MWFY Learning Outcomes - UEA MedSoc



righttop00rightbottomBen McCartneyMWFYDr. Bowater and Dr. WinpennyBy0Ben McCartneyMWFYDr. Bowater and Dr. WinpennyBy41122604581525MWFY Learning Outcomes00MWFY Learning Outcomes MED 0002Y - An Introduction to issues in Health Care – 2014-15Semester 1 - Week 3 - Genetics and Reproductive MedicineDescribe the biochemical and genetic basis of modern genetics and inheritance and discuss the concept of a single polypeptide chain encoded by a gene.5121910635000Nucleic acids are molecules that encode genetic information.They are nitrogenous bases connected to ribose sugar molecules which are linked together with phosphodiester bonds.DNA is a double stranded, helical Molecule.Each chromosome carries a DNA sequence that contains many genesGene - The functional unit of hereditaryStructure of the chromosome:center9525Genome - the total DNA in a single cell, representing all of the genetic information of the organism. Allele - One of several alternative forms of a gene occupying a given locus on a chromosome.List the tests available for pre-natal diagnosis of chromosome abnormalities and single gene disorders and describe how the process of DNA hybridisation and denaturation in relation to DNA structure is the basis for these pre-natal diagnoses.Amniocentesis - a needle is inserted in the womb, and amniotic fluid is extracted, this is because skin cells are coming off the baby and are in the amniotic fluid so we can extract the baby’s DNA from that. 2-3 weeks are needed before the result of the test are available this is because we need to wait for the cell to reach the necessary cell cycle stage where non-disjunction occurs. Performed between 14 and 20 weeks gestation.Fluorescence in situ hybridisation (FISH) - The first thing to do in order to carry our FISH is melt the DNA from metaphase cells and you need to have two single strands. Due to the human genome project, we have sequenced the entire chromosome, so we know the sequence of chromosome 21 and we can therefore design probes that can attach at different points specific to one chromosome which are fluorescent. We then cool the DNA and wash off the probes using a solution to remove and probes that are not attached. Can detect abnormalities in metaphase and interphase (non-dividing) cells. Results available within 24 hours.To isolate, sequence or manipulate the DNA molecule, we need to break it up into smaller fragments. This is done using restriction endonucleases (enzymes).Southern blotting - when we are looking for mutations in the Cystic Fibrosis gene, we want to check if a base sequence is present but also we want to look at the length of DNA carrying the mutation for example a mutation called ΔPhe 502 causes CF can be identified by measuring the length of DNA. This is because it is a deletion. Requires about 10ug of DNA.PCR- Amplifies DNA so that you can take an incredibly small amount of DNA (much less than 10ug need for southern blotting) and make enough DNA to look for mutations.Define the terms aneuploidy and trisomy and explain how aneuploidy arises during cell division.Aneuploidy - the absence of whole chromosome(s) or the presence of additional chromosome(s), the chromosome number is not an exact multiple of the haploid numberusually arises from non-disjunctionNon-disjunction – Failure of 1 or more pairs of homologous chromosomes or sister chromatids to separate normally during nuclear division which leads to an abnormal distribution of chromosomes. I.e. the chromosomes not lining up along the spindle.Trisomy - the presence of three copies, instead of the normal two, of a particular chromosomeTrisomy’s can be detected postnatal or prenatally, increasingly by employing DNA-based techniques, and confirmed by means of karyotyping (visualisation of the chromosome complement).List the basic conventions for using family trees (pedigrees) in medicine.Consultand - person seeking adviceProband - the affected individualDoctors can use a pedigree analysis chart to show genetic disorders are inherited in a family. They can use this to work out the probability (chance) that someone in a family will inherit a condition. This is called pedigree analysis.Male is put to the left or older sibling. Straight horizontal line means a couple or sibling, vertical line means child. Generations are indicated by roman numerals, oldest is I.List examples of diseases inherited as autosomal dominant and autosomal recessive traits.Autosomal dominant diseasesAutosomal recessive diseasesSex linked diseasesHuntingdon’s diseaseCystic fibrosisHaemophiliaMyotonic dystrophySickle cell anaemiaRed-green colour blindnessExplain and contrast the genetic diseases, Down Syndromesyndrome and cystic fibrosis.Down’s syndrome - is most commonly caused by the presence of a third copy of chromosome 21 in all cells. The birth incidence of trisomy 21 rises with increasing maternal age.CF is an autosomal recessive condition, owing to mutations in the CFTR (cystic fibrosis transmembrane conductance regulator) gene. The most common mutation, ΔF508, is a deletion (Δ signifying deletion) of three nucleotides that results in a loss of the amino acid phenylalanine (F) at the 508th position on the protein.The CFTR gene provides instructions for making a channel that transports negatively charged particles called chloride ions into and out of cells.Similar shared features (between DS and CF) include increased sodium content of parotid saliva, abnormal morphology of nailbed capillaries, autonomic dysfunction, an increased frequency of diabetes mellitus, and intestinal atresia (narrowing or absence of a portion of the intestine. This defect can either occur in the small or large intestine).Explain how cell division occurs – including the processes of mitosis and meiosis.Mitosis:Interphase The "resting" or non-mitotic portion of the cell cycle. It is comprised of G1, S, and G2 stages of the cell cycle. DNA is replicated during the S phase of InterphaseProphase - the first stage of mitosisThe chromosomes condense and become visible The centrioles form and move toward opposite ends of the cell ("the poles") The nuclear membrane dissolves The mitotic spindle forms (from the centrioles in animal cells) Spindle fibres from each centriole attach to each sister chromatidMetaphaseThe Centrioles complete their migration to the poles The chromosomes line up in the middle of the cell ("the equator")Anaphase Spindles attached to kinetochores begin to shorten. This exerts a force on the sister chromatids that pulls them apart. Spindle fibres continue to shorten, pulling chromatids to opposite poles. This ensures that each daughter cell gets identical sets of chromosomesTelophase The chromosomes de-condense The nuclear envelope forms Cytokinesis:Contractile ring (actin filaments contracted by the ‘motor’ myosin which) pinches cell until it splits into 2Meiosis:Prophase I The chromosomes condense and become visible The centrioles form and move toward the poles The nuclear membrane begins to dissolve The homologs pair up, forming a tetrad Each tetrad is comprised of four chromatids - the two homologs, each with their sister chromatidHomologous chromosomes will swap genetic material in a process known as crossing over (abbreviated as XO) Crossing over serves to increase genetic diversity by creating four unique chromatidsMetaphase I Microtubules grow from the centrioles and attach to the centromeres The tetrads line up along the cell equatorAnaphase I The centromeres break and homologous chromosomes separate (note that the sister chromatids are still attached) Cytokinesis beginsTelophase I The chromosomes may de-condense (depends on species) Cytokinesis reaches completion, creating two haploid daughter cellsProphase II Centrioles form and move toward the poles The nuclear membrane dissolvesMetaphase II Microtubules grow from the centrioles and attach to the centromeres The sister chromatids line up along the cell equatorAnaphase II The centromeres break and sister chromatids separate Cytokinesis beginsTelophase II The chromosomes may de-condense (depends on species) Cytokinesis reaches completion, creating four haploid daughter cells-46672536195000center714375430276019050MitosisDiscuss the ethical and legal issues around aborting a genetically abnormal foetus.Legal:Due to Abortion Act of 1967, abortion is legal in the UK up to 24 weeks and it can only be carried out in a hospital or a specialist licensed clinictwo doctors must agree that an abortion would cause less damage to a woman's physical or mental health than continuing with the pregnancyAbortion to take place ‘up to birth’ if:it's necessary to save the woman's life to prevent grave permanent injury to the physical or mental health of the pregnant woman if there is substantial risk that the child would be born with serious physical or mental disabilities Ethical:Take away the right of life from a being that can’t protect/defend itself and its rights (Sanctity of life)Deliberate killing of innocent 'humans'The foetus isn’t ‘owned’ and so we can’t choose what we want to do with itMoral discrimination between handicapped and ‘healthy’ foetusMorally repellent to force a woman to bear a child against her willAbortion laws deny women the absolute dominion that they have over their own bodies.Week 4 - Meningitis and ImmunologyDescribe the risk factors and causes (focusing on bacterial and viral infections) of meningitis.Risk Factors:Skipping vaccinations. If you or your child hasn't completed the recommended childhood or adult vaccination schedule, the risk of meningitis is higher.Age. Most cases of viral meningitis occur in children younger than age 5. Bacterial meningitis commonly affects people under 20, especially those living in community settings.Living in a community setting. College students living in dormitories, personnel on military bases, and children in boarding schools and child care facilities are at increased risk of meningococcal meningitis. This increased risk likely occurs because the bacterium is spread by the respiratory route and tends to spread quickly wherever large groups congregate.Pregnancy. If you're pregnant, you're at increased risk of contracting listeriosis - an infection caused by listeria bacteria, which also may cause meningitis. If you have listeriosis, your unborn baby is at risk, promised immune system. Factors that may compromise your immune system - including AIDS, alcoholism, diabetes and use of immunosuppressant drugs - also make you more susceptible to meningitis. Removal of your spleen, an important part of your immune system, also may increase your risk.Causes:.Meningitis usually results from a viral infection, but the cause may also be a bacterial infection. Less commonly, a fungal infection may cause meningitis. Because bacterial infections are the most serious and can be life-threatening, identifying the source of the infection is an important part of developing a treatment plan. Bacterial meningitis:A number of strains of bacteria can cause acute bacterial meningitis. The most common include: Streptococcus pneumoniae (pneumococcus). This bacterium is the most common cause of bacterial meningitis in infants, young children and adults. It more commonly causes pneumonia or ear or sinus infections.Neisseria meningitidis (meningococcus). This bacterium is another leading cause of bacterial meningitis. Meningococcal meningitis commonly occurs when bacteria from an upper respiratory infection enter your bloodstream. This infection is highly contagious. It affects mainly teenagers and young adults, and may cause local epidemics in college dormitories, boarding schools and military bases. There is a vaccine to help reduce the occurrence of this infection.Haemophilus influenzae (haemophilus). Haemophilus influenzae type b (Hib) bacterium used to be the leading cause of bacterial meningitis in children. But new Hib vaccines available as part of the routine childhood immunisation schedule have greatly reduced the number of cases of this type of meningitis.Viral meningitis:Viral meningitis is usually mild and often clears on its own. A group of viruses known as enteroviruses is responsible for most viral meningitis cases. These viruses tend to circulate in late summer and early fall. Viruses such as herpes simplex virus, HIV, mumps, West Nile virus and others also can cause viral meningitis.Describe the signs and symptoms of bacterial meningitis in babies and small children, and in adults.3P’s in children:Pain in limbsPale mottled skinPeriphery cold (hands and feet)Triad of fever, neck stiffness and loss of consciousnessRapid onset headachePhotophobia (dislike of bright light)Phonophobia (a fear of loud sounds)Possible signs of increased pressure in head (e.g. fits and seizures)Rash if septicaemia too (blood poisoning)– see belowKernig’s sign positive (unable to straighten leg due to hamstring stiffness)Non-blanching rash (doesn’t disappear when you press a glass to it) – can have meningitis without rash, but is a sign of septicaemiaDiscuss the laboratory investigations involved in the diagnosis of meningitis.Blood cultures - Blood drawn from a vein is sent to a laboratory and placed in a special dish to see if it grows microorganisms, particularly bacteria. A sample may also be placed on a slide to which stains are added (Gram's stain), then examined under a microscope for bacteria.Blood culture Coagulation screenBlood for PCRFull blood count (numbers of white cells)U+Es/CRP (Urea and electrolytes)Imaging - X-rays and computerized tomography (CT) scans of the head, chest or sinuses may reveal swelling or inflammation. These tests can also help your doctor look for infection in other areas of the body that may be associated with meningitis.Lumbar puncture - The definitive diagnosis of meningitis requires an analysis of your cerebrospinal fluid (CSF), which is collected during a procedure known as a spinal tap. In people with meningitis, the CSF fluid often shows a low sugar (glucose) level along with an increased white blood cell count and increased protein. CSF analysis may also help your doctor identify the exact bacterium that's causing the illness. If your doctor suspects viral meningitis, he or she may order a DNA-based test known as a polymerase chain reaction (PCR) amplification or a test to check for antibodies against certain viruses to check for the specific causes of meningitis. This helps to determine proper treatment and prognosis. Describe the treatment for meningitis (antibiotics).Immediate (in A&E or community):Suspicion of bacterial meningitis, especially meningococcal meningitis, may prompt administration of injection of antibiotics which is usually parenteral penicillin or cephalosporin.Empiric treatment (treatment by means that experience has proved to be beneficial):Broad spectrum antibiotic that treats N. meningitidis, S. pneumoniae and H. influenzae. E.g. Cefotaxime/ceftriaxoneNarrowing of antibiotic spectrum can be guided by blood culture and or CSF microscopy and cultureSuspicion of specific pathogens such as Group B streptococcus (neonates) or Listeria (neonates/pregnant/elderly)may prompt empirical use of other agentsDescribe the immune response to bacteria and viruses, and the principles behind disease prevention (vaccines).The human body has 3 lines of defence against pathogens:1. Barriers preventing entry2. Non-specific – generalised response3. Specific – giving a specific response to a specific pathogen or toxin.To Viruses:Via antibodies:Viruses can also be removed from the body by antibodies before they get the chance to infect a cell. Antibodies are proteins that specifically recognise invading pathogens and bind (stick) to them. This binding serves many purposes in the eradication of the virus:Firstly, the antibodies neutralise the virus, meaning that it is no longer capable of infecting the host cell.Secondly, many antibodies can work together, causing virus particles to stick together in a process called agglutination. Agglutinated viruses make an easier target for immune cells than single viral particles.A third mechanism used by antibodies to eradicate viruses, is the activation of phagocytes. A virus-bound antibody binds to receptors, called Fc receptors, on the surface of phagocytic cells and triggers a mechanism known as phagocytosis, by which the cell engulfs and destroys the virus.Finally, antibodies can also activate the complement system, which opsonises and promotes phagocytosis of viruses. Complement can also damage the envelope (phospholipid bilayer) that is present on some types of virusVia interferonsVirally infected cells produce and release small proteins called interferons, which play a role in immune protection against viruses. Interferons prevent replication of viruses, by directly interfering with their ability to replicate within an infected cell. They also act as signalling molecules that allow infected cells to warn nearby cells of a viral presence – this signal makes neighbouring cells increase the numbers of MHC class I molecules upon their surfaces, so that T cells surveying the area can identify and eliminate the viral infection as described above.Via cytotoxic cellsWhen a virus infects a person (host), it invades the cells of its host in order to survive and replicate. Once inside, the cells of the immune system cannot ‘see’ the virus and therefore do not know that the host cell is infected. To overcome this, cells employ a system that allows them to show other cells what is inside them – they use molecules called class I major histocompatibility complex proteins (or MHC class I, for short) to display pieces of protein from inside the cell upon the cell surface. If the cell is infected with a virus, these pieces of peptide will include fragments of proteins made by the virus.A special cell of the immune system called a T cell circulates looking for infections. One type of T cell is called a cytotoxic T cell because it kills cells that are infected with viruses with toxic mediators. Cytotoxic T cells have specialised proteins on their surface that help them to recognise virally-infected cells. These proteins are called T cell receptors (TCRs). Each cytotoxic T cell has a TCR that can specifically recognise a particular antigenic peptide bound to an MHC molecule. If the T cell receptor detects a peptide from a virus, it warns its T cell of an infection. The T cell releases cytotoxic factors to kill the infected cell and, therefore, prevent survival of the invading virusBacteria:Via complement-mediated lysis:When bacteria, such as Neisseria meningitidis, invade the body, they are attacked by immune proteins called complement proteins.Antibody mediated defence:Neutralization – Ab combines with secreted bacterial molecule (toxin) resulting in inactivation of toxin. Toxin + Ab is phagocytised and toxin degraded. Ab binds to bacterial adhesins resulting in the inhibition of colonization by the bacterial pathogen.Opsonisation – Ab binding and coating the surface of bacteria making the bacteria more susceptible to plement activation – Ab binding results in Complement activation and Complement components coating the surface of bacteria (C3b) making the bacteria more susceptible to phagocytosis (Gram pos) or direct killing by the MAC (Gram neg).After bacteria are ingested by phagocytosis, they are killed by various processes that occur inside the cell, and broken into small fragments by enzymes. Phagocytes present the fragments on their surface via class II major histocompatibility (MHC class II) molecules.Circulating helper T cells recognise these bacterial fragments and begin to produce proteins called cytokines. Two major groups of helper T cells are known as Th1 and Th2 cells. These cell types differ in the types of cytokine they secrete. Th1 cells predominantly produce interferon-g (IFN-g), which promotes cell-mediated immune mechanisms. Th2 cells produce mostly interleukin-4 (IL-4), which promotes humoral immunity by activating B cells. B cells make antibodies that stick to extracellular bacteria and prevent their growth and survival.Via cell-mediated immunity:Macrophage activation (MHC II (on the surface of antigen presenting cells such as macrophages, B cells and dendritic cells), Th1 response) - Phagosome containing phagocytised bacteria fuse with lysosomes resulting in killing of bacteria. Important against intracellular pathogenic bacteria.CTL’s; Cytotoxic Lymphocytes (MHC I (present on the surface of all nucleated cells) response) - Intracellular pathogenic bacteria expressing bacterial molecules on the surface of the infected cells with MHC I molecules are recognized by specific CTLs. CTLs lyse the infected cells releasing bacteria in the external milieu making them susceptible to activated macrophage phagocytosis. Again, important against intracellular pathogenic bacteria.MHC class 1 advertise what is happening in the cell as they present proteins that are produced within the cell. (the proteins could have been made by a virus). They work with cytotoxic T cells.384810012319000MHC class 2 present a phagocytised pathogen fragment, therefore show what is happening in that region/around the cell. They work with helper T cells.Vaccines:Stimulate protective adaptive immune response by expanding pool of specific memory cellsSubsequent natural infection induces fast, vigorous responseHarmless forms of the immunogen used to vaccinate e.g. killed or modified living organisms, fragments or toxoid333121027241500-285750291465Describe and recognise the different organs and cells of the immune system.Innate (Non specific therefore no memory):PMN/Neutrophil – Phagocytosis and killing of microbes Eosinophil – Killing of parasitesMacrophage - Phagocytosis and killing of microbes, activation of adaptive IR Mast cell – Expulsion of parasites by release of histamine, allergy Natural killer cell – Lysis of virally infected cells Dendritic cell - activation of adaptive IRAdaptive (specific so has memory):T lymphocytesOriginate from stem cells in bone marrow Maturation takes place in Thymus gland followed by migration to secondary lymphoid tissue Express T cell receptors which recognize antigens present on surface of antigen presenting cells (macrophages, dendritic cells, B cells)B lymphocytes Originate from stem cells in Bone marrow Maturation in bone marrow followed by migration to secondary lymphoid tissue Express surface receptor (antibody) specific for particular antigenFollowing exposure to antigen, differentiation into plasma cells and memory cellsLymphoblasts are immature cells which typically differentiate to form mature lymphocytes. Normally Lymphoblasts are found in the bone marrow.Thymocytes are hematopoietic progenitor cells present in the thymus. Thymopoiesis is the process in the thymus by which thymocytes differentiate into mature T lymphocytes. The primary function of thymocytes is the generation of T lymphocytes (T cells).Explain how immunisation works and describe the normal immunisation schedule.All forms of immunisation work in the same way. When someone is injected with, or swallows, a vaccine, their body produces an immune response in the same way it would following exposure to a disease but without the person getting the disease.center698500Discuss the difference between passive and active immunity.Passive immunity is the transfer of antibody produced by one human or other animal to another. Passive immunity provides protection against some infections, but this protection is temporary. The antibodies will degrade during a period of weeks to months, and the recipient will no longer be protected. The most common form of passive immunity is that which an infant receives from its mother.Active immunity is stimulation of the immune system to produce antigen-specific humoral (antibody) and cellular immunity. Unlike passive immunity, which is temporary, active immunity usually lasts for many years, often for a lifetime.Week 5 - Bone Disease and AnatomyRecognise anatomical terms such as anterior and lateral, and the layers of the body, in terms of the skin, fascia, muscles, bonesand bones around the hip joint.Anterior – Front of the body 52101754445000Posterior – Back of the bodyLateral - the side of the body or a body part that is farther from the middle or centre of the bodyThe nearer the area is to the point of reference – origin/point of attachment, the more proximal it is said to beThe further away the more distal it is said to be Fascia – are connective tissue fibres, primarily collagen, that form sheets or bands beneath the skin to attach, stabilize, enclose, and separate muscles and other internal organs.Discuss the basic anatomy of the hip.Figure SEQ Figure \* ARABIC 1: Anterior view of the hip joint2940054296410Figure 2: Posterior view of the hip jointFigure 2: Posterior view of the hip jointcenter000center127000center16510Figure 3: Ligaments - iliofemoral, ischiofemoral, pubofemoral – Limit hip extension0Figure 3: Ligaments - iliofemoral, ischiofemoral, pubofemoral – Limit hip extensionDescribe the role of muscles and ligaments in moving and limiting movement of the hip joint and relate it to the basic biomechanical principles that underpin the hip joint.Weight bearing ball and socket joint:As it is ball and socket, it gives a wide range of motionSynovial jointStabilityDeep socket which is further increased by the labrum - a cartilage extension of the acetabulum; it makes it deeper so it makes the joint a little bit more secure.Strong ligaments (bone to bone), join top of femur to acetabulum. Hold femoral head in placeMovementMobility inversely proportional to stabilityArticular cartilage to absorb shock and is smooth to make motion easierMusclesBack of hip - Gluteus muscles extend, abduct and keep the pelvis level when walkingInner thigh – Adductor muscles (pull inward)Hip flexors (thigh forward) – Iliopsoas (deep) and Rectus Femoris (one of the quad muscles)External rotators – Form inside pelvis and attach to back of upper femur. Help stabilise and rotate outwardsHamstring (back of thigh) – Extend the hip (pull it backwards)Describe how pain is transmitted from the hip joint to the brain i.e. as in osteoarthritis.Osteoarthritis causes the cartilage in a joint to become stiff and lose its elasticity, making it more susceptible to damage. Over time, the cartilage may wear away in some areas, greatly decreasing its ability to act as a shock absorber. As the cartilage deteriorates, tendons and ligaments stretch, causing pain. If the condition worsens, the bones could rub against each other. The joint capsule becomes thicker and more synovial fluid is produced making the joint swell.Following the excitation of pain receptors, the message to the brain is sent via one of two pathways. The fast pathway is characterized by myelinated, thin fibres that send messages quickly, giving a sensation of bright pain. The slow pathway is characterized by unmyelinated fibres that send messages much slower, generating a nagging pain sensation. The pain impulse is transmitted: from the site of transduction along the nociceptor fibres to the dorsal horn (where fibres from the slow pathway converge) in the spinal cord; from the spinal cord to the brain stem; through connections between the thalamus, cortex and higher levels of the brain.If you consciously distract yourself, you don't think about the pain and it bothers you less.People given placebos for pain control often report that the pain ceases or diminishes.This indicates that pain-influencing neural pathways must exist from the brain downward.Nerves the pass the hip joint:Obturator – medial compartment thighFemoral – anterior compartment of thighSciatic – posterior limbBegin to interpret X-ray data and relate the data to the clinically vulnerable areas of the hip joint, for example in osteoarthritis.BonesAre they in one piece?Are they a normal shape?JointsLook at the joint spaceLook for changes in the bone around the jointAnything elseIs there something that isn’t normally there e.g. metalwork from a previous operationOsteoarthritis specific:Joint space narrowing- superolateral directionMarginal osteophytes - smooth protrusions of bone and cartilage Subchondral (beneath cartilage) sclerosis - increased bone density or thickening in the subchondral layerSubchondral cysts - a fluid-filled sac that extrudes from the joint, consisting of thickened joint material (mostly hyaluronic acid, a substance found in normal joint fluid that serves to lubricate the joint)Remodelling- changes of shape of femoral head and neckDescribe the signs and symptoms of osteoarthritis.The most common signs and symptoms of OA include stiff and painful joints, limited range of movement, weakness and muscle wasting, and tenderness or inflammation of the joints too. You may also experience crepitus, which is described as a grinding or grating sensation felt in the joint when mon risk factors of osteoarthritis are as follows:Age – Osteoarthritis becomes more common as one gets older. If people over the age of 60 had an X-ray taken, there would be visible evidence to suggest they may have OA. However three quarters of these people would not be showing any symptoms.Sports – There are certain sports which increase the likelihood of developing OAOccupation –Jobs which require frequent kneeling or squatting have been proven to be linked to OA of the knee (carpentry, dock/shipyard work), while other jobs which may require heavy lifting or standing for prolonged periods of time have been linked to OA of the hip (construction work)Gender – Over the age of 55, women are almost three times more likely than men to be affected by OA. The reasons for this are not yet known.38385751778000Obesity – This puts an increased amount of stress on the weight-bearing joints such as the hip and knee, thereby increasing the risk of developing OA in those joints.Genetics – There is speculation regarding the role of genetics in OA. It is thought that point mutations in the genes coding for collagen type 2 affect the formation of collagen, causing it to degrade prematurely and result in osteoarthritis.Discuss osteoarthritis and its treatments: list the pros and cons of the treatment options.Osteoarthritis is usually treated by physiotherapy with muscle strengthening exercises, oral medications, hot and cold compresses to the painful joint, and removal of joint fluid, injection of medications into the joint, use of supportive devices such as crutches or walking sticks, and weight control (including proper nutrition to get vitamin D and calcium, which may help promote the healing process and rebuilding of bone). Surgery may be helpful to relieve pain when other treatment options have not been effective.The purpose of a new hip joint is to:relieve pain (as previously mentioned) elevate the function of your hipenhance your ability to move aroundimprove your quality of life Arthroscopy:Used to smooth a rough joint surface, remove loose cartilage or bone fragments. It may relieve pain but is only a short term improvement.Hip resurfacing surgery:This is most often done in younger, more active people who have pain and disability caused by a badly damaged hip.Hip Replacement: When other treatments haven't worked and damage to the joint can be seen on X-rays, this procedure is carried out. It involves surgery to remove the affected joint and replace it with an artificial joint (prosthesis).Procedure for total hip replacement:Hip IncisionTo begin the surgery, the surgeon makes an incision in the skin over your hip joint.Prepare the AcetabulumThe femoral head is then dislocated from the socket and removed from the end of the femur with a saw. The acetabulum (hip socket) is exposed and a reamer is used to create a smooth bone socket.Implant the Acetabular CupThe acetabular cup is carefully positioned into the socket. This cup is held in place using a number of methods depending upon surgeon preference and your bone quality. These methods may include bone cement to hold the cup in place; most cups are designed to allow bone to grow into the metal surface to hold the cup in placeImplant the Acetabular InsertAn acetabular insert is snapped into the cup. This may be made of durable plastic or ceramic.Implant the Femoral StemThe inside of the femur (thigh bone) is then cleared with various types of devices and a prosthesis is placed into the femur.Check Hip StabilityA trial ball is placed on the top of the femoral stem. The hip is evaluated for the type and amount of motion it has and the stability of the joint — that is, the inability of the ball to dislocate from the socket easily.Final ImplantsThe final ball is placed onto the femoral stem. The leg is evaluated again for stability and mobility and leg length equality. The surgeon will close the wound in layers with stitches and/or staplesExplain the gait cycle (how one walks).The 2 phases of the gait cycle:A complete gait cycle begins when one foot makes contact with the ground and ends when that same foot makes contact with the ground again. It is made up of two phases:Stance phase during which (part of) the foot touches the ground;Swing phase during which that same foot doesn't touch the ground.Stance phaseStance is considered the most important phase, because this is when the foot and leg bear your body weight. The stance phase can in turn be divided into three stages:Initial ContactMid-stancePropulsionLet's take a closer look at each of these gait cycle phases. Watch the right leg move through the gait cycle in the animation below.1. Initial ContactInitial contact is when your foot lands on the ground. It is the cushioning phase of the gait cycle. The knee flexes just before the foot hits the ground and the foot pronates (rolls in). This causes the foot and leg to act together as shock absorbers.The initial contact phase begins when the foot makes contact with the ground, usually heel first. It ends when the forefoot makes contact with the running surface. This moment is called 'foot flat' and it marks the beginning of the midstance phase.2. MidstanceDuring midstance the foot and leg provide a stable platform for the body weight to pass over. By now the foot should have stopped pronating. If the foot is still pronating at this time there is too much movement and instability.Also called single support phase, midstance is when the other foot is in swing phase, so all the body weight is borne by a single leg. This also means that the lower limb is particularly susceptible to injury.3. PropulsionPropulsion is the final stage of the stance phase. It begins immediately as the heel lifts off the ground. As the big toe turns upwards (dorsiflexes) the windlass mechanism comes into play, tightening the plantar fascia and helping to raise the arch of the foot. This mechanism is very important since it allows the foot to act as an efficient lever.Swing PhaseThe swing phase begins with 'toe off' and ends just before the foot makes contact with the ground again and a new gait cycle starts. This phase is important to set the foot and leg up in preparation for heel contact and the next stance phase.Muscle contraction:Muscles, which are attached to tendons, have a key role in the movement of skeletal muscle. Contract of the muscles can be described as having a domino effect, as it causes the tendon which it is attached to, to move relative to this, followed by the movement of the bone and joint. Muscle fibres consist of myofibrils made up of two proteins: actin and myosin. A nerve impulse is initially sent to a muscle fibre, causing calcium channels to open and enable Ca2+ ions to diffuse into the sarcoplasm. Calcium ions bind to troponin, resulting in tropomyosin to move and expose an available binding site on the actin. Myosin heads will then bind with this site to form an actomyosin cross bridge. The myosin head then tilts, causing the actin to also move relative to this (this requires ATP). ADP and inorganic phosphate are then released. ATP then binds with the myosin heads and is hydrolysed to form ADP and Pi. The head then flips away, and leaves the site exposed to enable another myosin head to attach.SSemester 2 - Week 4 - Diabetes, Biochemistry and HomeostasisDefine homeostasis and describe the components of a homeostatic system-44767521018500Homeostasis – maintaining a constant internal environment regardless of external changes. Maintained by the principle of negative ponents required:Detectors/Sensors – send signal to comparator (receptor cells, neural, measures variable in question) Comparator – compares the value, generate the effect (CNS, Brain) Effectors – Muscular, hormones, activated by comparator to restore variable to set point. Move the variable in an opposite direction to the change Variable – the thing changed/acted upon by the effectorNegative feedback, reverse an effect, switch itself off Positive feedback, increases response, needs a way to switch itself off – i.e. during labor, a hormone (oxytocin) is released which intensifies and increases the contractions. An increase in contractions, increases oxytocin release which continues until baby is born (switch off).Set point is actually a narrow range and not a single number. Detected by a regulator.Describe how glucose levels are controlled in the body and explain the role of insulin.Glucose is needed by cells for respiration. It is important that the concentration of glucose in the blood is maintained at a constant level. This is done by the cells in the islets of Langerhans, which is normally in a range of 4-6mmol dm-3. If the concentration rises or falls away from the ‘set point’, then alpha and beta cells in the islets detect the change and respond by releasing a hormone.What happens when blood glucose concentration rises?A rise in the blood glucose concentration above normal is detected by the beta cells (β-cells) in the pancreas. The β-cells synthesise a hormone called insulin. When blood with a high concentration of glucose reaches the islets, glucose is absorbed into the β-cells. The plasma membrane of a β-cell contains carrier protein molecules that transport glucose into the cells by facilitated diffusion. This stimulates vesicles of insulin to move to the membrane and release insulin into the capillaries. Insulin then circulates round the body in the bloodstream. It stimulates uptake of glucose by cells in muscles, adipose tissue and the liver. Insulin attaches to receptor molecules in the membranes of the cells in these tissues. Glucose cannot diffuse into cells through the phospholipid bilayer. All cells have carrier proteins that allow glucose to enter by facilitated diffusion, but the rate of uptake is limited by the number of carrier molecules. In muscles and adipose tissue insulin causes additional carrier proteins to join the membrane. By adding many more carrier proteins the rate of uptake of glucose from the blood is greatly increased. Liver cells already have large numbers of carrier proteins in their membranes. In the liver insulin speeds up glucose uptake in a different way. After the glucose has entered the liver cells it activates an enzyme that rapidly converts the glucose to glucose phosphate. This maintains a steep diffusion gradient between the blood and the liver cells. Other enzymes then synthesise the glucose phosphate to glycogen, a process known as glycogenesis. Glycogenesis also occurs in the muscles, replenishing the stores there. In fat storage tissue insulin activates enzymes that manufacture fatty acids and glycerol, which are then stored as fat. ANABOLIC STATE.Insulin secretion - glucose enters Beta-cell via GLUT 2 down its concentration gradient, glycolysis occurs, ATP is produced, inhibition of K channels, leads to depolarization, Ca channels open, calcium moves in, causes insulin to be released from secretory granules via exocytosisWhat happens when blood glucose concentration falls?The low concentration stimulates the alpha cells to secrete another hormone, called glucagon. Glucagon’s main effects are in the liver. It activates enzymes that break down the stored glycogen to glucose, which is then released into the blood. It can also activate enzymes that convert other substances to glucose, notably lactate and amino acids. This is a process called gluconeogenesis. Both of these effects increase the blood glucose concentration again so that it quickly returns to its normal value. In practice, there are constant adjustments to the amounts of insulin and glucagon being secreted. Much of the time both hormones are secreted in small quantities with the proportions adjusted to maintain the glucose concentration at a fairly constant level. CATABOLIC STATE..Describe the aetiology (cause), signs and symptoms of Type I diabetes.Type 1 diabetes is caused by a lack of insulin due to the destruction of insulin-producing beta cells in the pancreas. In type 1 diabetes - an autoimmune disease - the body’s immune system attacks and destroys the beta cells.Signs and symptoms:Frequent urination - The reason you make a lot of urine and become thirsty is because glucose leaks into your urine, which pulls out extra water through the kidneys.Excessive thirst Increased hungerWeight loss - insufficient insulin prevents the body from getting glucose from the blood into the body's cells to use as energy. When this occurs, the body starts burning fat and muscle for energy, causing a reduction in overall body weight.TirednessLack of interest and concentrationA tingling sensation or numbness in the hands or feetBlurred vision – high blood glucose concentration draws water from the eyesFrequent infectionsSlow-healing woundsVomiting and stomach pain (often mistaken as the flu)Fruity smell of breath - due to ketone bodies from fat metabolismCompare and contrast Type 1 and Type II diabetes.Type 2 diabetes - the most common form of diabetes - is caused by a combination of factors, including insulin resistance, a condition in which the body’s muscle, fat, and liver cells do not use insulin effectively. Type 2 diabetes develops when the body can no longer produce enough insulin to compensate for the impaired ability to use insulin.Auto-immune diseaseInsulin resistance (insensitive)Explain how diabetes is diagnosed.Diagnosing a patient with diabetes often begins with the analysis of symptoms.Random blood sugar test. A blood sample will be taken at a random time. Regardless of when you last ate, a random blood sugar level of 200 milligrams per deciliter (mg/dL) — 11.1 millimoles per liter (mmol/L) — or higher suggests diabetes.Fasting blood sugar test. A blood sample will be taken after an overnight fast. A fasting blood sugar level less than 100 mg/dL (5.6 mmol/L) is normal. A fasting blood sugar level from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) is considered pre-diabetes. If it's 126 mg/dL (7 mmol/L) or higher on two separate tests, you have diabetes.Oral glucose tolerance test. For this test, you fast overnight, and the fasting blood sugar level is measured. Then you drink a sugary liquid, and blood sugar levels are tested periodically for the next two hours. A blood sugar level less than 140 mg/dL (7.8 mmol/L) is normal. A reading of more than 200 mg/dL (11.1 mmol/L) after two hours indicates diabetes. A reading between 140 and 199 mg/dL (7.8 mmol/L and 11.0 mmol/L) indicates pre-diabetes.Urinalysis: A useful tool in diagnosing a potential case of diabetes is a urine test for the presence of glucose. Glycosuria is when glucose enters the urine and is a result of elevated blood glucose concentration. In an individual who is able to control blood glucose concentration within a suitable range glucose should not be present in the urine due to it being selectively reabsorbed back into the blood stream. This is a good diagnostic technique due to the speed and ease of the test but is not the most accurate as glucose being present in the urine can be an indication for a number of other conditions not related to diabetes.A1C Test (gold standard):The A1C test is used to detect type 2 diabetes and pre-diabetes but is not recommended for diagnosis of type 1 diabetes or gestational diabetes. The A1C test is a blood test that reflects the average of a person’s blood glucose levels over the past 3 months and does not show daily fluctuations. The A1C test is more convenient for patients than the traditional glucose tests because it does not require fasting and can be performed at any time of the day.The A1C test result is reported as a percentage. The higher the percentage, the higher a person’s blood glucose levels have been. A normal A1C level is below 5.7 percent.An A1C of 5.7 to 6.4 percent indicates pre-diabetesAn A1C above 6.0 percent should be considered at very high risk of developing diabetesA level of 6.5 percent or above means a person has diabetes.How is diabetesdiabetes is treated, and why are regular blood tests important?InsulinIn type 1 diabetes, the beta cells fail to produce insulin, as a result of which blood glucose levels cannot be lowered. In order to then increase insulin levels, insulin injections must then be given multiple times a day. Obtained from genetically engineered bacteria.The insulin can either be injected manually, or using pump which is strapped to the waist, allowing insulin to be continuously delivered via a needle in the subcutaneous tissue. If needed, insulin can also be delivered manually during meal times for example, when the patient touches a button on the pump. The pump is often preferred over manual injections as the insulin can be automatically administered overnight, the rate of which can be modified to suit the patient. There are however several risks associated with the pump, such as skin infections, ketoacidosis, and its cost.Other complications of insulin treatment in general include allergic responses (localized are more common than generalized), weight gain, hypoglycaemia and lesions or scarring as a result of improper technique.Diabetic dietGenerally, it is recommended that people with diabetes eat foods low in sugars and fats (saturated in particular) and high in fibre and carbohydrates – preferably those with a lower glycaemic index, thereby allowing for a slower absorption and preventing sudden peaks in blood glucose levels. Furthermore, due to the fact that most people with diabetes also suffer from hyperlipidaemia (putting them at a greater risk of cardiovascular disease), lipid-lowering foods are often incorporated into the diet and lipid-lowering drugs may often be used in addition.ExerciseAny increase in the levels of activity is encouraged. Studies show that the risk of progression to type 2 diabetes is reduced by 30-60% with regular exercise. Furthermore, aerobic training and resistance training have been proved to improve insulin sensitivity. However, certain medications do put the patient at a greater risk of hypoglycaemia after heavy exertion.TransplantationIn terms of transplantations, there are usually two options:Whole pancreas transplantationSurgical advances have improved the success rate of this procedure and can lead to a significant improvement in the quality of life for the patient. However, there is evidence to suggest the pancreas is able to survive better if is grafted together with the kidney.Islet transplantationIslets are harvested and injected into the portal vein. They then seed themselves into the liver. This method is thought to eliminate the risk of hypoglycaemia, but it does require fairly strong immunosuppressive therapy, which has costs of its own.Oral medicationGenerally, oral medication is given to patients with type 2 diabetes. However, both type 1 and type 2 diabetes increase the patients chances of developing cardiovascular disease, stroke and kidney disease (Nhs.uk, 2014) (Kumar and Clark, 2009). In order to reduce these chances, they may be advised to take certain medications:Statins – help reduce the blood pressureAspirin – often in low doses to reduce the risk of strokeACE inhibitors – inhibits ACE enzymes, reducing the production of angiotensin II (cause constriction of blood vessels), thereby causing blood vessels to dilate and reducing pressure. Also, they slow down the progression to kidney disease (Ogbru, 2013).Blood tests are important as it can help you:Judge how well you're reaching overall treatment goalsUnderstand how diet and exercise affect blood sugar levelsUnderstand how other factors, such as illness or stress, affect blood sugar levelsMonitor the effect of diabetes medications on blood sugar levelsIdentify blood sugar levels that are high or lowExplain the role of the clinical biochemistry department in the diagnosis and management of diabetes.Can measure:Random glucose levelFasting glucoseDo an oral glucose tolerance test Measure haemoglobin A1C.Discuss the psychological effects of a diagnosis of long term illness may have on an individual.Diabetes has a great impact on a person’s life as they then have to become accustomed to counting carbohydrates, testing blood glucose levels multiple times a day and dealing with both physical and emotional highs and lows. There is a high correlation between diabetes and depression. This can be due to fears about whether diabetes will affect their life expectancy, the complications that diabetes may bring about and whether or not the diabetes will cause serious physical impairment such as blindness or the need for limb amputation. Being diagnosed with diabetes can cause a number of psychological effects including:Anxiety – Fears about the future consequences of the disease on themselves and others around them.Denial – A defence mechanism in which the person avoids the consequences of the chronic health condition.Depression – A common reaction to being diagnosed with diabetes but sometimes delayed as it takes time for a person to realise the full implications of their health condition, particularly if they also go through stages of denial. Grief – Grieving day to day losses. Guilt – A negative reaction to self.Shame – The feeling of no longer being ‘healthy’ in the sense that the person now has a health condition that will always affect them.Week 5 - Epidemiology & Infectious DiseaseDefine epidemiology and explain its need and scope.Epidemiology is the study of how often diseases occur in different groups of people and why. It is the scientific method of investigation problem-solving used by disease detectives to get to the root of health problems and outbreaks in a community and to try to prevent future outbreaks from occuring.The scope of the field extends from study of the patterns of disease to the causes of disease and to the control or prevention of disease. What distinguishes epidemiology from other clinical sciences is the focus on health problems in population groups rather than in individuals.Key assumptions: Human disease does not occur at random Human disease has causal and preventive factors that can be identified through systematic investigation Epidemiology has three main aims:To describe disease patterns in human populations.To identify the causes of diseases (also known as aetiology).To provide data essential for the management, evaluation and planning of services for the prevention, control and treatment of diseaseDefine key epidemiologic terms, including prevalence, incidence, endemic and pandemic.Prevalence - snapshot of number of cases at a given timeIncidence - No. of new cases during a specific period of timeEndemic disease - The constant presence of a disease or infectious agent within a given geographic area or population group. I.e. The disease malaria is endemic to tropical areas of the world, such as those in South America or Africa. Malaria, however, is not endemic to Antarctica since it's not present there.Epidemic - The occurrence of more cases of disease than expected in a given area or among a specific group of people over a particular period of time. This term is very relative. For example, 1000 cases of malaria in a tropical nation may not be an epidemic, but 1000 cases of malaria in England would be an epidemic. That's because the 1000 cases of malaria in an endemic tropical area is considered to be a normal, constant amount of cases of malaria for a set period of time. However, since malaria is not endemic to England, even a small increase in the number of people affected by malaria in England would be considered an epidemic.Pandemic - An epidemic occurring over a very wide area (several countries or continents) and usually affecting a large proportion of the population.Describe the principles of communicable disease control (notifiable diseases).‘Notification of infectious diseases’ is the term used to refer to the statutory duties for reporting notifiable diseases in the Public Health (Control of Disease) Act 1984 and the Health Protection (Notification) Regulations 2010.Registered Medical Practitioners in England and Wales have a statutory duty to notify a Proper Officer of the local authority, often the CCDC (Consultant in Communicable Disease Control), of suspected cases of certain diseases. Diseases that are notifiable:AnthraxCholeraMalariaPlagueSmallpoxScarlet feverYellow feverWhy do we bother to notify the authorities of these diseases?Surveillance – accuracy of diagnosis is secondary, clinical suspicion is all is requiredCase management – depends on early detection and rapid structured investigationContact tracing & case finding – accuracy of outbreakGood laboratory service to confirm and diagnose casesPrevention of spread of diseaseDescribe the preventive methods to be used in controlling infectious disease, in particular malaria.Reducing the numbers of mosquitoes reduces transmission of the malaria parasite. Methods include; insecticide spraying, environmental management and biological control. Environmental management measures, such as covering wells and filling in ditches (with earth or oil), and keeping irrigation channels fast flowing, help reduce the number of mosquito breeding sIn unscreened accommodation, nets impregnated with insecticide (pyrethroid) are recommended as they are proved to be up to 50% more effective than regular nets. They help prevent the mosquito biting through the net and prevent the mosquito surviving around the net long enough to find any tears.ClothingCovering up will minimize accessibility to the skin for mosquitoes.AccommodationAir conditioning or a ceiling fan can reduce the likelihood of bites, due to the decrease in temperature. Doors or windows may be lined with a fine mesh netting to prevent mosquitoes entering.Describe the pathophysiology of malaria.Pathophysiology - the functional changes that accompany a particular syndrome or diseaseThe symptoms include:Fever, shivering, pain in the joints, headache, generalized convulsions, severe anaemia (due to ruptured RBC’s), and coma. The fever is associated with the rupture of the red blood cells and the released merozoites. Sequestration (net increase in the quantity of blood within a limited vascular area) of erythrocytes (red blood cells) in capillaries leads to organ damage and cerebral malaria. That’s because when the blood travels through our capillaries the spleen filters out old red blood cells. Old red blood cells are rigid and not so flexible. Infected red blood cells also rigid and have a different shape more spherical. This is seen especially P. falciparum where the infected red blood cells stick to then endothelial cells of capillaries.The parasite digest haemoglobin, producing a nontoxic product (metabolite hemozoin). The parasites derive energy from the anaerobic glycolysis of glucose to lactic acid; this may contribute to hypoglycaemia and lactic acidosis. They also reduce red cell membrane deformability and this results in haemolysis and accelerated splenic clearance which may contribute to anaemia.List the tests available for diagnosis of tropical diseases.Microscopic examinations (light microscopy – considered ‘gold standard’): Blood specimens: stained/thick/thin smears (e.g. Plasmodium sp.) Stool specimens: wet/stained preparations (e.g. helminth eggs) Tissue specimens: biopsies (e.g. Leishmania sp.) Sputum specimens: wet/fixed preparations (e.g. roundworm larvae) Urine: sediment (e.g. Schistosoma haematobium eggs) Immunochromatographic RDT’s (rapid diagnostic tests) This procedure utilizes a monoclonal antibody to a parasite antigen on an immunochromatographic strip to detect the parasite presence in the peripheral bloodIsolation of organisms: Tissue specimens: inoculation in culture (e.g. Leishmania sp., bacteria) Blood specimens: inoculation in mice (e.g. Trypanosoma cruzi) Detection of antibodies: Blood specimens: CATT (e.g. Trypanosoma brucei spp.) Serum/plasma specimens: IgM/IgA (e.g. Toxoplasma gondii) Molecular diagnosis: PCR with blood specimens can detect parasites below the threshold for microscopic identification. Under optimal conditions, it is able to detect a single parasite per mm3 of blood. This technique is particularly of use in cases whereby the parasite morphology is distorted due to prior antimalarial exposure, which mean it is difficult to identify on a microscope. However, the results are not available quickly and so it is most useful in confirming the malaria parasite species once diagnosis has been confirmed by using either RDT or smear microscopyImaging tests: Chest: X-rays: pulmonary tuberculosis (pulmonary TB)Discuss the options available to treat malaria.Determine which kind of species is causing the disease, this can be done by geographical location Determine the clinical status on the patient – good/bad health Knowledge of the geographic area where the infection was acquiredTreatment: Chloroquine-sensitive P. falciparum: oral chloroquine Chloroquine-resistant P. flaciparum: qunine sulphate + doxycycline /tetracycline/ clindamycin. Atovaquone-proguanil. Mefloquine P. Malaria: oral chloroquine P. vivax and P. ovale: oral chloroquine. primaquine (liver stage; G6PD deficiency) Chloroquine-resistant P. vivax: quinine sulphate + doxycycline/tetracycline/mefloquine Tissue schizonticides –i.e. Primaquine - destroys all the exo-erythrocytic (outside of RBC) forms, and act against the malarial parasites Plasmodium vivax and Plasmodium ovale in the liver. If the tissue schizonoticides are successful, then this will prevent the infection from spreadingBlood schizonticides – i.e. Chloroquine, Quinine, Proguanil and Sulphones - attack the erythrocytic forms of the malarial parasite, and therefore stop the infection Gametocytocides – i.e. Primaquine - act against gametocytes which are the sexual forms of the malarial parasite. Through the destruction of gametocytes, a mosquito is unable to transmit the parasite into a host Start treatment before diagnosis in case of falciparum as it can be deadly.Discuss where people can get help when falling ill after return from holidays abroad.GPAccident & Emergency The Hospital for Tropical Diseases London Liverpool School of Tropical Medicine (LSTM) 388620025146000Week 6 - Gastrointestinal System and PhysiologyDescribe the basic anatomy of the gastrointestinal tract.The digestive system prepares, moves and breaks down ingested food so it can be absorbed into the bloodstream to nourish cells and provide energy to the body, while indigestible products are disposed of as waste. There is the digestive tract as well as the accessory organs. The autonomic system, hormones and other chemicals control secretions. The tract itself is starting from the mouth and going to the anus. It’s a long epithelial (mucosa) lined muscular tube that is about 9 m long. Mouth -> Pharynx -> Oesophagus -> Stomach -> Small intestine -> Large intestine/colon -> Rectum -> Anus The accessory organs are: TeethSalivary glandsPancreasLiver Gall bladderThe general structure of the digestive tract:Mucosa – internal epithelium (either stratified for protection or columnar for absorption) moistened by glandular secretions, connective tissue, and smooth muscle layer autonomic and not under voluntary control. Submucosa - Connective tissue with blood vessels, nerves, and lymphatics Muscularis externa – 2 smooth muscle layers Inner circular layer for crushing and segmenting Outer longitudinal layer for moving Serosa - Outermost layer – smooth layer of cells which secrete serous fluid (lubricant)3962400-127444500The GI has a specific structural make up of layers that vary along the tract related to its function. For example in the oral cavity, pharynx, esophagus and the anus we aren’t absorbing anything. So their role is mainly for movement. We are therefore mainly concerned about protection that comes from the stratified epithelium and no serosa layer. As we move down we get columnar epithelium and in the small intestine it becomes more and more highly folded to increase the surface area in order to aid absorption and expansion. So in the small intestine we have plica and villi, which are tiny projections that allow for better absorption. Mucosa of the stomach simple columnar epithelium: Mucous neck cells – produce a sticky alkaline mucusGastric glands – secrete gastric juice Chief cells – produce protein-digesting enzymes (pepsinogens) Parietal cells – produce hydrochloric acid (HCl) and intrinsic factor Endocrine cells – produce gastrin Describe the physiology of the pancreas and its role in the gastrointestinal system.375285059245500Exocrine cells secrete digestive enzymes, which are then transported in pancreatic juice through the pancreatic duct and into the duodenum. Pancreatic juice contains pancreatic amylase, which is an enzyme used to breakdown starch, as well as enzymes that are involved in the partial digestion of proteins – for example, trypsin. Lipases, which are enzymes used to breakdown fat, and nucleases, which are enzymes used to digest nucleic acids, are also present in the pancreatic juice.The pancreas has two main functions:To make digestive enzymes which help us to digest food. Enzymes are special chemicals which help to speed up your body’s processes.To make hormones which regulate our metabolism. Hormones are chemicals which can be released into the bloodstream. They act as messengers, affecting cells and tissues in distant parts of your body.About 90% of the pancreas is dedicated to making digestive enzymes. Cells called acinar cells within the pancreas produce these enzymes. The enzymes help to make proteins, fats and carbohydrates smaller. This helps the intestines to absorb these nutrients. The acinar cells also make a liquid which creates the right conditions for pancreatic enzymes to work. This is also known as pancreatic juice.Pancreatic juice is alkaline, and this helps to neutralise the chyme (partly digested food soaked in gastric fluids) from the stomach. This alkalinity is due to the presence of bicarbonate ions (which are secreted by the duct cells), and these ions provide a neutral environment for the use of digestive enzymes from both the intestine and the pancreas.When chyme begins to emerge from the stomach, cells in the duodenum secrete secretin which stimulates the duct cells in the pancreas to the release bicarbonate ions into the pancreatic juice, which can then move through the pancreatic duct and neutralise the chyme. Discuss the physiological control of the release of digestive secretions from the stomach, pancreas and small intestine.Presence of food in the gastrointestinal tract stimulates smooth muscle in the main body of the tract and the gall bladder, relaxes the smooth muscle of the sphincters, and stimulates secretion and blood flow in salivary glands, pancreas and liver. Control is considered in 3 phases, depending on where the food is:Cephalic – This is due to the approach of food and presence of food in the mouth. Food in the mouth stimulates pressure receptors & chemoreceptors. This results in increased blood flow to the salivary glands & secretion of saliva begins the digestion of starch (through amylase). It also starts to stimulate the secretions of the stomach, pancreas and liver to prepare the digestive tract to perform its functions (digestion and absorption). The chemoreceptors stimulates the vagal nerve causing a release of gastrin. The gastrin stimulates the parietal calls of the stomach.Gastric – This is due to the presence of food in the stomach. This results in increased blood flow to the stomach, stomach distention and the secretion of gastric juice. There is smooth muscle stimulation in the stomach, which enables churning of the food as well as digestion. Food in the stomach also stimulates the secretion of pancreatic juices, bile and intestinal juices to prepare for when the chyme reaches the small intestine. Intestinal – When food is present in the small intestines. Gastric secretion and motility is inhibited (to prevent further emptying of the stomach – stomach stores food and food in small intestine is processed). There is stimulation of intestinal juice, pancreatic juice and bile. The blood flow to the intestines, pancreas and liver also increases. Amino acids and fatty acids stimulate the I cells in the duodenum to release cholecystokinin as well as a vagovagal enteropancreatic reflex that stimulates acinar cells. Cholecystokinin stimulates the secretion of more pancreatic enzymes, some bicarbonate secretion (although this is mainly done by secretin) and some release of bile from the gall bladder. Protons from the acidic chyme stimulate S cells in the duodenum to release secretin. The gall bladder is stimulated to contract and the sphincter of Oddi relaxes to allow entry of pancreatic juices and bile into the duodenum. These digestive juices enable digestion and absorption of complex nutrients within the small intestine.Discuss the aetiology (cause), signs and symptoms of pancreatic cancer.Risk factors:Age - mainly affects people who are aged 50 to 80Smoking and tobaccoDiet – high in fat, sugar and red or processed meatAlcoholBody weight and physical activitySome medical conditions i.e. diabetesFamily historyThe main symptoms that are associated with pancreatic cancer are as follows:Extreme weight loss - reduced exocrine function of the pancreas and lack of functioning pancreatic enzymes. The pancreas secretes digestive enzymes such as lipase which breaks down macromolecules in food such as lipids enabling it to be absorbed without this it is just egested. Another cause of extreme weight loss could be due to the cancerous cells depriving the healthy cells of nutrients. Jaundice - often results in a type of jaundice called obstructive jaundice. This results from the lack of movement of a pigment called bilirubin (break down product of haemoglobin) from the blood to the liver and then out of the body. The obstruction is often caused by the pancreatic tumour applying pressure to the bile duct which causes a blockage resulting in a build-up of bilirubin, as it cannot leave the gall bladder and enter the digestive system. The bilirubin then deposits in the blood and tissues resulting in a yellow pigmentation of the skin and the sclera. Along with these signs of jaundice a patient will most likely notice a darkening in the colour of the urine due to excess amounts of bilirubin and pale stools which results in lack of bilirubin as it is unable to enter the digestive systemSteatorrhea - This is the presence of excess fat in faeces which is foul smelling and floats due to its oily contents. Fat absorption is triggered by pancreatic lipases which help to break it down and so when someone is suffering from pancreatic cancer in which there is a lack of pancreatic enzymes fat absorption is greatly reduced which results in it being egested in the faces.Abdominal pain that radiates to the back - Cancers that grow in the tail or the body of the pancreas can grow fairly large and begin to press and apply pressure on surrounding organs which can result in significant pain. Many patients note as the disease progresses the pain becomes more constant and begins to radiate to the back this is due to the tumour pressing on a nearby collection of nerves called the celiac ganglion List the common obstructive (post-hepatic) causes of jaundice.Intra-hepatic jaundice:Caused by damage to liver cells produced by viruses, drugs, alcohol cirrhosis, or blockage of the intra-hepatic bile ducts, which leads to a failure of bile secretion.Extra-hepatic jaundice:Produced by a blockage of the extra-hepatic bile ducts. The obstruction may be due to gall stones in the biliary tree, or due to an enlargement of an adjacent organ, such as pancreatic cancer/carcinoma of the head of the pancreas.Describe the management of patients with pancreatic cancer.Chemotherapy – Post surgery to reduce the chance of recurrence or to relieve symptomsRadiotherapy – normally to shrink tumour so as to relieve symptomsSurgery:Surgery is usually the only way pancreatic cancer can be completely cured, however due to late diagnosis in most cases, the condition is usually too advanced and only 15-20% of people are suitable to have the surgery. Whipple – this is the most common operation used to treat pancreatic cancer, it involves removing the head of the pancreas. The end of the bile duct and the remaining part of the pancreas is connected to the small intestine, allowing bile and hormones and enzymes to still be released into the system. Distal pancreatectomy – this involves removing the tail and body of the pancreasTotal pancreatectomy – the entire pancreas is removed usually due to the position of the tumour.Explain bilirubin metabolism and excretion.Red blood cell (haemoglobin) after a while they stop working so we need to get rid of them and produce new ones, so they go to the spleen (and bone marrow) to be broken up to haem and globin. And the haem part goes through a pathway and forms bilirubin, which is a waste product. It’s also insoluble in water so the body cannot get rid of it. It’s not joined to anything so it’s called unconjugated bilirubin.We need to make it water-soluble so we can either excrete it. So it goes to the liver and the bilirubin is added to this glucuronic acid and at this stage it becomes conjugated so now it’s water-soluble. Then it goes from the liver into the intestines and this is where most of the water is reabsorbed, so conjugated bilirubin is absorbed into the blood stream. And then it goes into the kidneys so we can wee it out and that’s 95% of it. About 5% of it doesn’t get re-absorbed and stays in the bowels and it’s excreted in the faeces and it’s turned to stercobilinogen and that’s what makes the faeces brown. These points are useful for symptoms. Discuss why patients may choose not to visit their GP.Machoism The condition isn’t bothering themTherapeuticHaving to take medication, having to undergo a potentially embarrassing and personal examination or discussion.Practical Costs; time off work, time away from the family, cost of the travel to and from.EmotionalCosts; embarrassment or the feeling of being a nuisance to the Doctor.The sick role Costs; may be drawn out so patient may fear that others will think they’re putting it on, they will have to accept helpWeek 7 - Respiration and PharmacologyDescribe the anatomy and physiology of the respiratory system.Inspiration:Contraction of external intercostal muscles > ribs move up and out > increased front- to-back dimension of thoracic cavity > lowers air pressure in lungs > air moves into lungsContraction of diaphragm > diaphragm moves downward > increases vertical dimension of thoracic cavity > lowers air pressure in lungs > air moves into lungsExhalationrelaxation of external intercostal muscles & diaphragm > return of diaphragm, ribs, & ribs move down and in > restores thoracic cavity to pre-inspiratory volume > increases pressure in lungs > air is exhaledSurfactant decreases surface tension which reduces the effort needed to expand the lungs and reduces the tendency for alveoli to collapseControl of breathing:Chemoreceptors monitor pH of body fluidsHigher [CO2] forms more carbonic acid and lowers pHCentral (brain) chemoreceptors monitor CSF (cerebrospinal fluid)Peripheral chemoreceptors monitor arterial bloodLower pH causes rate and depth of breathing to increaseRemoves CO2 and pH rises again(Good example of homeostasis (negative feedback))Coordinated with regulation of heart rateLimited gain from breathing faster unless blood arriving faster tooUnder normal conditions oxygen level has little effectBreathing rate can also increase in panic, early stages of exercise etc. before CO2 level risesIdentify the causes of wheeze and recognise how to diagnose asthma.Wheeze - air forcing its way through the narrow airways produces a whistling noise. The narrowing of the airways can be caused by inflammation from asthma, an infection, an allergic reaction, or by a physical obstruction, such as a tumor or a foreign object that's been inhaled. Wheezing is also a symptom of bronchitis.To diagnose:Allergy testing - using a skin test, whereby you are given a dose of a possible allergen and the immune response is monitored: in particular the level of IgE.Peak expiratory flow rate (PEFR) - It measures (in one breath) how fast you can blow air out of your lungs, but is less accurate than a spirometry. To demonstrate the variable airflow limitation of asthma, measurements are taken upon waking, prior to using a bronchodilator and just before bed after using a bronchodilator. A ‘morning dip’ (a significant decline in maximum expiratory flow rate or MEFR) is evident in some asthmatic patients. It occurs early in the morning and results in a loss of sleep due to breathlessness and coughing.Spirometry - Can assess reversibility. It measures how much air you breath in and out and how fast you blow air out. Asthma diagnosed in patients that demonstrate a greater than 15% improvement in FEV1 (forced expiratory volume in 1 second) or PEFR after bronchodilator inhalation.Chest x-ray - to see whether the symptoms are due to another disease or a foreign object.Arterial blood gas - Only done in patients that are having a severe asthma attack. It allows us to measure the amount of oxygen and carbon dioxide in the blood, as well as acidity. It can reveal severe hypoxemia (low oxygen in blood) or hypercarbia (high level of carbon dioxide in blood) that is secondary to hypoventilation.Medical history - Doctors will ask about family history of asthma and allergies, as well as ask if the patient has any of the asthma symptoms and if so how frequent they are. The susceptibility to asthma can be inherited.Examination - Your doctor will listen to your breathing and look for signs of asthma or allergies. These signs include wheezing, a runny nose or swollen nasal passages, and allergic skin conditions (such as eczema). Asthma, eczema and hay fever are atopic (atopy refers to the genetic tendency to develop allergic diseases).List the types of drugs that can cause an acute asthma attack.Beta blockersNon-steroidal anti-inflammatory drugs (NSAIDs) They block the COX-1 enzyme, production of thromboxane (induces platelet aggregation and arterial constriction) and some prostaglandins (varying effects such as the contraction and relaxation of smooth muscle, the dilation and constriction of blood vessels, control of blood pressure, and modulation of inflammation) is decreased, and in patients with aspirin-induced asthma this results in the overproduction of leukotrienes (which are very pro-inflammatory). The combined effect is to promote inflammation in the airways, and thus asthma attack.Angiotensin-converting enzyme (ACE) inhibitorsDescribe how an acute asthma attack is managed in primary and secondary care.Primary care - health care provided in the community for people making an initial approach to a medical practitioner or clinic for advice or treatment.Nebuliser (its job is to get a liquid drug into an aerosol)– nebulised beta 2 agonist bronchodilatorsInitiating oral montelukast (block leukotriene (inflammatory mediators produced by leukocytes) effects)Refer to secondary careMeasure:Respiratory rate;Pulse rate;Peak expiratory flow (PEF);Oxygen saturationSecondary care - medical care provided by a specialist or facility upon referral by a primary care physician that requires more specialized knowledge, skill, or equipment than the primary care physician has.Measure oxygen saturationIncrease inhaler therapyAdd oral steroid (only to be prescribed long term with secondary care review)Other steroid sparing agentsAnti IgE therapyDescribe the types of organisms that can infect the lungs and the different investigations and treatments that are available for lung infections.The common cold (virus) Tonsillitis (bacterial or viral)Sinusitis (allergic reaction, trauma to face or allergies such as hay fever)Laryngitis (inhaled irritants such as chemical fumes, acid reflux, chronic sinusitis) Flu (influenza virus)Bronchitis (viral or bacterial) Pneumonia (most common bacterial, but can be fungal or viral)Tuberculosis (bacterial infection)Investigations available for lung infections:Blood tests or cultures. Blood tests may help tell whether antibodies to a specific organism that can cause pneumonia are present or whether specific viruses, such as influenza (flu) or respiratory syncytial virus (RSV), are present. A test for blood urea nitrogen (BUN) can help tell how serious an infection is. Doctors can use blood cultures to test for bacteria in your bloodstream.Oximetry. An oximeter can estimate the amount of oxygen in your blood. A sensor in a cuff or clip is placed on the end of your finger. This sensor measures how much oxygen is in your blood. The oximeter machine shows the result.Arterial blood gases. An arterial blood gas test can measure the levels of oxygen in a sample of blood drawn from your artery. Doctors use this test to find out whether enough oxygen is getting into your bloodstream from your lungs.Bronchoscopy. Bronchoscopy is a visual exam of the tubes leading to your lungs. This test is usually done by a pulmonologist (lung specialist). He or she inserts a small, lighted device through your nose or mouth into the tubes leading to your lungs. During the procedure, the doctor can obtain samples of tissue, fluid, or mucus.Lung biopsy. A lung biopsy is a test done on a very small piece of lung tissue to look for conditions such as lung cancer or fibrous tissue in the lungs (pulmonary fibrosis). Your doctor obtains lung tissue by inserting a needle into your chest between two ribs or by using bronchoscopy.Thoracentesis. Thoracentesis involves puncturing the chest wall to obtain fluid from the space around the lungs. Fluid obtained during the test can be checked for signs of infection or puted tomography (CT) scan. A CT scan uses X-rays to produce detailed pictures of structures inside your body. It may be used in people who are not responding to their treatmentTreatments:AntibioticsAnti-viralCough medications to reduce coughAntihistamines for nasal secretions and congestionNSAID’s for aches and feversDecongestantsBed restHydrationDescribe the different types of cellular receptor and their signalling pathway present in human cells.Signal transductionSignal molecule binds to receptorBinding causes a change in receptorChange in receptor causes an effect in the cell..The majority of cell surface receptors are G-protein-coupled receptors (GPCR or 7 trans-membrane (7TM) receptors)When an external signalling molecule binds to a GPCR, it causes a conformational change in the GPCR. This change then triggers the interaction between the GPCR and a nearby G protein.Ligand gated ion channelsopen to allow ions such as Na+, K+, Ca2+, or Cl? to pass through the membrane in response to the binding of a chemical messenger (i.e. a ligand), such as a neurotransmitter.Receptor (tyrosine) kinasescenter100393500Can transfer a phosphate group from ATP to a protein in a cell. An inactivated RTK receptor encounters a ligand. Upon binding, the receptor forms a complex of proteins that are phosphorylated. In turn, this phosphorylation affects other proteins in the cell. It can function as an "on" or "off" switch in many cellular functions.Discuss the difference between the structure and mode of action of different hormones in the body.Types of hormones:Proteins/polypeptides most of our body’s hormonesCan be small (3 amino acids) or large (100’s of amino acids) so have peptide bondsMade in rough ER -> Golgi apparatus ->Packaged into vesiclesReceptors in or on a cell surfaceTherefore initiate a cascade effect of secondary messengers inside the target cellSteroidsFrom lipids (cholesterol) so can pass through membrane and signal the receptor in the cell, therefore they are the primary messengerHave 4 carbon rings characteristic structureAffect transcription and translationi.e. Testosterone, oestrogen and progesteroneTyrosine derivatives:All derived from the amino acid tyrosineCan act like polypeptides (Catecholamine’s) and steroids (Thyroxine)Types of signalling:Autocrine - cell secretes a hormone or chemical messenger (called the autocrine agent) that binds to autocrine receptors on that same cell, leading to changes in the cell.Paracrine - a form of cell-cell communication in which a cell produces a signal to induce changes in nearby cells, altering the behaviour or differentiation of those cells.Endocrine - when cells need to communicate a message over a long distance, they can use the endocrine system. Endocrine signalling uses chemicals called hormones to send messages throughout the body. The hormones are released from the cell into the bloodstream and can travel around the entire bodyNeural Signalling - This transfer of information from the external environment, through neurons, and back again to the external environmentExplain what pharmacology is and describe key pharmacological concepts such as agonist, antagonist, half lifehalf-life etc.Pharmacokinetics - what the body does to drugs Pharmacodynamics - what the drugs do to the bodyAgonist - a substance which initiates a physiological response when combined with a receptor.Full agonist – a substance that completely activates a receptor leading to a cellular responsePartial agonist - a substance which partially initiates a physiological response when combined with a receptorAntagonist - a substance which interferes with or inhibits the physiological action of another. Binds to part of receptor which prevents agonist from stimulating a response (competitive (can be overcome by increasing agonist conc.) or non-competitive (can’t be overcome, usually dangerous drugs i.e. poisons))Half-life - the period of time required for the concentration or amount of drug in the body to be reduced by 1/2. Determines how often the medication has to be taken.Receptor - protein molecule which can selectively bind drug, hormone or neurotransmitterOral bio-availability – Proportion of a drug that passes into systemic circulation after taking as a tablet, as compared to IV injectionSelectivity - propensity of drug to affect one type of receptors more than othersTolerance - gradual decrease in effect over days / weeksWeek 8 - The Multidisciplinary Team and CommunicationDiscuss the issues that affect how people decide when, where and who to ask for health advicseCan ask:The internet - It is quick, easy to access and avoids certain complications that could possibly arise if you had to visit a doctor (i.e. having to organize a babysitter for children etc.) as well as being up to date (relevant) and free.Pharmacies – no need to book an appointment. They are usually local and so are easily accessible and can offer anonymity to patients. Moreover, they can offer patients help with many common conditions such as rashes and aches and will advise patients to visit their GP if need be. Lots of pharmacies are open until late and at weekends, which is useful if you start feeling unwell at 9pm and the local GPs are all shut. Can offer repeat prescription dispensing.Drop/walk in centres - popular since appointments are not needed and they are open 365 days a year. Offer access to nurses and sometimes doctors.Doctor – to diagnose, prescribe and answer questions to settle worries and/or fears.Friends/family – especially if they have gone through the same thing and so can share experiences and offer advice.34245551079500Describe the information that Amanda needs to be given about her brown inhaler and recognise who might give this information and how the information may be given?GP or other doctor can prescribe the inhaler. Information to be given:The role of each medication; in the case of asthma, about the two broad categories of asthma medication: preventative and relievers.Instruct patients about the proper techniques for inhaling medications.When to use the inhalerMonitor medication use and refill intervals to help identify patients with poorly controlled asthma. Describe Asthma management in general practice.GPs play a central role in the management of asthma in the community. This includes assessment, diagnosis, prescription of regular medications and education.Asthma Nurse - The role of the asthma nurse may include diagnosis and management of asthma. Their responsibilities include instructing inhaler technique, selecting and changing inhaler devices, supervising self-management plans, changing doses of treatment and withdrawing medication. Nurses play a major role in asthma education.Assess and record:Peak expiratory flow (PEF)Symptoms and response to self-treatmentHeart and respiratory ratesOxygen saturation (by pulse oximetry)Identify the different health professionals that have a role in the management of Asthma and describe their role?Triage Nurse – (in A&E)Assess the severity of a patient’s condition and determine where and in what priority the emergency physicians will care for them. The triage nurse carries out brief examinations and checks vital signs, such as temperature and blood pressure. May administer emergency/necessary treatment (nebuliser).A&E clerkMaintain the accuracy and security of confidential patient health records. They manage paperwork such as patient history forms, and admission and discharge documentsGPs Play a central role in the management of asthma in the community. This includes assessment, diagnosis, prescription of regular medications and education.Asthma Nurse The role of the asthma nurse may include diagnosis and management of asthma. Their responsibilities include instructing inhaler technique, selecting and changing inhaler devices, supervising self-management plans, changing doses of treatment and withdrawing medication. Nurses play a major role in asthma education.RadiologistChest radiographic imaging is an important tool in the examination of patients with an exacerbation of asthma. Initial imaging evaluation in most individuals with symptoms of asthma. It usually is more useful in the initial diagnosis of bronchial asthma than in the detection of exacerbations, although it is valuable in excluding complications such as pneumonia and asthma mimics, even during exacerbations.Smoking cessation councillorThe counsellor can provide information and guidelines on how to quit smoking; they may include referrals to outside organizations and provide support in telephone sessions, group interventions and individual sessions.Discuss the roles of multidisciplinary teams in patient care and recognise how good team work can be achieved.All doctors:Must make sure that you communicate relevant information clearly to:Colleagues in your teamColleagues in other services with which you workPatients and those close to them in a way that they can understand, including who to contact if they have questions or concerns. This is particularly important when patient care is shared between teams.Should not assume that someone else in the team will pass on information needed for patient care. You should check if you are unclear about the responsibility for communicating information, including during handover, to members of the healthcare team, other services involved in providing care and patients and those close to them.You should encourage team members to cooperate and communicate effectively with each other and other teams or colleagues with whom they work. If you identify problems arising from poor communication or unclear responsibilities within or between teams, you should take action to deal with them.Effective decisions are generally made by teams that are well led and have an emphasis on incorporating the views of the whole multidisciplinary team.How good teamwork can be achieved:Membership: two or more individuals work together toward a common goalCommon goal: the members have negotiated shared aims and goalsSocial organisation: the group develops or actively negotiates functional norms, roles, and relationshipsInterdependence between members: members succeed only if all succeed Productive involvement: all members are supported to contribute equally to the workload; resources and skills are identified early on and used effectively. Decisions are made by consensus.Effective communication and interaction: face-to-face and other modes of communication help to monitor group processes and dynamics, drive creativity and enable productive work practicesMutual interest: members focus on the interests of the group as a whole, and avoid personalising problems or differences of opinionCollective consciousness: members perceive themselves as belonging to the group even when the group is not togetherMutual trust: members listen to each other, respect contributions, help each other to clarify ideas, and show interest in each otherCohesion: group processes function smoothly without need for intervention, members are able to contribute equally to produce something greater than the individual parts, individual contributions are brought together seamlessly and within nominated deadlines, and members feel they have learnt something from the process and from the other group members. Recognise the importance of good communication within effective teams and describe how good communication can be achieved both within teams and between teams and the patient.Teams that communicate complete projects in a quicker and more efficient amount of time than others. They also are more accurate in their work than others. Effective communication also allows team members to understand their roles and the roles of everyone else on the team. It also gives room for understanding among the team members for what needs to be munication plays a big part in patient satisfaction, a patient is more likely to feel satisfied with their treatment and feel the health care professional took their problem seriously if the information is explained clearly and if they were provided viable options.Good communication can be achieved by:Being conscious of verbal and non-verbal communicationNo jargonBe transparent – same info to all members to keep all members adequately informedPostureTouchEye contactFacial expressionGesturesBuilding rapport by being:Non-judgementalEmpathicSupportiveDeal sensitively with embarrassing or disturbing topics including physical examinationParalinguistic-tone of voice, pace, pitch, and volumeLISTENING-3257552483485Open focused questions00Open focused questionsright3928745Closed questions00Closed questionsright855980Broad open questions00Broad open questions361950292735Describe the Cambridge-Calgary model of communication skills.152400121919Discuss why patients may choose not to follow the doctor’s advice.Don’t believe in the treatmentForgetFinance – take half the amount to delay renewing prescriptionFear of dependence/addictionIndividual doesn’t notice any improvementDon’t like what we hearWomen are more likely to participate in regular visits to healthcare professionals (due to childbirth and contraception prescriptions) compared to men, and as a result, will form more trusting relationships with these healthcare individuals and are more likely to follow any advice givenWeek 9 - Cancer, Health Economics and Histopathology Identify the different health professionals that have a role in the diagnosis and management of breast cancer and describe their role.A medical oncologist Specialises in treating cancer with chemotherapy (the use of drugs to kill cancer cells, usually by stopping the cancer cells’ ability to grow and divide) or other medications, such as targeted therapy and oral (in pill form) chemotherapy.A surgical oncologist Specialises in the removal of the tumour and surrounding tissue during an operation. A surgical oncologist also performs biopsies (the removal of a small amount of tissue for examination under a microscope).A radiation oncologist Specialises in treating cancer with radiation therapy (the use of high-energy x-rays or other particles to kill cancer cells).AnaesthetistA doctor who specializes in giving drugs or other agents (like gasses) that cause a total loss of feeling or relieve pain, most often during surgery. The drugs may put the patient into a deep sleep so they not aware of procedures or surgery.Pathologist A doctor who specializes in diagnosing and classifying diseases by lab tests and by looking at tissue and cells under a microscope. The pathologist determines whether a tumour is cancer, and, if cancer, the exact cell type (where it started) and grade (how fast it likely will grow).Plastic surgeon A surgeon who specializes in changing the way a body part looks or in rebuilding or replacing removed or injured body parts. In reconstruction (rebuilding body parts), the surgeon may use tissue from the patient or some special material with the right consistency to hold a shape or form over time.Radiologist A doctor with special training in diagnosing diseases by interpreting (reading) x-rays and other types of imaging studies that make pictures of the inside of the body.Describe the role of the histopathology department at the core biopsy, sentinel node and excision sample stage.Histopathologist’s diagnose disease in;BiopsiesSurgically removed organs.They also are able to provide information on the stage of the cancer, the prognosis for the patient and the management of the patient (treatment and therapy etc.)Preparing the specimen:Orientate the specimen.Ink the surface of the specimen, this is the coloured stain that you see. Palpate the tissue (examine by touch, cancerous tissue is stiffer than healthy tissue).Cut the tissue into transverse (cross direction) sections.Sample the tissues appropriately under the microscope.Core biopsies uses a larger needle (about as thick as a pencil lead) to obtain a sample (sometimes several samples) of breast tissue from the area of concern. Because tissue is taken rather than cells it gives more detailed information.In this type of biopsy the pathologist can see the cells in place within the piece of breast tissue that has been removed. So it is possible to tell a non-invasive cancer from invasive breast cancer with this test. It can also show how abnormal the cancer cells are (the grade) and whether they have receptors for hormones or particular treatments (i.e. HER2/neu).A sentinel lymph node biopsy is a surgery that takes out lymph node tissue to look for cancer. A sentinel node biopsy is used to see if a known cancer has spread from the original cancer site. A sentinel node biopsy may be done instead of a more extensive surgery called lymph node dissection. But if cancer is found in the sentinel lymph node at the time of surgery, more surgery may be needed to remove additional lymph nodes.3448685000Describe the Nottingham Prognostic Index and describe how a histopathologist can grade tumours.The Nottingham prognostic index (NPI) is used to determine prognosis following surgery for breast cancer.The index is calculated using the formula:NPI = [0.2 x S] + N + GWhere:S is the size of the index lesion in centimetresN is the node status: 0 nodes =1, 1-3 nodes = 2, 4+ nodes = 3G is the grade of tumour: Grade I =1, Grade II =2, Grade III =3However treatment results have greatly improved since then. So it may not give as good an outlook (prognosis) as you actually have, if you are having treatment now.List the treatment regimes available for treating breast cancer and discuss the histopathological information that is required and the guidelines used to make treatment decisions for breast cancer.Treatment options depend upon several factors such as:Stage of the cancer (localised or metastasised)Type of breast cancerHER2/neu, oestrogen and progesterone receptor levels in tumourWhether tumour is triple-negativeSize, growth and how likely the tumour is to recurPatient’s age, general heath and menopausal statusWhether the cancer has just been diagnosed or has recurredOptions:Chemotherapy Involves the use of cytotoxic drugs treat neoplastic diseases. These drugs do this by killing dividing cancer cells and interfering with cell production. It is administered by an infusion into a vein though some can also be taken as tablets. Drugs that are given this way travel through the blood stream so they usually act in all parts of the body - a systemic treatment.Radiotherapy (RT)Involves the use of high-energy x-rays or other types of ionising radiation to kill cancer cells or keep them from growing. Radiation does this by directly hitting and damaging DNA or indirectly by producing free radicals in water adjacent to DNA which will then damage the DNA. RT causes the DNA double-strand to break, impairing the function of that particular cell. Although cells can repair some of the damage, residual breaks lead to cell death (apoptosis). If a cell in unable to repair the breaks, it will die when it tries to divide; this is the desired effect against a tumour (mitotic cell death)SurgeryBreast-conserving surgery: removal of the cancer but not the breastLumpectomy (wide local excision) – removal of a tumour and small amounts of surrounding normal tissue; not recommended to patients with cancers larger than 3-4cm due to poor cosmetic results.Quadrantectomy (partial mastectomy) – removal of the breast that has cancer and some normal tissue around it. The lining over the chest muscles below the cancer may also be removed.Total (simple) mastectomy: surgery to remove the whole breast that has cancer and some of the lymph nodes under the arm for biopsy. Around 30% of all breast cancers are unsuitable for breast-conserving surgery and so require a mastectomy (Harmer, 2011).Modified radical mastectomy: surgery to remove the whole breast that has cancer, many lymph nodes under the arm, the lining over the chest muscles and sometimes, part of the chest wall muscles.HerceptinHerceptin is a recombinant monoclonal antibody that is used as treatment for HER2 positive breast cancer. This accounts for approximately 1 in 5 cases of breast cancer where, due to a mutation, the HER2 gene is overexpressed and many HER2 receptors are present, resulting in the increased proliferation of the cells, resulting in a tumour. It can be administered alongside chemotherapy, or on its own, but is generally given after the patient has undergone two courses of chemotherapy.ArimadexArimadex is an aromatase inhibitor (AI). AI’s limit the amount of oestrogen produced by the body after menopause. Before menopause, the ovarian tissues produce high levels of oestrogen, which aromatase inhibitors have little effect on. After menopause however, the peripheral tissues still produce small quantities of oestrogen. This production of oestrogen can be significantly reduced with the use of aromatase inhibitors, thereby making the cancer less likely to return.After menopause, the body still makes small amounts of oestrogen by changing hormones called androgens into oestrogen. Androgens are produced by the adrenal glands, which are above the kidneys. A hormone called aromatase changes androgens into oestrogen. Aromatase is produced mainly by fatty tissue.Describe the principles and scope of health technology assessment and discuss the role of health economics in the medical decision not to prescribe herceptinHerceptin to Mrs Smith.Health economics is a branch of economics concerned with issues related to efficiency, effectiveness, value and behaviour in the production and consumption of health and health care. The application of health economics reflects a universal desire to obtain maximum value for money by ensuring not just the clinical effectiveness, but also the cost-effectiveness of healthcare provision.Herceptin is offered to all women with breast cancer carrying the HER2 (15-25%) protein on their cancer cells. Herceptin attaches to the HER2 protein. If your breast cancer cells don't have this protein, Herceptin won't work. HER 2 is detected by:Fluorescence in situ hybridization (FISH), which detects gene amplification by measuring the number of copies of the HER2 gene in the nuclei of tumour cellsImmunohistochemistry (IHC), which measures the number of HER2 receptors on the cell surface and therefore detects receptor overexpressionHerceptin can control the growth of cancer cells that produce too much of a protein called HER2 (human epidermal growth factor receptor 2). Some breast cancers have large amounts of HER2 and they are called HER2 positive cancers. HER2 makes the cancer cells grow and divide. When Herceptin attaches to HER2 it can make the cells stop growing and die. The problem is treating a patient for one year with Herceptin costs the NHS ?90,831 per patient. The combination of a relative high drug price, long treatment duration and the large population it is targeting can pose a financial burden on the health-care systemDescribe the anatomy and physiology of the lymphatic system-60960016637000The lymph system is the body's drainage system. It is composed of a network of vessels and small structures called lymph nodes. The lymph vessels convey excess fluid collected from all over the body back into the blood circulation. Along the way, however, these fluids are forced to percolate through the lymph nodes so that they can be filtered. Harmful organisms are trapped and destroyed by the specialized white blood cells, called lymphocytes that are present in these nodes. Lymphocytes are also added to the lymph that flows out of nodes and back to the bloodstream. Since the lymphatic system does not have a heart to pump it, its movement depends on gravity and the motions of the muscle.The main functions of the lymphatic system are as follows: the main function of the lymphatic system is to collect and transport tissue fluids from the intercellular spaces in all the tissues of the body, back to the veins in the blood system; it plays an important role in returning plasma proteins to the bloodstream.Digested fats are absorbed and then transported from the villi in the small intestine to the bloodstream via the lacteals and lymph vessels.Lymph transports large molecular compounds (such as enzymes and hormones) from their manufactured sites to the bloodstream.Lymph nodes perform three functions:They filter the lymph, preventing the spread of microorganisms and toxins that enter interstitial fluids.They destroy bacteria, toxins, and particulate matter through the phagocytic action of macrophages.They produce antibodies through the activity of B cells.The function of the thymus is to promote the maturation of T lymphocytes. Immature T cells migrate through the blood from the red bone marrow to the thymus.The functions of the spleen include the following:Filter the blood. Macrophages in the spleen remove bacteria and other pathogens, cellular debris, and aged blood cells. There are no afferent lymphatic vessels, and unlike lymph nodes, the spleen does not filter lymph.Destroy old red blood cells and recycles their parts. It removes the iron from heme groups and binds the iron to the storage protein.Provide a reservoir of blood. The diffuse nature of the red pulp retains large quantities of blood, which can be directed to the circulation when necessary. One third of the blood platelets are stored in the spleen.The spleen is active in immune responses. T cells proliferate in the white pulp before returning to the blood to attack non-self-cells when necessary. B cells proliferate in the white pulp, producing plasma cells and antibodies that return to the blood to inactivate antigens.Discuss the molecular basis of cancerCancer describes disorders that share the common feature of uncontrolled cell growth, leading to a mass of cells known as a tumour/neoplasm.Mutation:Produce cells that fail to differentiate normallyLead to deregulationAllow the cell to grow abnormallyWhen this happens, either necrotic cell death or apoptosis should kick in:Tumour suppressors - inhibit proliferationLoss of function of a gene that is involved in cell proliferation/ growthThey remove the gene’s inhibitory role in the regulation of cell growth and proliferationExample is the retinoblastoma gene RB1makes RB1 protein that interacts with components in cell cycle stopping uncontrolled proliferation When the RB1 protein is active (gets phosphorylated by CDK) it binds to a complex that allows the cell cycle to enter into the S phase. When the protein complex has RB1 attached it doesn’t allow the cell cycle to go to S phase therefore no S phaseProto-oncogenes (involved in normal cell growth regulation) which can become oncogenes when mutated. An example is RAS (rat sarcoma gene).Mutated RAS protein remain in an active form and cause cell growthDNA repair genes In some cases defects in these repair mechanisms lead to genome instability,Genome instability can lead to DNA breaks, abnormal chromosome numbers, widespread mutations in somatic cells that can cause proto- oncogenes to become oncogenes and tumor suppressor genes to become inactivatedDescribe the pharmacology of Herceptin and Arimidex.Herceptin binds to the HER2 receptors, therefore preventing the cancer cells from growing further by preventing the epidermal growth factor protein from entering the cells. Secondly, it takes part in a process known as antibody-dependant cell-mediated cytotoxicity (ADCC) by flagging the cancerous cell for destruction by the immune system. There are also pre-clinical studies, which suggest that it may help enhance the effects of chemotherapy, but further research is yet to be conducted.Arimadex is an aromatase inhibitor (AI). AI’s limit the amount of oestrogen produced by the body after menopause. It works by preventing the action of an enzyme in the body called the aromatase enzyme. The aromatase enzyme is involved in the production of the female sex hormone, oestrogen. Before menopause, the ovarian tissues produce high levels of oestrogen, which aromatase inhibitors have little effect on. After menopause however, the peripheral tissues still produce small quantities of oestrogen. This production of oestrogen can be significantly reduced with the use of aromatase inhibitors, thereby making the cancer less likely to return.After menopause, the body still makes small amounts of oestrogen by changing hormones called androgens into oestrogen. Androgens are produced by the adrenal glands, which are above the kidneys. A hormone called aromatase changes androgens into oestrogen. Aromatase is produced mainly by fatty tissue.Week 10 – Obesity & Public Health Describe the physiological control of appetite.Stretch receptors in the stomach and duodenum send a signal to the brain to let us know that we have had enough to eat and where the food is. The absorption of nutrients is another signaling mechanism.GLP-1 is released when we take food in. (↑ insulin secretion, ↓ glucagon secretion, promotes insulin sensitivity)In obesity these regulators aren’t working properly and we don’t have the same energy output, so more energy comes in that goes out.Short-term regulation of food intake in order to stop us from over eating done by nervous impulses sent by stretch receptors:CCK – pancreatic enzyme secretion, satiety signalReleased from small intestine in response to nutrients (e.g. FAs)Influences satiety by action on CCK receptors located in peripheral vagal afferent terminalsGLP-1, PYY important for maintaining glucose homeostasisPYY released from intestine after meal in proportion to meal size. It’s a satiety signal.Evidence suggests peptide reduces food intake by action on inhibitory presynaptic NPY Y2 receptors on arcuate nucleus NPY neuronsGhrelin stimulates food intakeReleased from stomach during fasting & before meals, falls within an hour of food intakeActivates NPY-expressing neurons in arcuate nucleusLong-term regulation of food intake:GlucostaticHypoglycaemia (low blood sugar) produces hungerIncreases firing of glucose-sensitive neurons in hunger centre while also decreasing firing in neurons in satiety centreAlso activates orexin-containing neurons in LHAInsulin satiety signal Mechanism exists for transport of insulin across BBBInsulin receptors expressed in appetite-controlling areas of the brain (Arcuate nucleus)Insulin deficiency leads to hyperphagia in uncontrolled type 1 diabetesLeptin satiety signal Leptin secreted by fat (adipose) cells, plasma leptin levels rise with increasing fat storesLeptin receptors expressed in appetite-controlling areas of the brain (arcuate nucleus)Leptin deficiency is uncommon cause of obesity, instead leptin resistance results from defects in transport across BBB or impaired intracellular signallingInteracts with insulin and its production, it inhibits insulin release whilst insulin stimulates leptin release. The main controller is the brain in the hypothalamic area and there are certain areas that we know are important:Satiety centreLocated in ventromedial nucleus (VMN)Electrical stimulation of this centre elicits sensations of satiety (even in presence of food)Lesion of this centre causes continuous food intake (hyperphagia: wanting to eat something) even in absence of needHunger (feeding) centreLocated in lateral hypothalamic area (LHA)Electrical stimulation of this area elicits voracious appetite (even after adequate amount)Lesion of area causes complete and lasting cessation of food intake (aphagia)Paraventricular, dorsomedial & arcuate nuclei have major roles in appetite controlIf we look at the arcuate nucleus we have two types of neurons that cause us to decrease or increase food intake. If you stimulate these neurons they will elicit a response. There are interactions between these neurons.Insulin, leptin and CCK cross the blood brain barrier and interact with these neurons and they do that by attaching to their receptors, and if you stimulate them, they will reduce food intake.Ghrelin on the other hand which we know is a stimulant interacts with the neurons on the other side of arcuate nucleus and stimulation of those neurons leads to increase food intake.Defective signalling of melanocortin system leads to obesity e.g. MCR-4 mutations.The neurons that increase food intake are orexigenic stimulate either neuropeptide Y or AgRP (Agouti-related protein), these are neurotransmitters that are being produced by these neurons that cause stimulations of neurons higher up the hypothalamus. The AgRP have receptors to leptin and insulin but this time they inhibit these neurones. So not only are you stimulating neurones that reduce food intake, you are also inhibiting the neurones that increase food intake.Equally if you stimulate these neurones like ghrelin does, they can inhibit these neurones, so stimulation of food intake will inhibit the satiety neurones.Discuss the physiological (normal function of the body) effects of obesity on the body.Increase risk of many diseases and conditions such as:Coronary Heart DiseaseThere is both an indirect and direct correlation between coronary heart disease and obesity and in individuals with an increased BMI there is an increased risk of suffering from coronary heart disease. Obesity causes it indirectly by causing hypertension, dyslipidaemia and reductions in HDL cholesterol which then in turn increases the risk of CHD and also directly by increasing the build-up of a waxy substance referred to as plaque inside the coronary arteries. It is found that in a 14 year prospective study with middle aged women who had a BMI less than 23 and another group of women who had a BMI of over 25 there was an increased risk of coronary heart disease by up to 50% in the group with greater BMI .High blood pressureThe risk of having high blood pressure greatly increases when an individual has a BMI classified as obese this can be due to a number of reasons. A high fat diet can cause the deposition and build-up of plaque within the arteries which narrows the lumen and causes an increase in blood pressure. Additional fat tissue within he body increases the demand for oxygen in several areas which causes an increase in blood pressure to cope with this demand not only this but it also means blood must be pumped through additional blood vessels and so blood pressure may increase to allow this. Extra weight can raise the individuals heart rate and reduce the ability to transport blood through blood vessels this all contributes to an increases risk of hypertension. Type 2 DiabetesType 2 diabetes is responsible for at least 90% of all cases for diabetes and its link with obesity is extremely significant. A person who is obese has a seven times greater risk of developing this type of diabetes in comparison to an individual of a healthy weight. A person with type 2 diabetes has significantly reduced sensitivity to insulin and there are several possible reasons as to why obesity can cause this. Abdominal obesity may cause fat cells to release pro-inflammatory chemicals these can make the body less sensitive to insulin which disrupts its function it is also though that obesity can trigger changes to the body’s metabolism that cause adipose tissue to release increased amounts of fatty acids, glycerol , hormones and pro inflammatory cytokines which can develop insulin resistance .OsteoarthritisObesity is noted as one of the most significant and most preventable risk factor for osteoarthritis and there have been numerous studies which have notes an undeniable link between BMI and osteoarthritis of the hip, knee, foot and hand. Although the correlation is not fully understood it is believed that increased pressure on joints such as the hip and knee due to increased weight load can cause the breakdown of cartilage not only this but it may be due to an alteration in the gait of an individual who is obese. Arthritis is considered a low-grade systemic inflammatory disease and obesity can increase the levels of pro inflammatory cytokines.Other diseases/conditionsThere are numerous other conditions and diseases which obesity is a major risk factor for such as stroke, this is greatly linked with an increased risk of CHD and hypertension with narrowed lumens of blood vessels and a build-up of plaque within the blood vessel this can increase the risk of clots forming and if a clot was to form in a blood vessel which is close to the brain this can cause a stroke. Obesity can also cause Sleep Apnoea which can cause pauses in breathing during sleep and shallow breathing in general this can be caused by an excess of fatty deposits around the neck which constricts the airways. Obesity has been known to cause reproductive problems particularly in women where it can cause infertility and disruption of the normal menstrual cycle. Obesity can also increase the risk of many other diseases and conditions such as cancer (particularly colon, breast, endometrial and gall bladder), Obesity hyperventilation syndrome and gall stones.How is fat metabolised in the body?When food sources exceed the immediate needs of the body, excess energy is then metabolised and stored as dietary triacylglycerol’s in fat cells. Food travels to the stomach where it is digested into its components including fats. These components then travel into the small intestine where bile salts from the gall bladder emulsify the relatively insoluble, non-polar dietary fats to form micelles. Triacylglycerol’s form micelles with non-polar cores and are surrounded by bile salts during solvation. The R groups of the triacylglycerol’s are non-polar so they point toward the centre of the micelles. The micelles then continue down the small intestine. Here an enzyme called pancreatic lipase degrades the triacylglycerol’s into fatty acids and glycerol via hydrolysis. The fatty acids and glycerol are absorbed into the intestinal mucosa.In the small intestinal mucosa, the fatty acids and glycerol are then resynthesized into triacylglycerol’s then they are packaged with apoprotiens and cholesterol into blood soluble complexes called chylomicrons. These chylomicrons move across the blood vessel membrane and into the blood stream. The chylomicrons are released into the lymphatic system – they do not go directly into the bloodstream, as they are too large to pass through the walls of the capillary. The lymphatic system eventually merges with the veins, at which point the chylomicrons travel through the blood stream and have two possible fates. The lipoproteins can travel to fat cells (adipocytes) for storage, or to muscle cells (myocytes) for breakdown as fuel for energy. For storage of fat in adipocytes, the triacylglycerol is split on the wall of the blood vessel by the lipoprotein, lipase, into fatty acids and glycerol. These components travel into the adipocyte cell and are stored as triacylglycerol’s in fat droplets. If you were exercising after eating, the dietary fat would instead be utilised by muscle cells as energy. Another scenario that arises during exercise is when the muscles quickly use up the small amount of the body’s stored glycogen. In this case, energy stored as fat droplets in adipocytes gets released to bring energy reserves to the respiring tissues. First epinephrine or glucagon leaves the bloodstream and binds to the receptor molecule found in the membrane of the adipocyte. This allows adenyl cyclase to convert ATP into cAMP. Now the cAMP binds to a protein kinase and activates it. The activated protein kinase binds to the triacylglycerol lipase, activating it. Once activated, the triacylglycerol lipase is able to break into its components. The fatty acid molecules are then picked up by the protein serum albumin in the blood stream. The serum albumin travels through the blood vessels and releases the fatty acid molecules in myocytes as needed. Finally the fatty acids undergo beta-oxidation. This process releases CO2 and ATP energy for the myocyte to use.Discuss the role of nutrition in maintaining a healthy body weight and what goes wrong in obesity.Obesity is created by an imbalance of energy. Calories consumed > Calories usedThe same amount of energy IN and energy OUT over time = weight stays the same (energy balance)Discuss the epidemiology of obesity in the UK. Why do different regions have different prevalence?Socio-economic classLower paid jobs and longer working hours -> less nutritious and high fat diets.Minority ethnic groupsObesity prevalence rates are also higher (and lower) in some ethnic groups in comparison to the general population. In 2004, among the ethnic minority groups, Black Caribbean and Irish men had the highest prevalence of obesity (25 percent each) compared to the 23 percent in the general population.AgeOverweight and obesity rates vary significantly as a function of age in both men and women. This is partly because of a natural progression in the increase in body weight with ageing. Data from the 2005 Health Survey for England indicate overweight and obesity levels peaked in individuals between 55-74 years of age with 77.4 percent of adults being overweight or obese compared to the general population rate of 65 percent.?Describe how the social determinants of health are related to weight gain in childhood, includingincluding genetics, behaviours (nutrition and exercise), the social and built environment.Behavioural factors In prevalence not due to increase in calorific value but due to decrease in activity levelsHigh-fat dietsSnackingConsumption of energy-dense foodsAlcohol consumptionSmokingDecrease in activity levels due to labour saving devices such as carsGenetic factorsMutations of melanocortin-4 receptor (MC4R)Prader-Willi syndrome (childhood obesity with abnormal appearance and CNS function)Mutations in leptin geneSpecific causes (a few cases of obesity)Endocrine factors (Hypothyroidism, Cushing’s syndrome, Hypopthalamic tumours, Insulinoma)Drug Treatments (Tricyclic antidepressants, sulphonylurea drugs, corticosteroids, some oral contraceptive pills)Other social determinants of health:Access to educational, economic, and job opportunitiesAccess to health care servicesQuality of education and job trainingNutrition and exerciseTransportation optionsSocial norms and attitudes (e.g., discrimination, racism, and distrust of government)Access to mass media and emerging technologies (e.g., cell phones, the Internet, and social media)Apply the principles and application of primary, secondary and tertiary prevention of disease to managing childhood obesity.Primary prevention involves the “preventing of a disease before it occurs…and is the most effective way to improve health and control costs”Encourage physical activity and decrease sedentary activity, especially screen time.No or almost no sweetened beveragesBehavioural Counselling: Eat a healthy breakfast everyday Limit meals outside of the home, especially fast food Family meals 5-6 times per week Fruits and VegetablesAppropriate portion sizesTaxing foodSecondary prevention strategies attempt to diagnose and treat an existing disease in its early stages before it results in significant morbidity (relative incidence of a disease). Screening for diabetesCommunity level weight loss and exercise programsFood and activity monitoring, and creation of short-term diet and physical activity goals.Tertiary prevention treatments aim to reduce the negative impact of established disease by restoring function and reducing disease-related complications.Weight control surgeryMeal replacement or very low calorie dietPharmacologic interventions Figure 3: Nuffield Council on Bioethics ladder of interventionDemonstrate how to begin a discussion on obesity with a patient.Demonstrate how to begin a discussion on obesity with a patient.Ask the patient if he/she would be comfortable with discussing general health including weight.Ask about the patient’s weight history and how excess weight has affected his/her life.Ask patient if he/she would consider lifestyle changes to lose weight and improve healthAsk patient about previous attempts to lose weight. What were the most successful and least successful?Ask about the patient’s physical activity level and attitude toward exercise.Ask patient about the level of support he/she can expect from family and friends.Ask about potential barriers to success.Ask what the patient’s weight goals are.Explain that even a small weight loss of 10 percent of initial weight can lower health risks.Ask patient if he/she would like help with diet and physical activity.Select two or three measurable, achievable goals and discuss steps needed to achieve them.Week 11 – Psychology for Medicine: An Introduction-257175229870Nicotine Eeffects on whole organismIncreased heart rateCardiac contractilityIncreased blood pressureDecreased skin temperatureMobilisation of blood sugarIncrease in FFA in bloodIncrease catecholaminescatecholamine levels in blood i.e. adrenaline and noradrenalineArousal or relaxation as it stimulates the sympathetic and parasympathetic nervous system00Nicotine Eeffects on whole organismIncreased heart rateCardiac contractilityIncreased blood pressureDecreased skin temperatureMobilisation of blood sugarIncrease in FFA in bloodIncrease catecholaminescatecholamine levels in blood i.e. adrenaline and noradrenalineArousal or relaxation as it stimulates the sympathetic and parasympathetic nervous systemDescribe the physiological effects of smoking and drinking (nicotine and alcohol)right69215Nicotine Eeffects at the cellular levelIncreased synthesis and release of hormonesActivation of tyrosine hydroxylase enzymeActivation of several transcription factorInduction of heat shock proteinsInduction of oxidative stressEffects on apoptosisInduction of chromosome aberrationsInduction of sister chromatidechromatid exchange00Nicotine Eeffects at the cellular levelIncreased synthesis and release of hormonesActivation of tyrosine hydroxylase enzymeActivation of several transcription factorInduction of heat shock proteinsInduction of oxidative stressEffects on apoptosisInduction of chromosome aberrationsInduction of sister chromatidechromatid exchangeEffect of alcohol:Effects on cardiovascular systemCutaneous vasodilation, causes warm feeling but actually increases heat lossEffects on endocrine systemsDiuresis familiar effect – caused by inhibition of ADHEffects on GI tractEthanol increases salivary and gastric secretionEffects on liverMost serious long term consequenceIncreased fat accumulation, leads to hepatitis and finally hepatic necrosis and fibrosisEffects on lipid metabolism, platelet function & atherosclerosisEffects on foetal developmentFoetal alcohol syndrome (FAS)Describe the effect of exercise on the body.Increase in heart rate due to adrenaline and an increased demand for oxygenBreathe deeper and quicker to get more oxygen into your lungs which is detected by chemoreceptors detecting a decrease in pHBody temperature increases due to an increase in metabolismSweat to reduce the increase in temperatureAching muscles due to glucose being respired anaerobicallyArterioles dilate to make sure blood pressure doesn’t get too highEffects of regular training:The heart pumps more blood per beat and the muscles becomes thicker therefore stronger.The recovery rate becomes quicker.Number of red blood cells increases.The resting pulse rate becomes lower.In the muscle cells there is an increased number of mitochondria to increase rat of energy production and increased capability to store glycogen for energy.You can work harder for longer.The number of capillaries increases.The cardiovascular system becomes more efficient.The muscles, bones and ligaments become stronger which helps cope with additional impact.Decreases your risk of various health conditions such as stroke, type 2 diabetes, depression and CHD.Describe the physiological basis of addictionNicotine and alcohol are both “dependence-producing” drugs and stimulate the reward centres of the mesolimbic system. Although both ultimately lead to an increased amount of dopamine being produced, they do so in different ways.Nicotine stimulates tyrosine hydroxylase, which is used in a series of reactions to produce more dopamine.Alcohol is absorbed into the bloodstream and interacts with GABA receptors in the ventral tegmental area, nucleus accumbens and amygdala, which then results in the increased production of dopamine. (Alcoholics do have hypo function of mesolimbic system).With elevated dopamine levels, the reward pathway is activated. This reinforces the associated behaviour, thereby making the behaviour more likely to be repeated.Discuss different definitions of healthHealth is a state of complete, physical, mental, and social wellbeing and not merely the absence of disease and infirmity. - Inclusive but too broad and unrealistic as a definition?Antonovsky (1987) proposed we should perhaps think of it on a continuum instead, from optimal wellness to death.center2159000We think of health in 6 different ways:Not having symptomsHaving physical or social reservesHaving healthy lifestylesBeing physically fitPsychological wellbeingBeing able to functionDiscuss the relevance of psychology to medicinePsychology is the scientific study of the mind and behaviour.Treating the person, not the disease is crucial and psychological factors such as thoughts, emotions, personality and personal experience makes each person unique so should be considered in treatment.There is a strong link between physical and psychological health so one side should not be pare and contrast the biomedical and biopsychosocial approaches to healthcareBiomedical approach:Assumes all disease can be explained using physiological processesTreatment is for the disease, not the personPsychological and social processes are separate; it separates body and mind (dualism)Biopsychosocial approach:Does take into account biological, psychological and social factors when diagnosing and treating an individualExtended to include factors such as ethnicity and culture.A holistic approachcenter33655Discuss the importance of health behaviour and health behaviour changeHealth behaviours are behaviours that effect our health positively or negatively.Importance of health behaviour:If we understand why people carry out health risk behaviours we can help them changeHealth promotion programmes can then be tailored to target the causes of the harmful behaviourTo be effective, we have to know the main causes for behaviours for different groups of people.Outline key psychological models that explain and predict health behaviourHealth Belief model:Susceptibility: The patient’s belief of how susceptible they are to the negative consequences of carrying out the behaviour.Severity: How severe the consequences of the action are.Costs: the pros (of carrying on) and cons of stopping the action.Benefits: of stopping the behaviour.Cues to action: an event that has made them think about their actions. Can be internal or external. Health motivation: how motivated are they to change their health behaviour. “Readiness”.Perceived control: how much control do they think they have to change their behaviour?The Stages of Change model:Focused on preventing relapse back to addiction.?It has five stages, but the stages do not have to go be progressed through in order, it depends on the patient.?The five stages are:Pre-contemplation -?Where there is no intention to change behaviour in the foreseeable futureContemplation -?The individual is seriously contemplating a change in behaviour.Preparation/Determination -?The individual decides that they want to change their behaviour and starts to show small signs of behavioural change in conjunction with this.Action -?The individual puts their decision into action and shows large behavioural changes in an effort to combat their addiction. <6 months.Maintenance -?The individual continues their efforts to prevent relapse and to consolidate gains made in treatment. 6+ months (stability).Theory of planned behaviourBehavioural beliefs: your thoughts on the behaviour that you are carrying outAttitude: The patient’s evaluation of the behaviour (is it good or bad). The pros and cons.Normative beliefs: your belief on what others around you think of the actions you are carrying out.Subjective norm: the pressure (or not) that you receive to engage in a particular behaviour. Control belief: Patient’s belief regarding ability to quit. Do you have the internal resources you need (i.e. willpower) and the external resources (i.e. money).Explain how we can apply these models to influence behaviour change in clinical practice.Health psychology models Aim to explain why people carry out health behaviours and can be used to develop health behaviour interventions in clinical practice.In a clinical setting we can use Health Belief Model’s to find out what stage the patient is in and also to explain to patients the pros and cons of their chosen behaviour.Suspected questions:What is the difference between disease and illness?Illness is used to describe a person who is in a poor state of health (what the patient feels). A disease is an abnormal condition that affects the body of an organism, often caused by pathogens (what the patient has). ................
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