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34 Cards in this Set
- Front
- Back
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Where are nociceptors
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Dorsal Root Ganglia. Sensory neurons that detect pain.
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What are Baroreceptors
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Sensors located in blood vessels.The low-pressure baroreceptors have both circulatory and renal effects; they produce changes in hormone secretion, resulting in effects on the retention of salt and water; they also influence intake of salt and water. The renal effects allow the receptors to change the mean pressure in the system in the long term.
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What are Chemoreceptors
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Sensory receptor that tranduces chemical signal into action potential.
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What are Osmoreceptors
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An osmoreceptor is a sensory receptor primarily found in the hypothalamus of most homeothermic organisms that detects changes in osmotic pressure.
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Endospore formation
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Starvation of these microbes causes sporulation, a dramatic 8 hour programme that ultimately creates a spore. Uses one of two potential division sites. Replicates and stretches DNA. Stage 2 steptation occurs, dividing cell into two seperate compartments. Each contains chromosone. Mother cell engulfs small spore, resulting in structure encircled by two membranes. MOther cell is destroyed.
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Antibiotic Resistance
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due to genetic modification caused when bacteria is exposed to but not killed by antibiotic. This causes antibiotic to modify the cell wall and eject a long hair like appendage named a pillus to notify the other bacteria to mutate in the same fashion.
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Streptokinase
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Lyses and dissolves clots designed to trap bacteria so that they are able to then roam freely
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Capsules
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Some bacteria produce a sticky layer of polysachinides and secrete this as a layer over the cell. This layer of slime helps mainatin bacteria's virulance, resist phagocytosis and will help it adhere to a host cell. While the capsule underneath will help it from drying out.
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Reservoirs of infection
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Many common infectious diseases have human reservoirs. Diseases that are transmitted from person to person without intermediaries include the sexually transmitted diseases, measles, mumps, herpes.
Human reservoirs may or may not show the effects of illness. Asymptomatic carriers are those who never experience symptoms despite being infected and infecting others. |
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Portal of Exit
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Portal of exit is the path by which a pathogen leaves its host. The portal of exit usually corresponds to the site where the pathogen is localized. For example, influenza viruses exit the respiratory tract, Sarcoptes scabiei in scabies skin lesions, and enterovirus 70, a cause of hemorrhagic conjunctivitis, in conjunctival secretions
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Portal of Entry
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The portal of entry refers to the manner in which a pathogen enters a susceptible host. The portal of entry must provide access to tissues in which the pathogen can multiply or a toxin can act. Often, infectious agents use the same portal to enter a new host that they used to exit the source host. For example, influenza virus exits the respiratory tract of the source host and enters the respiratory tract of the new host.Many pathogens that cause gastroenteritis follow a so-called “fecal-oral” route because they exit the source host in feces, are carried on inadequately washed hands to a vehicle such as food, water, or utensil, and enter a new host through the mouth. Other portals of entry include the skin (hookworm), mucous membranes (syphilis), and blood (hepatitis B, human immunodeficiency virus).
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Host susceptibility
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Dependant on immune status of person
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Describe the hepatic portal system
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The venous blood from the GI tract drains into the superior and inferior mesenteric veins; these two vessels are then joined by the splenic vein just posterior to the neck of the pancreas to form the portal vein. This then splits to form the right and left branches, each supplying about half of the liver.
On entering the liver, the blood drains into the hepatic sinusoids, where it is screened by specialised macrophages (Kupffer cells) to remove any pathogens that manage to get past the GI defences. The plasma is filtered through the endothelial lining of the sinusoids and bathes the hepatocytes; these cells contain vast numbers of enzymes capable of braking down and metabolising most of what has been absorbed. The portal venous blood contains all of the products of digestion absorbed from the GI tract, so all useful and non-useful products are processed in the liver before being either released back into the hepatic veins which join the inferior vena cava or stored in the liver |
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Describe coronary circulation
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The heart needs its own reliable blood supply in order to keep beating- the coronary circulation. There are two main coronary arteries, the left and right coronary arteries, and these branch further to form several major branches. The coronary arteries lie in grooves running over the surface of the myocardium, covered over by the epicardium, and have many branches which terminate in arterioles supplying the vast capillary network of the myocardium.
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Describe the pulmonary circulation
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The veins bring waste-rich blood back to the heart, entering the right atrium throughout two large veins called vena cavae. The right atrium fills with the waste-rich blood and then contracts, pushing the blood through a one-way valve into the right ventricle. The right ventricle fills and then contracts, pushing the blood into the pulmonary artery which leads to the lungs. In the lung capillaries, the exchange of carbon dioxide and oxygen takes place. The fresh, oxygen-rich blood enters the pulmonary veins and then returns to the heart, re-entering through the left atrium. The oxygen-rich blood then passes through a one-way valve into the left ventricle where it will exit the heart through the main artery, called the aorta. The left ventricle's contraction forces the blood into the aorta and the blood begins its journey throughout the body.
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Explain therapeutic index with an example
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The ratio between the toxic dose and the therapeutic dose of a drug, used as a measure of the relative safety of the drug for a particular treatment. For example the therapeutic index for morphine morphine, a sedative, antidepressant, and analgesic and emetic is 70:1
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Explain hepatoxicity with relation to a drug
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Hepatotoxicity (from hepatic toxicity) implies chemical-driven liver damage. Because the liver plays a central role in transforming and clearing chemicals it is susceptible to the toxicity from these agents. Certain medicinal agents, when taken in overdoses and sometimes even when introduced within therapeutic ranges, may injure the organ. Morphine for example can damage the liver by causing hydropic degeneration.
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Neprotoxicity
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Nephrotoxicity is a poisonous effect of some substances on the kidneys. For example, morphine is not recommended for chronic use in renal insufficiency due to the rapid accumulation of active, nondialyzable metabolites that are neurotoxic.
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Drug interactions
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Drug interactions occurs when the effect of a particular drug is altered when it is taken with another drug, or with food. Coadministration of morphine and codiene may increase side effects such as dizziness, drowsiness, and difficulty concentrating.
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When does the first stimulation for cytoxic t cells take place?
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The first stimulation occurs when the antigen is present on the cell surface by the MHC 1 molecule and T cell receptor.
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When does the second stimulation for cytotoxic t cells take place?
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Second stimulation happens when IL2 from a CD4 helper T cell excretes – acting as a Paracrine. The CD8 cytotoxic T cell then divides to produce cloned offspring-Some are “activated” and can kill infected tissue cells quickly- others are memory cells which will react very fast the next time the same antigen is engulfed by tissue cells in the future
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How does pain travel
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Fast pain travels via type Aδ fibers to terminate in the dorsal horn of the spinal cord where they synapse on dendrites of the neospinothalamic tract. The axons of these neurons cross the midline (decussate) through the anterior white commissure and ascend contralaterally along the anterolateral columns. These fibres terminate on the ventrobasal complex of the thalamus and synapse with the dendrites of the somatosensory cortex. Fast pain is felt within a tenth of a second of application of the pain stimulus and is a sharp, acute, prickling pain felt in response to mechanical and thermal stimulation. It can be localised easily if Aδ fibres are stimulated together with tactile receptors
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How does morphine act on the body?
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The precise mechanism of the analgesic action of morphine is unknown. However, specific CNS opiate receptors have been identified and likely play a role in the expression of analgesic effects. Morphine first acts on the mu-opioid receptors. The mechanism of respiratory depression involves a reduction in the responsiveness of the brain stem respiratory centers to increases in carbon dioxide tension and to electrical stimulation. It has been shown that morphine binds to and inhibits GABA inhibitory interneurons. These interneurons normally inhibit the descending pain inhibition pathway. So, without the inhibitory signals, pain modulation can proceed downstream.
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What are adrenergic receptors?
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The adrenergic receptors (or adrenoceptors) are a class of G protein-coupled receptors that are targets of the catecholamines, especially norepinephrine (noradrenaline) and epinephrine (adrenaline).
Many cells possess these receptors, and the binding of a catecholamine to the receptor will generally stimulate the sympathetic nervous system. |
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What are specific reactions of beta 1 stimulation
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Increase cardiac output by increasing heart rate (positive chronotropic effect), conduction velocity (positive dromotropic effect), and stroke volume (by enhancing contractility—positive inotropic effect).
Increase renin secretion from juxtaglomerular cells of the kidney. Increase ghrelin secretion from the stomach.[12 |
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MHC I molecules
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MHC class I occurs on all nucleated cells—in essence all cells but red blood cells—and presents epitopes to killer T cells, also called cytotoxic T lymphocytes
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Receptors for water soluble hormones
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Water soluble or protein based ligands (such as hormone glucagon) are unable to pass through phospholipid bilayer. They attach to a receptor on the plasma membrane resulting in either opening of the integral protein or channel allowing ligand to enter or initiate a second messenger system within cell.
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Afterload
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Afterload is the ventricular pressure at the end of systole (ESP). Ejection stops because the ventricular pressure developed by the myocardial contraction is less than the arterial pressure. This determines the end-systolic volume (ESV). Because the EDV equals the presystolic volume for a given beat of a ventricle, then the pre- and postsystolic volumes define the stroke volume (if the valves are fully functioning and there are no ventricular-septal leaks). The product of stroke volume and heart rate determines the cardiac output—the primary function of the heart.
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Preload
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Preload is the end-diastolic volume (EDV) at the beginning of systole. The EDV is directly related to the degree of stretch of the myocardial sarcomeres. This
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End Systolic Volume
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End-systolic volume (ESV) is the volume of blood in a ventricle at the end of contraction, or systole, and the beginning of filling, or diastole.
ESV is the lowest volume of blood in the ventricle at any point in the cardiac cycle. The main factors that affect the end-systolic volume are afterload and the contractility of the heart. |
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Venous return
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Venous return refers to the flow of blood from the periphery back to the right atrium, and except for periods of a few seconds, it is equal to cardiac output
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Teratogenecity
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Of, relating to, or causing malformations of an embryo or fetus. In the case of morphine vasoconstriction of the placenta causes reduced blood and oxegyn flow to the fetus, resulting in fetal abnormalities.
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Adverse reactions
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The gastrointestinal effects of morphine are mediated primarily by μ-opioid receptors in the bowel. By inhibiting gastric emptying and reducing propulsive peristalsis of the intestine, morphine decreases the rate of intestinal transit. Reduction in gut secretion and increased intestinal fluid absorption also contribute to the constipating effect.
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Where does pain begin?
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In the periphery when free nerve endings are stimulated. Nocioreceptors tranduce noxious stimuli into neuronal action potential that propel centrally to the spinal cord and then to the brain.
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