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166 Cards in this Set
- Front
- Back
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What are the four different types of tissues?
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-epithelial tissue
-connective tissue -muscular tissue -nervous tissue |
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What are simple squamous epithelia for?
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-slippery surfaces (anti-clotting, anti-adhesion)
-passive diffusion |
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What is a basement membrane?
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-basal lamina: type IV collagen, proteoglycans, and glycoproteins (size and charge filter)
-reticular fibers: type III collagen wrapped in glycoprotein (anchor basal lamina to underlying general connective tissue) |
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How is transitional unstretched epithelium different from stratified columnar?
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Transitional unstretched epithelium has obvious gaps between surface cells and the basement membrane is wavy.
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How is transitional stretched epithelium different from stratified squamous?
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Transitional unstretched epithelium has very pink surface cells and they are frequently binucleated.
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What are simple cuboidal epithelia for?
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-moderate structural rigidity for tubes
-increased activity of the cell -small ducts, secretory portion of glands |
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What are simple columnar epithelia for?
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-high structural rigidity for tubes
-high activity of the cell -most cells possible for simple epithelium -small intestine, fallopian tube |
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What are pseudostratified columnar epithelia for?
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-all properties of simple columnar
-regeneration of basal cells -areas subject to damage but high activity -upper respiratory tract |
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What are stratified cuboidal epithelia for?
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-good strong wall of tube
-not very active cells -duct of sweat glands |
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What are stratified columnar epithelia for?
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-very strong wall of tube
-ducts leading to nipple of mammary gland |
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What are stratified squamous epithelia for?
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-best protection against outside
-surface cells cannot absorb or secrete -skin (keratin), esophagus (no keratin) |
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What are transitional epithelia for?
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-protection
-stretch -urinary bladder |
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What are the differences between microvilli and cilia?
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-microvilli cannot be resolved, cilia can
-microvilli are for absorption, cilia are for sweeping (movement) -cilia have basal bodies, microvilli do not |
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What are goblet cells for?
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secrete mucus
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What do serous exocrine glands secrete? What do their cells look like?
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-watery proteinaceous secretion
-nucleus is rounded and euchromatic -cytoplasm is pink or blue |
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What do mucous exocrine glands secrete? What do their cells look like?
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-secrete proteoglycan (slippery, sticky, or protective, as needed)
-basally squished, heterochromatic nucleus -pale staining cytoplasm |
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What are examples of exocrine glands which are not mucous, serous, or mucoserous? What do their cells look like?
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-eccrine sweat glands
-sebaceous glands -pale cells -rounded fairly euchromatic nuclei |
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How can a mucoserous gland be distinguished from an "other" gland?
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-mucoserous has squished heterochromatic nuclei
-"other" has central rounded euchromatic nuclei |
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What do myoepithelial cells do?
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They contract to accelerate secretory product to the surface in response to nervous or hormonal stimuli.
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What are the different types of secretion by cells of a gland?
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-merocrine (exocytosis) 99% of the time, e.g. sweat
-apocrine (part of membrane is secreted along with product), e.g. lipid secretion into milk -holocrine (whole cells), e.g. sebaceous glands, ova, sperm, hair |
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What does neoplasia mean?
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new growth - either benign or malignant
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What does metaplasia mean?
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cell growth which is abnormal to the area/tissue, but otherwise ok
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What does dysplasia mean?
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focal abnormal appearance and behavior
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What does anaplasia mean?
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cells have multiple morphologies and have lost differentiated characteristics of the cells of origin
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What does connective tissue consist of?
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-ground substance
-fibers -cells (fat cells, fibroblasts, smooth muscle cells, small vessel cells, nerve cells, stem cells, leukocytes) |
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What is ground substance?
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-proteoglycans
-peptidoglycans -glycosaminoglycans -large glycoproteins -soluble factors -plasma filtrate |
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What is Hurler's syndrome?
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A disorder of ground substance characterized by short stature, hernias, and mental retardation.
-problems with nutrient/waste flow -improper morphogenesis -improper tissue growth -product accumulation in lysosomes, cell malfunction |
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What is hyaluronate?
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-the most important non-sulfated glycosaminoglycan
-viscosity of 0.2 - 48 mL/g -abundant in vitreous humor, synovial fluid, skin |
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What do sulfated glycosaminoglycans do? What are some examples?
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-impart a charge to ground substance
-chondroitins -keratans -dermatans -heparans |
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What does ground substance do?
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-holds water
-charge and size barrier -contributes to physical properties of connective tissue -regulates morphogenesis (migration recognition and growth factor activation) -facilitates cell migration by coating cells |
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What is the structure of elastic fibers?
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-collagen-like fibrillar protein, fibrillin
-elastin filler, which is made similarly to collagen |
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What are type I collagen fibers used for?
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-bone
-skin -tendon -fibrocartilage |
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What are type II collagen fibers used for?
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-elastic cartilage
-vitreous humor |
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What are type III collagen fibers used for?
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-skin
-reticular fibers -vessel walls |
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What are type IV collagen fibers used for?
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basal lamina
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In type I collagen biosynthesis, what modifications are made to the α-chain?
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-cleavage of signal sequence in rough ER
-hydroxylation of Pro and Lys residues |
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What is prolyl hydroxylase? What is necessary in order for it to function?
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-hydroxylates prolines on the α-chain
-Vit C, Fe, and O2 are cofactors |
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What is the purpose of hydroxylating prolines on the α-chain?
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hydroxyprolines are necessary for the formation of the triple helix (procollagen) in the rough ER
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What is scurvy?
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A deficiency in Vit C which leads to inability to form a stable triple helix. Therefore the procollagen is degraded in the rough ER.
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What is the purpose of hydroxylating lysines on the α-chain?
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It is necessary for the formation of tropocollagen into collagen fibrils (assisted by lysyl oxidase).
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What could inhibit the formation of collagen fibrils from tropocollagen?
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-defect in lysyl hydroxylase (Ehler's Danlos VI)
-defect in lysyl oxidase (Marfan's Syndrome) or Cu deficiency -defect in procollagen peptidase (Ehler's Danlos I) -glycosylation of hydroxylysines |
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What does lysyl oxidase do? What is necessary in order for it to function?
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-oxidizes certain hydroxylysine residues in the triple helix to aldehydes, this promotes cross-linking
-copper is a cofactor |
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What does procollagen peptidase do?
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Cleaves the nonhelical ends of procollagen to make tropocollagen
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What is the difference between type I collagen and type II collagen?
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Type II fibers are more highly glycosylated. This reduces cross-linking of tropocollagen into fibers, so the collagen fibers are thinner for type II.
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How is type III collagen different from types I and II?
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-more glycosylation than type I, less than type II
-fibers are intermediate thickness between types I and II -glycoprotein coat, forming reticular fibers |
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What are the distinguishing features of type IV collagen biosynthesis and structure?
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-propieces are not cleaved
-highly glycosylated -no fibers, just randomly arranged fibrils (filter) |
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What are the symptoms of Ehler's Danlos?
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-type I collagen is like type IV (or type II)
-hyperextensibility -fragility -skin overelasticity |
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In what disease does basement membrane accumulate outside the cell? What are the consequences?
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Diabetes; contributes to cardiovascular disease, peripheral neuropathy, kidney failure.
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What type of fibers are most prominent in the wall of the aorta? What happens if these fibers cannot be crosslinked?
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Elastic fibers; if there is a crosslinking defect (as in Marfan's Syndrome), patient usually dies of aortic aneurysm.
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Which enzyme is necessary for crosslinking of elastin?
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lysyl oxidase
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What are the effects of aging on connective tissue?
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-production and molecular weight of glycosaminoglycans decreases (holds less water)
-lower turnover of collagen, more crosslinking, UV damage, type III synthesis turns over to type I -lower turnover of elastic fibers, UV damage |
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Which cells of the connective tissue are "citizens" (born and live in CT)?
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-fibroblasts
-smooth muscle cells -small vessel/nerve cells -stem cells -fat cells |
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Which cells of the connective tissue are "permanent residents" (arise in bone marrow)?
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-macrophages
-mast cells |
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Which cells of the connective tissue are "transient aliens" (may or may not be in the CT at any given time)?
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-neutrophils
-eosinophils -basophils -lymphocytes |
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What do fibroblasts do? What do they usually look like?
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-major producers of collagen and connective tissue
-very little cytoplasm and heterochromatic nucleus (inactive) |
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What do smooth muscle cells do? What do they usually look like?
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-produce elastin fibers
-contract (when in groups) -pink cytoplasm (form actin) and euchromatic nucleus (active) |
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What do white fat cells do?
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-calorie storage
-insulation/cushioning -leptin/adiponectin production → reduce food intake |
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What do brown fat cells do?
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thermogenesis (by mitochondria)
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What do stem cells do?
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-participate in angiogenesis
-give rise to other connective tissue cells |
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What is contained in the granules of mast cells?
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-histamine
-heparin (activates some growth factors) -chymase (degrades connective tissue, activates kinin and clotting) -chemotactic factors for neutrophils, eosinophils -GAGases (degrade glycosaminoglycans) |
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What products are made by mast cells upon activation?
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-leukotrienes (like long-lasting histamine)
-prostaglandins -hydroxyarachidonates (neutrophil chemoattractant) -platelet activating factor |
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What events occur in the second exposure to an allergen that do not occur during the first exposure?
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-crosslinking of allergen by IgE
-granule content release by mast cells, basophils |
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What type of leukocytes contain enzymes that degrade histamine and leukotrienes?
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Eosinophils (feedback inhibition of inflammation)
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What types of solute movement (through cells/tissue) exist?
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-bulk flow/convection
-diffusion -transport |
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What is the partition coefficient (K)?
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[solute] in lipid / [solute] in water
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What types of solutes diffuse easily through the plasma membrane?
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-gases
-small uncharged polar molecules |
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What types of solutes diffuse with difficulty through the plasma membrane?
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-water
-urea |
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What types of solutes cannot diffuse through the plasma membrane?
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-large uncharged polar molecules
-charged/polar molecules -ions |
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Why is the lipid solubility of a drug important?
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determines:
-rate of absorption from the GI tract -accumulation of body fat -persistence in the body |
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Why is aspirin absorbed through the stomach quickly?
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The acid form (neutral) and charged form are in equilibrium at pH of 3.5. Since the stomach is more acidic, the equilibrium is shifted toward the neutral form, which is easily absorbed through membranes.
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Why would a molecule have a permeability coefficient that is much higher than expected based on its oil-water partition coefficient?
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Transporters exist for those molecules in an actual membrane, and they are actively brought into the cell.
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Why would a molecule have a permeability coefficient that is much lower than expected based on its oil-water partition coefficient?
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These molecules are poisons which are actively pumped out of the cell.
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What are the four types of membrane transit?
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-simple diffusion
-ion/water channels -facilitated transport -active transport |
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What is the structure of an aquaporin?
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-homotetramers
-each monomer has 6 transmembrane α-helices and 2 re-entrant loops -5 pores/homotetramer (1 pore in the middle) |
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What are aquaporins for?
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-allow water molecules to pass in single file
-some allow glycerol and/or urea to pass |
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What are cation gradients used for?
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-generate membrane potential and action potential
-regulate cell volume -secondary active transport to accumulate nutrients and expel wastes |
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What is the difference between a transporter and a pump?
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A pump uses ATP, a transporter doesn't.
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What is the difference between primary and secondary active transport?
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-primary uses ATP hydrolysis, secondary uses the diffusion of some other molecule.
-primary uses a pump, secondary uses a cotransporter or an exchanger |
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What do integrins do? What is their basic structure?
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-mediate cell-matrix and cell-cell signaling
-2 non-covalently associated transmembrane glycoprotein subunits, α and β -attached to actin filaments -interact with cellular tyrosine kinases |
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What are some ligands of integrins?
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-fibronectins
-laminins -immunoglobulin counter receptors -fibrinogen |
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How can integrins be activated?
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formation of focal contacts - assembly of actin filaments with actin binding proteins and integrins; it is how the cell attaches to the substratum
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How do integrins contribute to mitogenic signaling?
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integration of signals:
-when integrin binds fibronectin, FAKs are activated -FAKs are involved in the Ras-MAPK pathway; if the integrin is not bound then Ras-MAPK will not work even if there are growth factors |
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How are tumor cells able to exhibit anchorage-independent growth?
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-less fibronectin
-can proliferate without substrate attachment |
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What happens when mechanical force is applied to a fibronectin bound to an integrin?
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The cell is induced to produce:
-RhoA GTPases -stress responses -reorganization of focal contacts |
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What do cadherins do? What types of interactions do they have?
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-associate with actin filaments and adherens junctions
-homophilic interactions |
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What do CAMs (immunoglobulin superfamily) do? What types of interactions do they have?
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-bind some integrins
-heterophilic and homophilic interactions |
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What do selectins do? What types of interactions do they have?
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-found in blood cells and endothelial cells
-mediate extravasation of blood cells -heterophilic interactions (with lectins) |
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How is cell overgrowth prevented?
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-growth factor availability
-contact inhibition |
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How does E-cadherin suppress tumors?
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-Hyp. 1: Upon E-cadherin homophilic interaction, β-catenin is sequestered, blocking Wnt-induced cell proliferation
-Hyp. 2: E-cadherins facilitate a juxtacrine pathway that inhibits cell division |
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What is Delta/Notch signaling? What happens if it is disrupted?
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-all cells have Delta and Notch
-one cell's Delta binds an adjacent cell's Notch, which turns off Delta -the "winning cell" inhibits Notch and promotes Delta -if Delta/Notch signaling is disrupted, developmental patterning is lost |
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What is the difference between neurotransmitter-mediated and neuropeptide-mediated signaling?
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-neurotransmitters are faster and act on ion channels
-neuropeptides are slower and act on GPCRs or enzyme-linked receptors |
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What is the phenotypic consequence of a mutation in E-cadherin 1?
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-familial gastric cancer
-colon cancer |
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What are the reversible cellular changes that result from decreased ATP?
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-Na+/K+ ATPase breaks → swelling (hydropic change)
-glycolysis increases → lactic acid buildup (pH drops) -ribosomes detach from ER (protein synthesis decreases) |
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What are the irreversible cellular changes that result from decreased ATP?
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-cell membrane breaks down
-calcium enters cell -mitochondria die (Ca+ kills them) -lysosomal membrane breaks -lysosomal enzymes digest cell |
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What is the difference between hypertrophy and hyperplasia?
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-hypertrophy is increase in size (of the cell)
-hyperplasia is increase in rate of cell division, and can lead to hypertrophy (of the tissue) |
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How can necrosis be recognized microscopically?
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-pyknosis: nucleus becomes condensed and deeply basophilic
-karyorrhexis: pyknotic nucleus fragments -karyolysis: nucleus loses staining and dissolves -increased eosinophilia |
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What is coagulative necrosis?
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-the default type
-protein denaturation -tissue is preserved in original morphology |
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What is liquefactive necrosis? Where does it normally occur?
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-enzymatic degradation
-dead tissue becomes amorphous -any kind of brain necrosis is liquefactive regardless of mechanism |
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What is enzymatic fat necrosis? What does it look like?
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-injury to the pancreas results in release of digestive enzymes
-when the enzymes react with triglyceride esters, fatty acids are produced -fatty acids + calcium = soaps -grossly: chalky white areas -microscopically: looks like dead fat cells with blue material |
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How does non-enzymatic fat necrosis occur?
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Trauma to subcutaneous adipose tissue
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What is caseous necrosis?
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-pink amorphous material in the center of granulomas
-often caused by TB -resembles crumbled cheese |
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What is gummatous necrosis?
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-in the center of granulomas, looks like caseous necrosis microscopically
-grossly looks firm and rubbery -often caused by syphilis |
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What is the difference between dry and wet gangrene?
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-dry gangrene is coagulative necrosis
-wet gangrene is dry gangrene that got infected |
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What is gas gangrene?
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Necrotizing, rapidly spreading infection caused by anaerobic bacteria.
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What is steatosis? Where in the body does it normally occur?
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Accumulation of triglycerides in parenchymal cells; it normally occurs in the liver but occasionally in the heart or kidney.
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What is acute fatty change?
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-microvesicular fat accumulation
-high percentage of free fatty acids (toxic) with triglycerides -central nucleus is visible |
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What is chronic fatty change?
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-single, large, membrane-bound lipid droplet
-nucleus is displaced to the side |
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What is the difference between fatty change and fatty infiltration?
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Fatty change involves triglycerides in parenchymal cells. Fatty infiltration involves adipocytes between parenchymal cells.
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What is hematin?
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Also known as formalin pigment, occurs in areas of hemorrhage fixed in acidic formalin (probably the result of acid formalin reacting with Hb).
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What is hemozoin?
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A pigment produced by the malaria parasite as it breaks down hemoglobin.
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What is bilirubin?
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Pigment derived from hemoglobin breakdown. Unconjugated birirubin is the opened porphyrin ring; conjugated bilirubin is the ring with glucuronide, it is water-soluble and innocuous.
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What causes accumulation of unconjugated bilirubin? What are the effects?
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-kernicterus (lack of enzymes that conjugate bile) → neurons are yellow and they die
-biliary obstruction → toxic injury and necrosis of liver cells, cirrhosis, chronic liver failure -hemorrhage or infarction → bilirubin forms yellow crystals of hematoidin at the site |
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What is lipofuscin?
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Wear and tear pigment (fine, granular, golden-brown) that accumulates due to membrane damage. Increases with age, malnutrition, and chronic wasting disease.
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What is Wilson disease?
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Autosomal recessive defect in copper excretion which causes cell damage and necrosis → cirrhosis and hepatolenticular degeneration.
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What is the Keyser-Fleischer ring?
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A greenish-brown ring discoloration at the sclerocorneal junction caused by copper accumulation in the Descemet.
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What causes local edema?
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-hydrostatic pressure increases
-oncotic pressure is decreased (loss of plasma proteins) -lymphatics are blocked -increased vascular permeability |
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What is the difference between transudate and exudate?
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Exudate has more proteins and cells and it is involved in inflammation, transudate is for the non-inflammatory response.
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What causes systemic edema?
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-congestive heart failure
-hypoproteinemia |
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What is anasarca?
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extreme systemic edema
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What is the difference between metastatic and dystrophic calcification?
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-metastatic has elevated [Ca2+], dystrophic has normal [Ca2+]
-in metastatic, Ca2+ deposits everywhere (lung, bone, kidney), in dystrophic, Ca2+ deposits in abnormal areas (causes tumors, scarring, necrosis) |
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What is the most robust nutritional method of extending life span?
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calorie restriction
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Why do Snell dwarf mice have an extended lifespan?
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They have a point mutation in the PitI gene, so no somatotrophs (GH), thyrotrophs (TH), or lactotrophs (Prl).
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Why do Ames dwarf mice have an extended lifespan?
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They have a point mutation in Prop1 gene, so no GH, LH, or Prl.
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Why do GHR/BP knockout mice have an extended lifespan?
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They have IGF-I reduced by 90%.
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Why do P66shc knockout mice have an extended lifespan?
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P66shc is a cytoplasmic transducer of mitogenic signals and involved in stress response.
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Which types of mice have an extended lifespan due to mutations in genes that are related to insulin or insulin growth factor?
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-IGF-I receptor knockout mice
-Klotho overexpressing mice -FIRKO mouse |
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In the Baltimore study of aging, what were some characteristics noted of long-lived humans?
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-lower body temperature
-lower plasma insulin levels -higher plasma DHEA levels |
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What is Metformin?
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-probable calorie restriction mimetic
-reduces risk of all forms of cancer in diabetic patients |
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How is the sensitivity of a new test determined?
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new test positives / gold standard positives
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How is the specificity of a new test determined?
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new test negatives / gold standard negatives
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What is sensitivity?
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Percentage of tests which detect true positives
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What is specificity?
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Percentage of tests which detect true negatives
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What is the likelihood ratio?
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How much a test result will change the odds of having the disease
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How is the LR+ calculated?
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sensitivity / 1 - specificity
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How is the LR- calculated?
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1 - sensitivity / specificity
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What is the predictive value?
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The probability that a patient with a positive result does have the disease, or the probability that a patient with a negative result does not have the disease.
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How is the PV+ calculated?
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true positives / new test positives
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How is the PV- calculated?
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true negatives / new test negatives
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How are pre-test odds of having a disease calculated?
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prevalence / 1 - prevalence
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How are the post-test odds of having a disease calculated?
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pre-test odds x likelihood ratio
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What are epidermal pegs/dermal papillae for?
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they help keep the epidermis and dermis together, fingerprints
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What is the difference between a regular blister and a blood blister?
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a regular blister is the fluid filled pocket that forms when cells in the epidermis separate, a blood blister is formed when the epidermis and dermis separate (capillaries break)
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Why do basal skin cells only divide during sleep?
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Proliferation growth factors complex with epinephrine, which deactivates them. while sleeping, the levels of epinephrine are decreased, and this allows the growth factors to act.
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What are the types of clear cells? What do they have in common?
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-melanocyte
-Merkel cell -Langerhans cell -γδ T lymphocytes all are clear and have dendrites |
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How do melanocytes work?
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-embryologically late migrating cells
-make melanin from tyrosine in granules -exocytose the granules, and basal cells/prickle cells endocytose them |
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Why do variations in skin color occur?
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-rate of synthesis of melanin
-size of melanin granule -ability of other cells to endocytose melanin -type of melanin (pheomelanin vs. eumelanin) |
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What are Merkel cells?
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-modified nerve endings
-very fine mechanoreceptors -contain neurotransmitter granules |
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What are Langerhans cells?
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-skin macrophages
-graft rejection -contact dermatitis |
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What are γδ T lymphocytes for?
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-anti-inflammatory
-anti-skin cancer |
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What are prickle cells? Why are they prickly?
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-main structural cells of epidermis
-they look prickly because they are only joined by desmosomes |
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What are examples of epidermal involutions? What are they for?
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-hair follicles
-sweat glands -sebaceous glands they provide outgrowth sites for the repair of skin |
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How do goose bumps work?
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Cold initiates contraction of the arrector pili muscle which squishes the skin in the angle to make a goose bump. This squeezes sebum out of the sebaceous gland and also makes the hair stand up straighter.
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What hormone promotes hair growth and what inhibits it? How is this different in the sebaceous gland?
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Estrogen promotes hair growth, testosterone + some pituitary factor inhibits it. In the sebaceous gland it is the opposite.
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What are free nerve endings for?
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-pain
-fine motion detectors |
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What are Krause end bulbs for?
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sense cold
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What are Ruffini corpuscles for?
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-sit on collagen fibers
-stretch receptors |
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What are Meissner's corpuscles for?
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-Schwann cells arranged parallel to skin
-detect lateral movement of skin -frequent in dermal papillae/ridges |
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What are Pacinian corpuscles for?
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-very large deep pressure receptors in the hypodermis
-tell when bladder is full -Schwann cells are perpendicular to skin |
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What is the Donnan potential?
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membrane potential affected by the presence of impermeable macromolecules
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What is the Nernst potential?
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equilibrium potential caused by the balance of an electrostatic and chemical potential gradient when one of two ions is permeable
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What is required in order to have a membrane potential?
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-gradient
-selectivity |
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How is the Nernst potential calculated?
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60 x log ([out]/[in]) / charge
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What three factors determine realistic flow across membranes?
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-partition (K)
-diffusion (D) -permeation (P) |
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What is the difference between hemochromatosis and hemosiderosis?
|
-hemosiderosis is iron buildup in cells (can be local or systemic)
-hemochromatosis affects entire organs (can be primary or secondary) |
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What does trichrome stain do?
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stains collagen
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What does congo red stain do?
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stains amyloid
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