) have contractile tissue |
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| Nervous tissue |
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| -Neurons are large cells responsive for conveying electrical stimuli -Glia are smaller supporting cells (50:50 – 90:10) -Neuropil is cellular (not extracellular) material between cell bodies- cell processes of glia and neurons |
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| Ectodermal origin |
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| epidermis, nervous system, cornea, lens |
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| Mesodermal origin |
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| dermis, circulatory system, kidney, skeletal muscle, connective tissue, lymphatic system, excretory system, mesothelium |
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| Endodermal origin |
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| GI (stomach, intestines, epithelial lining), lungs, liver, pancreas, bladder |
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| 3 cellular domains |
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| cytosol, intercisternal, nuclear |
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| Rough ER functions |
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| protein synthesis for extracellular, transmembrane proteins, lysoyme enzymes post-translational modification: proteolysis, glycosylation, sulfation, folding |
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| SER function |
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| synthesis of steroids, cholesterol, trigylcerides (in liver) detoxification carbohydrate metabolism - glycogenolysis Ca++ storage (in sarcoplasmic reticulum) |
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| COP II |
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| Anterograde transport from trans ER --> Cis Golgi Network |
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| COP I |
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| anterograde & retrograde transport throughout golgi retrograde back to trans ER constitutive secretion transmembrane protein |
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| Clathrin |
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| vessicle coat in regulated secretion & lysosomal targeting |
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| microfilament energy needs |
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| need ATP hydrolysis to breakdown, but not to grow (from - to + end) |
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| microtubule structure |
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| alpha & beta tubulin --> heterodimer - 13 pairs usually Cilia/flagella = 9 doublets + 2 pairs in center Centrioles / basal bodies = 9 triplets |
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| Intermediate junctions |
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| cadherins bridge membranes anchor to alpha & beta catenin in membrane then connect to actin |
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| Desmosomes |
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| 'spot junctions' cadherins connect membranes cadherins connect to desmoplakin desmoplakin connects to intermediate filaments (keratin) |
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| Hemidesmosomes |
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| -integrins span membrane -anchor to laminin & collagen -which bind to RGD-rich fibronectin |
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| Monocytes |
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| form macrophages, microglia, osteoclasts |
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| Neutrophils |
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| phagocytosis |
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| basophils |
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| histamine (vasoidlator) & heparin (anticoagulant) in allergic response |
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| Eosinophils |
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| moderate allergic response by reducing inflammation -parasitic attack |
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| Lymphocyte |
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| plasma cells T cells - which mature in thymus B cells - which mature in bone marrow |
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| Collagen synthesized by... |
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| fibroblasts (I, III), osteoblasts (type I), chondroblasts (type II), epithelial cells (type IV - basement membrane) |
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| LCT |
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| made of mostly type I, with some reticular & elastic fibers mostly found around vessels & nerves, under epithelia, subcutaneous layer of skin, between organs & tissue |
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| rDCT |
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| type I tendons & ligaments |
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| irDCT |
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| mostly type I collagen protects against multidirectional force seen in dermis, periosteum, perichondrium, heart valves |
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| Hylaine cartilage |
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| located on articular ends of long bone (but with no perichondrium), nose, larynx, trachea, bronchi, ribs -made of type II collagen surrounded by vascular perichondrium (except in articular cartilage & epiphysial plates) |
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| Elastic cartilage |
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| found in ear & epiglottis Type II collagen + elastic fibers (elastin & fibrllin) |
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| Fibrocartilage |
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| found connecting ligaments & tendons to bone (enthesis) Type I collagen does not do appositional growth |
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| centrioles |
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| function in cellular organizing 2 centrioles = centromere, which = MTOC 9 triplets microtubules splay out from the centrioles |
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| 3 cellular domains |
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| nucleus intercisternal space cytosol |
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| 4 types of tissue |
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| Epithelial Connective Contractile Neural |
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| H&E Staining |
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| Hematoxylin: stains basophilic substances blue Eosin: stains acidophilic substances pink |
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| Nuclear Pore Complex (NPC) |
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| Cytoplasmic Ring Middle Ring Nucleoplasmic ring |
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| Cell cycle check points |
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| G1 - environment S - DNA damage G2 - replication completion M - correct alignment on metaphase plate |
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| RER functions |
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| 1. synth proteins 2. new membrane for nucleus after cell division |
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| SER functions |
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| 1. detoxify drugs 2. breakdown carbs 3. synthesize steroids 4. Ca2+ dynamics in sarcoplasmic reticulum |
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| Protein synth in RER steps |
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| signal sequence on protein --> SRP --> SRP receptor --> translational pause while ribosome brought to ribophorins on RER --> translation continues --> signal sequence cleaved by signal peptidase --> protein released in RER 2. Misfolded --> proteases |
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| Golgi transport |
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| - lysosome/endosomes - plasma membrane - secretory granules |
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| Clathrin |
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| transport from CGN to lysosome/endosomes transport to secretory vessicles |
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| COPII |
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| Anterograde from RER to CGN |
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| COP I |
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| retrograde from CGN -> RER inter-cisternal transport constitutive secretion |
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| Inclusion cell disease |
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| defective enzyme for tagging enzymes (M6P) autosomal recessive |
