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48 Cards in this Set
- Front
- Back
- 3rd side (hint)
Is pepsinogen or pepsin the active enzyme? |
Pepsin is active form. Pepsinogen is inactive enzyme. Acid activates |
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Mucosa (convoluted so large SA for absorption and secretion, also houses GALT), Submucosa (connective tissue allows elasticity), Muscularis Externa (longitudinal and circular muscles allows movement), Serosa (lubricates and prevents friction with digestive organs) |
GI TRACT |
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Liver makes bile, bile stored in gall bladder (also concentrates bile). Lingual lipase is... Lipase forms... |
Produced in mouth, starts fat digestion in mouth and also works in stomach. Pancreatic lipase used in small intestine (duodenum). Monoglycerides and fatty acids, which can diffuse into cell, triglycerides are then resynthesised in SER, secreted as chylomicrons into lacteals |
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Fat soluble vitamins follow fat absorption pathway (A, D, E, K). Water soluble vitamins absorbed by diffusion except for... |
Vitamin B12, binds to intrinsic factor which is produced in stomach, can then bind to complexes on CSM of epithelial cells and is taken in by endocytosis. |
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Microvilli are made of... Cilia are made of... |
Actin microfilaments (microvilli can't move) Microtubules (cilia can move) |
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Adherens, Desmosomes, Tight, Gap junctions (contains connexins)
Hemidesmosomes...
Gap junctions... |
Attach cells to the basement membrane
Allow cell-cell communication via passage of small substances. E.g found in neurons for rapid electrical transmission and in cardiac muscle for ionic transmission |
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3 uses of basement membrane |
Filtration, control of movement of molecules between tissues. Compartmentalisation, separation of epithelium and connective tissues. Tissue regeneration, act as a scaffold and guides new cells to correct locations, allow repair after damage. |
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3 types of exocrine ducts |
Merocrine (most common), fusion of vesicles with membrane, lose cargo by exocytosis, no loss of cytoplasm. Apocrine, fusion of vesicles with membrane, lose cargo and part of the cytoplasm too. Holocrine (holo=death), cell undergoes programmed cell death (apoptosis) and product is released. |
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Cells that secrete- Protein... Steroid (or lipids)... Mucin... |
Large RER, large nucleus Large SER, lots of mitochondria Developed Golgi (lots of glycosylation and protein modification) |
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Bone is a connective tissue |
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Cancer often results from epithelial cells as... |
They have a high mitotic index (divide more often) |
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Functions of connective tissue (3 things) |
Provides form and support (structural integrity)
Has immune cells (immune response) Thermoregulation |
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Connective tissue made up of cells and the extracellular matrix (blood plasma, bone, collagen and elastin).
Fibroblast cells help to synthesise the ECM, cells secrete parts of it (collagen and elastin) and it's assembled outside the cells. Fibroblasts also produce...
What is fibronectin? |
Elastin fibres, central core of elastin with fibrillin microfibrils surrounding.
Fibronectin is a glycoprotein which mediates adhesion between cells and ECM |
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3 types of connective tissue |
Loose, less collagen, used for defence and undergo swelling (inflammatory response).
Dense irregular, mainly collagen, provides strength and resists stretching/distention
Dense regular, mainly collagen, many parallel fibres (tendons and ligaments) with fibroblasts inbetween. Tendons have no elastic fibres so don't stretch |
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Collagen... Elastin fibres... |
Made of tropocollagen sub-units, forms triple helix. Covalent bonding between and within helices increases strength. Made of central elastin molecule and surrounded by fibrillin microfibrils. Produced by fibroblasts. |
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ECM uses (3 things) |
Structural support Anchors cells Retains growth factors (specifically done by GAG's) |
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Cellular components of connective tissue and function.
Have both fixed (5 things) and wandering cells (2 things). |
Fibroblasts- synthesise elastin and collagen
Mast cells- immune response
Adipose cells- lipid storage
Myofibroblasts- synthesise fibres and assemble ECM. Seal wounds closed by contracting on the sides of cut.
Macrophages- phagocytic cells
Wandering, Lymphocytes and plasma cells (immune response) |
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Areas of the body with a lot of adipose tissue (lots of adipose cells present) such as the hypodermis... |
Act as heat insulators, as adipose cells store lipids. Also absorb shock and act as a food store. |
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Epidermis Dermis Hypodermis |
Many functions Supporting tissue, mostly collagen and elastic fibres Insulator, lots of adipose cells |
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Gastrointestinal control systems respond to many types of stimuli |
Sight of food (cephalic=head), acidity, volume of (stomach=gastric), conc. of specific digestive products (intestinal).
Reponse can be neural (autonomic nervous system) or hormonal either endocrine (into blood) or paracrine (into luminal contents) |
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Stimulus-->Receptor... |
Central nervous system, uses autonomic nervous system, travels to enteric nervous system, endocrine cells, hormone released into blood (or not released anymore), hormone presence / absense has a response to effector cells, leads to response |
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Mastication is... Peristalsis is... |
Chewing food, increases surface area A sequence of contraction and relaxation of muscles that moves chyme, food through lumen of digestive system |
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High osmolality means high concentration of dissolved particles/salt so is a factor to show digestion is occurring in lumen of both stomach and intestines. For example when there is a high osmolality (conc of dissolved particles/salt) in the intestines (H+ and nutrients also increase when this occurs), receptors against luminal membrane detect this, autonomic nervous system involved, CCK released (causing bile to be released into small intestine from the gall bladder) and secretin released as well (which stimulates secretion of bicarbonate into duodenum (neutralises H+), secretin also inhibits gastrin (this means when secretin produced, less H+ produced by parietal cells in stomach). |
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Gastrin
Secretin
CCK
(Both secretin and CCK cause 2 effects each) |
Stimulates release of H+ from parietal cells in stomach. Stimulated by cephalic response E.g sight, taste of food. And by peptides in stomach.
Inhibits gastrin, and stimulates release of bicarbonate into duodenum (neutralises acid). Stimulated when digestive products enter duodenum (specifically H+).
Stimulated by increase of digestive products in duodenum, causes increased release of digestive enzymes from pancreas into small intestine, also causes the release of bile from where it's stored in the gall bladder into the intestine. Emulsifiers fats. |
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Main factor that results in gastric emptying (by increasing strength of contraction in stomach) is...
Other factors (in duodenum) include... |
Volume of chyme in stomach Increased H+, increased osmolality, increased fats, increased distension of walls. |
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Filling of stomach, receptive relaxation occurs (stimulated by eating), increases volume so can eat more food. Mixing occurs at antrum of stomach (end) |
Peristalsis causes mixing |
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3 types of gastric exocrine secretory cells |
Mucous cells (produce alkaline mucus to protect lining of mucosa from stomach acid. Stays on lining only) Parietal cells (HCL secreted, stimulated by gastrin) Chief cells (pepsinogen secreted which is activated by HCL into pepsin) |
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HCL produced in cephalic phase and gastric phase, but production is inhibited in intestinal phase (secretin inhibits gastrin) |
Gastrin stimulates production of HCL from parietal cells |
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Pepsin is functional (activated) enzyme, pepsinogen is precursor. Once pepsin is produced it catalyses its own production (autocatalytic, positive feedback). |
Original pepsinogen secretion due to nervous response |
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Secretin and CCK work together (both have 2 effects). Gastrin is opposite to secretin. Secretin inhibits gastrin and stimulates HCO3- release by pancreas into duodenum.
What originally stimulates the production of gastrin (leading to H+ release by parietal cells)? |
The presence of peptides in the stomach stimulates gastrin production. |
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Regulation of secretin by H+ entering duodenum? |
Detected by chemoreceptor, leads to production of secretin, travels in the blood to pancreas, acts here to increase production of bicarbonate (HCO3-), more bicarbonate travels to duodenum to neutralise acids. Secretin also inhibits gastrin |
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Effects of increasing fatty acid and amino acid concentrations in the duodenum (conc of digestion products) and how this comes about? |
Chemoreceptor detects change, nerve signals (autonomic) cause increased secretion of CCK, CCK travels in the blood to the pancreas, stimulates enzyme production here, more enzymes enter duodenum and increased digestion occurs. Also bile is released from gall bladder into duodenum |
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Parietal cells Chief cells Both active in the stomach (exocrine cells) |
Secrete H+ Produce pepsinogen |
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Peptides in the stomach lumen stimulate production of gastrin (peptide hormone) which stimulates parietal cells to secrete H+. Very low pH inhibits gastrin, so H+ of stomach is not excessively high, negative feedback |
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It is important that we control the rate of gastric emptying as we cannot control the rate of absorption |
True |
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Resting potential, Na+K+ ATPase pump, 3Na+ out, 2K+ in, also leaky K+ channels are open so K+ leaves cells. Membrane potential is -70mV (polarised membrane).
Depolarisation caused by... |
External stimuli, E.g mechanical stretching causes Na+ channels to open, Na+ rapidly enter, if stimulus large enough (greater than threshold value) then an action potential is generated, is propogated along neurone. All action potentials are same size (all or nothing response) but a greater stimulus causes more frequent action potentials. |
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EPSP-IPSP cancellation occurs when a cell receives information from an inhibitory and an excitatory synapse. No overall effect. Spatial (multiple neurones) or temporal (one neurone firing very frequently) |
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Removal of neurotransmitter by hydrolysis and reuptake (active) ensures discrete signals only. Also repolarisation takes time, ions need time to return to correct side of membrane. |
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Contraction of skeletal muscle occurs when Ca2+ is in sarcoplasm (released from sarcoplasmic reticulum) and ATP is available. Relaxation occurs when Ca2+ is reuptaken into sarcoplasmic reticulum. Myosin ATPase needed to hydrolyse ATP to provide energy.
Action potential moves through... |
T-tubules (in skeletal muscle cells), causes Ca2+ to be released from lateral sacs (terminal cisternae) of the sarcoplasmic reticulum into cytosol, foot proteins allow Ca2+ to pass through to bind with troponin. |
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How do muscles work to delay fatigue? |
Asynchronous recruitment of fibres, some fibres are resting while others contract. Combine many motor units (that can have different numbers of muscle fibres) for larger contraction. |
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Twitch, summation (muscle fibre restimulated before its completely relaxed), tetanus (maximum sustained contraction) |
Tetanus leads to fatigue or muscle damage. |
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Creatine is phosphorylated (at rest) to form phosphorylcreatine which is used as an energy store in muscles. During exercise it is dephosphorylated and the phosphate released is used to form ATP (from ADP). Fatigue happens when... |
Lactic acid is produced in muscles and ATP can no longer be produced. |
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3 major types of muscle fibres |
Slow-oxidative, SLOW CONTRACTION, enzymes for oxidative phosphorylation, high resistance to fatigue, many mitochondria. Fast-oxidative. FAST CONTRACTION, enzymes for oxidative phosphorylation, intermediate resistance to fatigue, many mitochondria. Fast-glycolytic, FAST CONTRACTION, has enzymes for anaerobic respiration, few mitochondria, low resistance to fatigue. |
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Smooth muscle structure and how it is different to skeletal |
Doesn't form myofibrils, forms diamond lattice. At rest, myosin cannot bind to actin- myosin light chains need to be phosphorylated for that to occur. Troponin is not present, tropomyosin is present but does not cover binding sites. Crosslink can form across entire length of myosin so... |
Greater shortening than skeletal muscle, as actin filaments can be pulled further along relative to myosin. |
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Smooth muscle contraction
Begins with Ca2+ being released from the sarcoplasmic reticulum, enters sarcoplasm via membrane channels (no t tubules in smooth muscles), Ca2+ binds to... |
Calmodulin, this activates MLCK (myosin light chain kinase) which phosphorylates the light chains in myosin heads, this increases myosin ATPase activity so myosin can interact with actin (crosslink).
Ca2+ removal is slow, longer contraction. Also graded response (proportional to how much Ca2+). |
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Multi unit smooth muscle Single unit smooth muscle |
Contraction occurs as multiple units, each unit functions independently, and each one has to be stimulated for contraction. Contraction occurs as a single unit, more efficient but slower |
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Single unit smooth muscle can be phasic or tonic |
Phasic, contracts in bursts, each contraction stimulated by an action potential. Tonic, always partially contracted, has a low resting potential (near 0). |
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Cardiac muscle is pretty similar to skeletal muscle (troponin, tropomyosin, actin-myosin sliding filament mechanism, striated, t tubules). However it has autorhythmic beating (contractions), and no summation can occur because of the long plateau phase (long refractory period) due to Ca2+ in slow. Na+ in fast first, then Ca2+ in slow, then K+ out fast. Myogenic, stimulates itself. Affected by sympathetic and parasympathetic systems. SAN controls heart beat first because..., then... |
Because it has the fastest rate of Depolarisation. AVN then Purkinje fibres after that. 2nd action potential cannot be triggered until membrane returns to correct potential of -90 |
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