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Digestive System: Processes, Regulation, and Functions, Exams of Physiology

Barry UniversityPhysiology

All about Physiology in paragraph form

Typology: Exams

2019/2020

Available from 09/11/2021

arianeleconte
arianeleconte 🇺🇸

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Ch 15. Digestion
- Gastrointestinal system: composed of both GI tract (mouth->pharynx-> esophagus->
stomach->small intestine -> large intestine -> rectum and accessory glands such as
salivatory glands, liver, gallbladder, pancreas.
- Primary function is to transfer substances from the external environment to the internal
environment.
- Digestion is without regulation and designed for maximum absorption. It does not
regulate reabsorption but instead produces indigestible substances not absorbed in our
body.
- Gastrointestinal system is composed of both the GI tract and accessory organs
- Ingestion -> digestion -> secretion (salvia, acid, bicarbonate gets secreted outside the
body) -> absorption of break down products (active transport) -> motility (move food
down to anus -> defecation of undigested material
Functions of Gastrointestinal organs
- Mouth pharynx and esophagus
oMouth: site of ingestion
oMechanical digestion through matsifcation. AS we chew food, our teeth help
making the particles smaller while mixing the particles with saliva made up of
water, mucin to lubricate, electrolytes to buffer, lysosomes to kill bacteria,
salivary amylase starting the chemical digestion process, calicrim gives positive
feedback system with gradicin for more salivia to be released. These help
potential pathogens and moisten and buffer the bolus.
oAutonomic nervous system regulates the secretion of salvia. Both
parasympathetic and sympathetic stimulation will increase salvia secretion
however parasympathetic does it to a much greater degree. Once bolus is
formed, propulsion begins. Deglutition or swallowing center in the medulla
olbongata to coordinate the muscle groups so bolus moves down to esophagus
and finally the stomach, using peristalsis. Two phases of deglutition:
Buckle phase: voluntary (roll tongue to force bolus into pharynx)
Pharyngeal-esophageal phase: involuntary (swallowing coordinating
movement from pharynx to esophagus)
- Stomach
- Mechanical digestion and propulsion occur together through peristaltic contractions to
get peristaltic waves of contraction that start in the cardiac region of the stomach and
work across to the pyloric region.
oReceptive relaxation: stomach inhibits background contractions so stomach gets
bigger to allow contents to come in. Continues as you add food.
oChime, an acidic and hypertonic fluid inside the stomach that decreases the
amount of contractions in the stomach, gets squeezed out and goes into the
small intestine with each contraction. The rest of the majority of chime gets
dumped back into the middle of the stomach through retropulsion.
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Ch 15. Digestion

  • Gastrointestinal system: composed of both GI tract (mouth->pharynx-> esophagus-> stomach->small intestine -> large intestine -> rectum and accessory glands such as salivatory glands, liver, gallbladder, pancreas.
  • Primary function is to transfer substances from the external environment to the internal environment.
  • Digestion is without regulation and designed for maximum absorption. It does not regulate reabsorption but instead produces indigestible substances not absorbed in our body.
  • Gastrointestinal system is composed of both the GI tract and accessory organs
  • Ingestion -> digestion -> secretion (salvia, acid, bicarbonate gets secreted outside the body) -> absorption of break down products (active transport) -> motility (move food down to anus -> defecation of undigested material Functions of Gastrointestinal organs
  • Mouth pharynx and esophagus o Mouth: site of ingestion o Mechanical digestion through matsifcation. AS we chew food, our teeth help making the particles smaller while mixing the particles with saliva made up of water, mucin to lubricate, electrolytes to buffer, lysosomes to kill bacteria, salivary amylase starting the chemical digestion process, calicrim gives positive feedback system with gradicin for more salivia to be released. These help potential pathogens and moisten and buffer the bolus. o Autonomic nervous system regulates the secretion of salvia. Both parasympathetic and sympathetic stimulation will increase salvia secretion however parasympathetic does it to a much greater degree. Once bolus is formed, propulsion begins. Deglutition or swallowing center in the medulla olbongata to coordinate the muscle groups so bolus moves down to esophagus and finally the stomach, using peristalsis. Two phases of deglutition:  Buckle phase: voluntary (roll tongue to force bolus into pharynx)  Pharyngeal-esophageal phase: involuntary (swallowing coordinating movement from pharynx to esophagus)
  • Stomach
  • Mechanical digestion and propulsion occur together through peristaltic contractions to get peristaltic waves of contraction that start in the cardiac region of the stomach and work across to the pyloric region. o Receptive relaxation: stomach inhibits background contractions so stomach gets bigger to allow contents to come in. Continues as you add food. o Chime, an acidic and hypertonic fluid inside the stomach that decreases the amount of contractions in the stomach, gets squeezed out and goes into the small intestine with each contraction. The rest of the majority of chime gets dumped back into the middle of the stomach through retropulsion.

o Rate of contraction of the stomach muscles will be influenced by pacemaker cells and environment in the stomach and intestine. Pacemaker cells depolarize more slowly allowing for a decrease in the rate of contractions. The acidity of the chime influences the activity of pacemaker cells

  • Chemical digestion takes place through two pathways: breakdown of proteins through pepsin. Chief cells secrete pepsinogen activated to pepsin by HCI secreted by parietal cells. Pepsin takes proteins and breaks them down to peptides. o Pepsin works well in low acidity environments in the stomach. Once pepsin enters the small intestine, bicarbonate ions from the pancreas increase the pH to deactivate pepsin.
  • Small intestine o Most of absorption takes place in the small intestine o Mechanical digestion and propulsion occur together. As the peristaltic waves form across the stomach, mechanical digestion also occurs through segmentation. Segmentation contracts and relaxes neighboring portions of tubes. o Chemical digestion: break down food products down to subunit so that it can be absorbed through diffusion or transporters  The pancreatic juice has bicarbonate ions to buffer the hydrogen ions that come from the HCI secretion in the stomach to bring pH of chime back to neutrality.  Chemical digestion of carbohydrates through amylases  Maltases – complex -> individual sugar molecules (maltose, sucrose)  Sucrase –  Lactase –  Trypsin – protein digestive enzymes  Chymotrypsin – specific amino acid sequence  Carboxypeptidase - takes off amino acids from carboxy terminus  Aminopeptidase - takes off amino acids from amino terminus  Lipases – break down fat molecules  Nucleases – break down nucleic acids o Liver produces bile o Absorption can be active (driving force for passive process) or passive transport  Fats are absorbed directly into the lacteals tot the lymphatics to get to the general circulation  Proteins and carbohydrates go into the capillaries and the portal system to the liver where they will be processed
  • Large intestine o Propulsion  What is left of the chime gets moved through three ways: peristalsis,  Mass movements: long slow contractile waves that force material towards rectum

increases, intestinal cells release secretin to stimulate the release of bicarbonate ions from the pancreas and liver. This will buffer the hydrogen ions and decrease the amount of acid secreted in the stomach which will decrease the hydrogen ions further and decrease ethe contraction starting in the antrum of the stomach. Phases of GI control

  • Ways of regulating GI tract primarily divided upon where the stimulus location is going to be. The cephalic phase one of the long reflex pathway, is initiated through the head. Sympathetic and parasympathetic nerves feed in to regulate the nerve plexus flexible within the gastrointestinal tract to either increase or decrease secretion and motility. The gastric phase involving both long and short reflexes, moves the food into the stomach. It uses the hormone gastrin to decrease the acidity of the stomach. As the environment in the stomach becomes diluted with the food you ingest, you start to break down proteins with pepsin to form peptides to help mediate the long and short reflexes for the stomach to go through mechanical digestion, propulsion and chemical digestion.
  • In the intestinal phase, most absorption takes place here. Chime gets added to the small intestine and creates tension, hydrogen ions from the HCI secreted in the stomach, hormones and breakdown products such as peptides all trigger the intestinal phase of the GI control. Hormones such as cholecystokinin (CCK) and glucose dependent insulinotropic peptide (GIP) will regulate activity between different organs so it is the most efficient with the digestive process. Mouth, pharynx and esophagus
  • Chewing: activate somatic motor neurons to close jaw and as jaw closes, to activate mechanoreceptors to inhibit the somatic motor neuron creating rhythmic contractions making enzymes work much more efficiently.
  • Saliva, secreted into the buckle cavity based on the activation of chemoreceptors and pressure receptors, mixes with the food ingested with the help of the lubrication from the mucus to form the bolus and eventually swallow.
  • Swallowing comes from the swallowing center and medulla oblgaota. As the phase of swallowing gets triggered and creates a peristalsis wave, respiration and inspiratory neurons are inhibited to continue the swallowing in the pharynx and eventually to the esophagus.
  • How food gets ingested: move bolus into esophagus, constrict the upper esophageal sphincter and get a peristalsis wave which pushes the bolus down into the stomach. As we get to the stomach, the lower esophageal sphincter relaxes and opens up to dump the bolus into the stomach. If lower esophageal sphincter fails to keep the stomach acid out, as a result a heartburn rises. Stomach (FIGURE)
  • The stomach generally secretes two products: hydrochloric acid and pepsinogen. The HCI secretion occurs in the parietal cells. Partial cells are stimulated to secreted HCI by many factors such as parasympathic activity, hormones such as gastrin and histamine, distension of stomach, low acidity, production of peptides and excessive caffeine. To

inhibit the partital cells, the pH must decrease, increased osmolarity and nutrient content, distention of the small intestine and CCK and secretin to regulate the secretion.

  • CO2 and H20 create carbon hydrogen ions. The hydrogen pump on the apical surface pumps the hydrogen out to get a chloride shift with bicarbonate ions. The bicarbonate enters the blood increasing the pH while hydrogen ions go into the lumen. The chloride can now come down the gradient with the help of chloride channels. Chloride can also come down with withs sodium creating sodium chloride so the sodium gets recycle with the sodium potassium ATPase so end up with chloride coming in and balancing the charge of the proton pump. Pepsin secretion (FIGURE)
  • Stimulate the release of pepsinogen (inactivated) from the chief cells with the exposure of HCI. The pancreas and stomach make zymogens to be activated after they are activated. Thus, once pepsin is activated, a positive feedback cycle occurs activating more pepsinogen to pepsin. The pepsin eventually breaks down the proteins to peptides. However, once pepsin is moved to the small intestine and the pH is increased, it is inactivated and must be digested and absorbed. Gastric motility
  • Stomach moves in multiple ways such as receptive relaxation inhibits the muscles of the stomach from contracting. The swallowing center combined with the parasympathetic nervous system triggers the receptive relaxation as it initiates the movement of food toward the stomach. Once food enters the stomach, the activity of pacemaker cells become regulated to regulate the rates of the peristaltic contractions. As the peristalsis moves towards the pyloric sphincter, a retropulsion is exerted, or In other words, the food gets dumped back into the middle of the stomach so only a Small amount of chime gets released
  • Pacemaker cells determine the rate of contraction while neural and hormonal inputs will determine the force of the contractions. How much contractile strength we get will be regulated through hormones and neural input Vomiting
  • Vomiting center is in the medulla omblagata it is adaptive because it causes us to regurgitate potential toxic foods causing reserves peristalsis. Starts at the contractile rate at the pylorus and workback towards lower esophageal sphincter for food to come out. Dehydration, acid base problems, low fluid problems like bulimia are results of excessive vomiting Pancreas
  • Secrete both hormones (endocrine function) and digestive enzymes and bicarbonate (exocrine function) ions outside the body
  • Parasympathetic nervous system, CCK, presence of fats and amino acids in the digestive tract causes the secretion of zymogens from the pancreas o Trypsinogen: activated to tripsin through an enzyme called enterokinase. Found in the apical membrane of intestinal cells. Tripsin then activates the lipase, nucleases, and other protases as well as break down proteins into peptides. Enzymes are stimulated through neural and hormonal activity, driven by the environment within the small intestine

the body to produce energy, carbon dioxide and water. During the absorptive state, glucose is the major energy source for every cell in the body. However, some of the glucose gets stored as a complex carbohydrate, glycogen, occurring in two primary locations: the muscle (for anaerobic fibers whom use glucose as an energy source) and the liver (site of glucose production during post absorptive state). As a result, large branches of chains of glucose molecules are used as storage and converted to fat in adipose tissue. In the fat cells, glucose gets converted into fatty acids and glyceropholate combining to form the actual fat, triacyclglycerols. The liver, as it plays an important for glucose synthesis, takes the glycogen produced, to produce fatty acids and glycerophosphates to make triacyclglycerols. Triacyclglycerols then combine with proteins and amino acids to form very low density lipoproteins or (VLDL) having a lot of fat contained in them. VLDL get released into the blood and cells until they are digested by a degrading enzyme, lipoprotein lipase, taking the fat molecules and breaking them down into fatty acids and glycerol. This lipoprotein is now concentrated In the endothelium capillary within adipose tissue and get broken down into glycerol and fatty acids which will diffuse into the cells converting it to triacyclglycerols.

  • Glucose and amino acids will be freed up from complex carbs into individual glucose molecules to enter the blood. Glucose molecules Used by most cells into produce energy, CO2 and water. During absorptive state, glucose is the major source in the body to run the metabolism. Muscle and liver store glucose molecules.
  • Glucose gets converted into fatty acids and glycerophosphate as triacyclglycerols. Liver primary site of glucose synthesis to combine to proteins that have very low density lipoproteins (mainly fat) for a VLDL release from the liver cells to travel through blood until digested by lipoprotein lipase
  • Most of glucose taken up by liver ends up as fat in the adipose tissue. PACKAGED AS A VLDL. Triacyclglycerols metabolism (FIGURE)
  • Triacyclglycerols (fat) in GI unit get broken down with the help of lipases, bile salts, micelles so they can diffuse across the cell membrane to then get resynthesized in the smooth endoplasmic reticulum and converted to chylomicrons to be released in the lacteals and travel through the lymphatic system to the general circulation to the cells. Where lipoprotein lipase is activated, the large fats can be broken down to fatty acids and glycerol phosphates to make triglycerides. In the end, it is taking the fats that were absorbed and storing them in adipose tissue. The fat that is obtained during the absorptive state for storage comes from fats that were absorbed glucose converted in the adipose tissue Amino acids metabolism (FIGURE)
  • Amino acids in the GI tract are Used for protein synthesis. Amino acids are brought into the muscle, liver and other cells. The muscle makes contractile proteins by storing amino acids as proteins and in the liver. Excess amino acids become deaminated by going through citric acid cycle for the liver to use for energy instead of using glucose. The deaminated amino acids get converted to fatty acids to add into glycerophosphates

so Triacyclglycerols is produced as well as VLDL’s. All in all, excess energy gets stored as fat Postabsorptive State: occurs when nutrients are done being reabsorbed and energy stores are being used (FIGURE)

  • Producing glucose to maintain glucose levels without absorbing glucose
  • During the post-absorptive state , there are two sets of reactions: one that produces glucose or gluconeogenesis reactions and those that allow the cells to use something other than glucose as an energy source which can be termed the glucose sparing reactions
  • Pathways that produce glucose: the liver is the primary source of gluconeogenesis. What occurs is the glycogen that was made during the absorptive state gets taken to finally free the glucose to get secreted into the blood and let the nervous tissue maintain its metabolism. The glycogen stored in the muscle also gets ran through glycolysis to form pyruvate and lactate secreted by the muscle cells to go the liver. Once in the liver and they are then resynthesized into glucose from the glycogen molecules.
  • Also in the muscle, there is a breakdown of proteins to amino acids and released in the blood and carried back to the liver (major pathway for glucose production). Once into the liver, amino acids are deaminated taking the amine group and forming urea and keto acids. These keto acids then convert them back to glucose.
  • Glycerol can also be converted back into glucose. In the adipose tissue, triacyclglycerols are broken down glycerol and fatty acids, shifting it off to the liver and converting it into glucose. Glucose is being produced in the liver from fat molecules, from glycogen, from converting glycogen and from amino acids from the breakdown of proteins and muscles. Glucose sparring reactions (FIGURE)
  • Maintaining glucose in the body by decreasing the usage of glucose by other tissue by increasing the usage of fats for energy in those systems. That then leaves the glucose produced in liver for the nervous system to use it as energy making a three carbon backbone and long chain fatty acids to be transferred to liver and reincorporated into glucose synthesis. Side chains or short fatty acids get distributed to the tissues and liver. The livers primary function in this case is for energy production and the conversion of ketones to be released to the tissues for energy production. Ketones and fatty acids are both used by vast majority of the tissues for energy productions and to maintain metabolism.
  • Build up resources from Absorptive state for the postabsorptive state Endocrine and Neural Control of the Absorptive and Postabsorptive states
  • Under both endocrine and neural control
  • The pancreas very important in the digestive function because of its endocrine and exocrine functions.
  • Beta cells produce insulin
  • Alpha cells produce glucagon
  • Bone growth, a living tissue, determines maximum height. o The compact bone surrounds the spongey bone. The spongey bone is an area where growth occurs. The long bone contains the epiphyses located at the ends of the bone and in the middle contains the epiphyseal growth plate. Within the growth plate are osteoblasts and osteoclasts working to elongate the bone. On the distal end of the bone, osteoclasts work in converting the bone back into cartilage to make it the growth plate move toward the end. On the proximal side of the bone, cartilage gets reverted back into bone through the help of osteoblasts thus, osteoblasts and osteoclasts are always remodeling the bone under the influence of hormones.
  • Two big growth periods: o First years of life o Puberty
  • Estrogen causes fusion of the epiphyseal growth plate sooner than testosterone, hence why men are taller than women.
  • Environmental factors influencing growth o Nutritional state: how many calories you receive and what kind of food stuffs you take in.  Too many nutrients: overweight o Presence or absence of disease
  • Hormonal influences on growth o Growth, thyroid, estrogen, ACTH hormones o Growth hormone : secreted by anterior pituitary, stimulates mitosis by stimulating insulin growth factor 1. Growth hormone also increases uptake of amino acids, protein and RNA synthesis, ribosome synthesis, and mitosis to help stimulate cells to grow o Too much growth hormone = giantism (acromegaly) o Too little growth hormone = dwarfism o Too much growth hormone as adult: acromegaly (certain area gets big)  Produce insulin like growth factor 1 (IGF -1 = somatomedin C), giantism, dwarfism, acromegaly o Thyroid hormone : important in growth and development. Thyroid hormone has a permissive effect to growth hormone and necessary for proper development of the nervous system after birth. If one cannot not produce enough thyroid hormone, it Is resulted to creatism because nervous system does not develop (mental retardation) o Insulin : required for normal growth. Insulin will bind to insulin like growth factor 1 to stimulate growth o Sex hormones : responsible for pubertal growth spurt. In puberty, gonads are activated to produce estrogen and testosterone to stimulate growth in long bone. Sex hormones increase the secretion of growth hormone and less of the release of somatostatin to get the closure of that upper epiphyseal growth plate.

o Cortisol : Cortisol is released under periods of stress and inhibits growth by inhibiting DNA synthesis and bone growth. It helps In breaking down protein rather than building up protein o Compensatory growth : regenerates during adulthood. Occurs when damage or loss of an organ precipitates, and the remaining portions grow back to the initial mass of the organ before the damage or donation occurred. Regulation of total body energy expenditure

  • As we take up energy, we are also forming caloric balance by taking in nutrients with the digestive system, breaking them down into their components parts, modifying and storing during the absorptive state and eventually breaking down into CO2 and H (urea forming) while releasing heat and providing energy o Metabolic rate: determines how energy balances. Ones metabolic rate is the amount of energy you use per unit time (measure oxygen consumption to determine MR) o Determinates of MR: influenced by age (young = increases) , sex (testosterone = higher MR), height and weight, pregnancy, body temperature, environment temperature, activity levels (more activity = higher MR) , awake or asleep o Basal MR: at rest in postabsorptive state decrease if increased age or size or sex  Determinates of basal MR:  Amount of thyroid hormone and epinephrine increase the use of ATP which increases heat thus, increasing MR  Eating  Muscle activity or change in muscle tone influences basal MR  Hyperthyroid: eat a lot  Hypothyroid: always cold (not generating heat) o Total body energy balance –  food intake = internal work + external work + - storage  if the amount you eat is less than the internal and external work then the access comes from storage o Control of food intake (FIGURE)  Glucagon, neuropeptide y, drexins  Inhibit to stop eating: stretch receptors, decrease in plasma glucagon, increase in plasma glucose CH.19: Regulation of body temperature As temperature becomes Increased, the time of excitation contraction coupling decreases thus, the rate of tension increases
  • Poikilotherms: animals that have changing body temperature
  • Homeotherm: same constant body temperature
  • Ectotherm: animals get heat for thermoregulation from outside
  • Endotherm: generate heat inside

hypothalamus. Feeding into the hypothalamus are thermoreceptors deep in the viscera, CNS or peripheral in the appendages and surface of the body in the thorax

  • Peripheral receptors give us more info about the environment and how its changing
  • Deep thermoreceptors represent the cores temperature (what we try to regulate - appendages decrease temperature when it is cold so we loose less heat and conserve that heat for the core rather). Periperhy thermal receptors are eimportant because they give the ability to start a response before a change in the bodys temperature starts o Regionalhetrothermie: different temperatures in different parts of the body based on where it is o Acclimatization: in cold temperatures = loose heat to the environment which causes body temperature to drop triggering all the heat production mechanisms to bring or maintain normal body temperature o Feet forward reflexes: give the ability to minimize deviation in any particular variable, or temperature.
  • Heat production and heat loss: mechanisms to balance the heat budget in the body o Amount of heat produced/ lost will determine where equilibrium temperature will be. If heat is being lost into the environment, it must be generated more to balance it out. o Heat production is produced through chemical reactions in the body
  • Two ways to influence heat production : increase voluntary activity o Muscle activity: skeletal muscle is the primary source of heat production and is highly aerobic  Change/increase muscle tone by decreasing body temperature  Increase body temperature decrease muscle tone  Shivering: simultaneous activation of flexors and extensors around a joint  Hypothalamus feeds into motor cortex and stimulates both flexors and extensors to activate and vibrate. (uses energy) o Changes to metabolism (nonshivering thermogenesis) is an increase in metabolic rate with chronic exposure to the cold. With extended exposure to cold weather, the thyroid hormone, having a caloric effect, increases which causes all of the cells to work faster and burn more energy to produce more heat. The stimulation of epinephrine to stimulate the breakdown of metabolic pathways is also used for heat production as it gears up the catabolic and energy usage pathways.  Brown fat having a lot of mitochondria, and a the protein thermadulin, allows for the break down of food stuffs to run electrons down the electron chain letting hydrogen ions pass through the thermaduin molecule, allowing for the burn of energy without ATP. All of the energy reserves get broken down to generate heat.
  • Heat loss (has to be present if we have heat production to maintain body temperature e. Heat production = heat loss)
  • Four mechanisms of heat transfer

o Radiation: A significant amount of potential heat exchange takes place through radiation. The main radiative heat source is the sun but everything at absolute 0 radiates energy. We can lose or gain energy through radiation. (go under lamp for heat) (raised to the fourth power) o Conduction: heat transfer between objects in contact with one another. The constant can influence the rate of conduction depending on the surfaces that are in contact o Convection: in contact with medium (moving the medium over the surface of the body which allows for a transfer of heat more rapidly (fan). With convection, we get more heat transfer as long as its moving in the right direction  Can be free or forced  Free convection: you are warmer than the air around you. as warmer = less dense (warm air next to skin = becomes less dense) Causing a change in the density of the air which causes the air to move to forced convection  Forced convection (more common): wind is flowing over your body to transfer heat more rapidly. o Evaporation: a way one can lose heat. Loose 580 per gram per water we can evaporate. How much evaporation occurs depends on the partial pressure of water or the relative humidity in the environment vs the surface of the skin. By altering the area and the amount of water created, this allows for the evaporation of water and the ability to maintain the normal body temperature set point  By Increasing the amount of sweat produced, the amount of sodium decreases in the sweat so there isn’t any problems with sodium balance. Also, by increasing aldosterone, reabsorption of sodium in the gland occurs.  If exposed to cold, the production will increase as more heat is being lost to the environment. By increasing insulation, fat layers get built loosing less heat to the environment. By decreasing body temperature, shivering will start to initiate, allowing much greater control of vasoconstriction that takes place in the periphery.

  • When exposed to cold, increase the heat production by increasing insulin to loose less heat to environment.
  • Fever: regulating at a higher temperature (fibral response) fight potential pathogen better o Endogenous pyrogens: stimulate response for body temperature to increase to fight immune response more efficiently
  • Exercise: may cause hypothermia as activity is increased thus increasing heat production. Heat production may become greater than heat loss resulting in an increase in body temperature. o Body temperature primarily gets regulated through vasomotion and sweating changes

in killing potential pathogens by producing oxygen free radicals (desruptive to DNA and protein synthesis – dangerous to cells). Paraoxzysome (a neutralizer organelle) then, take the oxygen free radical and turn it into water and oxygen to eliminate them. Some neutrophils release a harmful chemicals to kill pathogen while killing self in process. b. Natural killer (NK) cells – roam around the body by a process known as immunological surveillance. They Go through the blood, lymphatics, within extracellular fluid and look for cancerous or virous affected cells to attack and destroy it. These cells Move cancers before you know you are sick and are Activated by interferon c. Inflammation – can be stimulated by a variety of stimuli (heat, frostbrite, UV light, physical trauma). Helps to localize potential area preventing the spread to neighboring areas. Helps to prepare the area for repair. Phagocytes are the key cell types in an inflammatory response. (phagocytes are used for inflammation responses Clinical types of inflammation : rubor et tumor cum calorr et dolor = redness and swelling with heat and pain Basic physiological changes that occurs during inflammatory responses : i. Trigger changes to physiology of the area which lead to redness, swelling and pain: release inflammatory chemicals which causes Vasodilation and increased vascular permeability. Many of these chemicals cause a local vasodilation which causes Hyperemia which occurs when there is an increase in blood flow which would cause redness and heat because core temperature is now brought to the area of inflammation. As vascular permeability becomes increased, more fluid comes out of capillary into the extracellular fluid which, overtime, causes a swelling. The pain is due to the pressure on the nerve endings because of the swelling activating the pain receptors ,and competition for oxygen and nutrients. ii. Phagocyte margination – activating phagocytes around the body while inflammation is taking place. Leukocytosis inducing factor: trigger neutrophil activation through a positive chemotaxis. Once at area of inflammation, phagocytes attach to capillary wall through margination, then, the movement to go to extracellular fluid though diapedesis, neutrophil exudation: neutrophils get to site of inflammation through margination and diapedesis. (first line of defense) Neutrophils phagocytize things that should not be there. Monocytes enter the area of inflammatory response, and differentiae to macrophages to replace neutrophils. d. Antimicrobial substances: three main categories i. Complement system – (series of 30 proteins which are involved in various immune responses to help amplify the immune response) Three groups or individual complement proteins:

  1. C5-C9 = membrane attack complex (MAC) C1 initiates the classical complement pathway

a. membrane attack complex (MAC) : C5,c6,c7,c9 make up this membrane. Have both hydrophilic or hydrophobic components to form a hole in a cell and ultimately kill the cell. b. C3B: an opsonin which inserts self in forieg/affected cell and puts “handle” on that cell for phagocyte to engulf it c. C1: come off an the antibody when binded to an antigen to trigger activation of M.A.C (membrane attack complex) to lyse cell ii. Interferon : a chemical release by virus affected cells. Decreases the rate of cell division and decreases the ability for the virus to multiply. Activates natural killer cells and macrophages. If a cell is infected , it starts to make this chemical to alert the other cells iii. Defensins : group of substances of peptides that are released on the skin epithelium both hydrophilic and hydrophobic and insert self and polymerize to form a hole in cell to cause death to the cell. e. Fever: systemic response where a class of chemicals called pyrogens, reset the hypothalamic thermostat.  Body temperature is that regulated to a higher level. Increase temperature to fight immune reaction  Pyrogens cause the thermostat to turn to a warmer temperature to increase rate of chemical reactions thus Causing the liver and spleen to absorb iron and zinc out of blood (slowing the rate of multiplication of pathogen  Fibral response is good as it increases the ability of body to fight reaction to potential pathogen Specific body defenses – fight a single antigen. A pathogen triggers immune response to amplify and destroy that one pathogen or amplify a response to a pathogen that is present giving a lot of cells to fight pathogen. Produces memory cells giving the ability to react more rapidly if exposed to the same pathogen

  • Specific body defenses are Antigen specific meaning they will fight a single antigen
  • Specific body defenses are Systemic working throughout the body, in the blood, lymph, extracellular fluid, lymph nodes (not localized)
  • Has memory cells that react more rapidly if exposed to same pathogen again A) Specific defenses use Lymphoid organs as a defensive strategy a. Primary lymphatic ctissues: contains bone marrow that produce white blood cells and thymus. This teaches cell the difference between cell vs non cell and prevent an autoimmune disease. Once cells are released they aggregate to secondary lymphatic tissues b. Secondary lymphatic tissues: lymph nodes, spleen, tonsils B) Cells of the Immune system: Four primary types of cells used: a. Lymphocytes: B and T cells. i. B cells will become immunocompetent within bone marrow (self vs non- self).
  • IGA: dimer secreted onto epithelial surfaces gibing four rbinding sites to preven pathogen
  • IGM: first of antibody classes made up of 5 antibodies held together Sub mediated immune response: uses T cells, recognize antigens that are incorporated into the surface of the body’s own cells to amplify the immune response Colonial secretion of T cells (FIGURE)
  • T cells must recognize both self and non self before the process of proliferation
  • MHC class 1 protein with antigen = phytotoxic T cell
  • MHC Class 2 protein in antigen= t helper cell, suppressor t-cell
  • Macrophage produces the IL-1 to activate the T – helper cells giving a positive feedback response to stimulate the differentiation of particular types of T cells.
  • B cells and T cells = t cells see the MCH protein and antigen. B cells only see antigen to trigger activation 5 major classes of T cells
  • Phytotoxic t cell : are cell killers. Only T cells that are involved in direct contact with an infected cell. Once MCH 1 protein and antigen are recognized, proriferrin vesicles are released onto the infected cell to kill it. Similar to nonspecific defenses. Produces cytokines
  • Cytokines: released by phytotoxic T cell onto the affected cell. T cell comes into contact with the foreign cell, phytotoxic releases a protein, proferrin, by exocytosis. The proferrin inserts self into the membrane, polymerize and forms a hole to kill the cell. (similar to a non specific system)
  • Produce various interferons, macrophage activating factors to keep activity in a particular region and immune cells. Immune cells talk through cytokines. T helper cells activation (FIGURE)
  • Help the immune response in terms of activation and amplification of the immune system. T helper cells regulate activity instead of killing foreign cells directly. However there is a Need for activity of T helper cells to amplify other immune cells. T helper cells help to stimulate multiplication of response in specific immune systems. They Recognize class 2 MCH protein and antigen, doing this through a negative feedback pathway. Illustrated by aids virus, attacks and inhabit T helper cells.
  • T helper cells Come in variety of forms: TH 1 (T helper 1 cell) TH 1 is activated by interleukin 12 (IL-12) that is secreted by dendritic cell 1 class of cells. Macrophages stimulate dendritic cell with interferon gamma to activate IL-12 and TH 1 cells
  • TH2 are stimulated by DC2 cells. IL – 4 also helps in the activation of TH 2 cells. Secondarily activation and may not have to see antigen to be activated
  • TH 17 cells produce IL – 17 (primary product being produced) and inhibited by interferon gamma while stimulating TH 1
  • IL 23 is important for TH 17 cells survival

o No TH 17 cells = autoimmune diseases (TH 17 suppresses any autoimmune function: keep from attacking self cell)

  • TsubFH (follicular helper T cells): found in lymphoid organs to mediate the activity of naïve and memory B cells. IL 21 triggers this type of cell to amplify B cells
  • Third category of T cells: suppressor T cells o Regulatory T cells particularly regulating phytotoxic cells. Prevent amplification from getting out of hand. Prevent excess antibody production o Appear to be important in suppressing autoimmune disorders. Activated by IL – 2 produced by helper T cells and macrophages  TS-1 (active early) simulated by IL- 12 and iL-2 to trigger activation of TS- to suppress the response o TS -3 shuts everything off
  • Fourth category of T cells: Delayed hypersensitivity : involved with cell meditated allergies and chronic inflammation. Release chemicals that activate the immune system when exposed to an antigen. These cells are Activated by macrophages (must recognize Class 2 MCH protein and antigen) as it multiplies, memory cells are being produced.
  • Memory T cells: allow for faster secondary response
  • TsubC-M (central memory T cells): primarily work against viruses and bacteria. Secrete IL-2 and work against virus infected, cancer infected and bacteria affected cells. Memory cells secrete IL 4 and interferon gamma for phytotoxic T cells, thus less able to generate a large number of different cell types. (sub categories: TsubEM-TsubEMR - effective memory t cells)
  • TSCM (stem memory cells) distinctive cell markers that appear to be apart of phytotoxic cells but can self renewal if activated
  • Alpha beta T cells: have alpha beta marker (all t cell types have this)
  • Gamma delta T cells: controls regulation of TH -2 cells. Unique because they lack alpha and beta markers. A bit strange as they developed outside the thymus. Important in dampening autoimmune reactions Stimulated by recognition of self only proteins with the help of glycolipids (MIC proteins: mike A and mike B activate these cells)
  • B alpha 14 natural killer T cells: cross between a natural killer cell and phytotoxic T cell, involved in the direct killing of cancerous/tumorous cells. Important in the liver. Confined to the liver and move around the blood stream.
  • Killer cell (K cell): white blood cells involved in direct killing lacking T cell antigens and have own self distinct markers. They lyse cells coated with antibodies, this process is known as antibody dependent cell meditated (ADCC) works similar to phytotoxic T cells (putt a hole and kill it) 1. Very low lipoprotein is hydrolyzed by the enzyme lipoprotein lipase and glycerol and fatty acids 2. Majority of fat produced during absorptive state ends up in the adipose tissue 3. Majority of blood glucose in the postabsorptive state comes from the metabolism from muscle