Patho. Test 2
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204 terms
Terms | Definitions |
|---|---|
 Define are hypersensity disorders | Characterized by excessive or Inappropriate activation of the immune system. Also a normal immune response that occurs inapropiately. |
| Type I Hypersensitivity | immediate- massive anaphaylactic response; can be life threatening |
| Type II Hypersensivity | Antibody-Mediated - anti-bodies are attacking things that they shouldnt |
| Type III Hypersensivity | Immune-Complex Mediated - antigen and antibody bound together |
| Type IV Hypersensivity | T-cell mediated - delayed reaction |
| What two main cells are associated with Type I hypersensitivity? | Helper T-cells and Mast cells |
| What is the first step in a Type I Hypersensitivity reaction? | Exposure to antigen |
| What is the second step in a Type I Hypersensitivity reaction? | Production of AB(IgE) against the antigen |
| What is the third step in a Type I Hyper. Reaction? | The IgE coats the surface of mast cell |
| What is the last in a Type I Hyper. Reaction? | Upon second exposure denauring of IgE coated mast cells. Release of histamine, prostaglandins, leukotienes. |
| What systemic, life threatening symptoms occur during anaphylaxis and why? | Hypotension, bronchospasm, edema, angioedema, itching, and G.I. cramps. |
| What are five treatments for anaphylactic shock? | Drugs to raise BP, Drugs to dialate airways, antihistamines, intravenous fluids, and corticosteroids. |
| Which two antibodies mediate Type II Hypers. reaction? | IgM, IgG |
| What binds the binding antibody to the antigen? | 1. Activation of Complement 2. AB-mediated cell lysis 3. Opsonization and Phagocytosis(attration of the microphages) |
| What attack is activated by the Complement + Antibody? | Membrane Attack Complex |
| Which receptors are involved in Grave's disease and what do they do? | TSH receptors of thyroid. Antibodies bind to the receptors and overactivate them, (hyperthyroidism) |
| Which receptor is involved in Myasthemia Gravis and what do they do? | ACh receptors. The block ACh so the muscles can no longer contract. (paralysis) |
| What usually preceeds the type II hypers. sens. disorder? | Occurs after widespread Bacterial Infection |
| Where do the AB-complexes deposit into? | blood vessel walls |
| What is vasculitis? | Inflammation of the vessels |
| What is glomerulonephritis? | Inflammation of kidneys |
| Whats is serum sickness? | Widespread deposition of AB-AG complexes in tissues and blood. |
| What are the effects of serum sickness? | vasculitis, joint pain, renal damage, pain fever, rash, lymphadenopathy |
| Give three antigens that cause serum sickness? | Penicilin reaction, Food reaction, and insect venom |
| How does inflammation effect Glomerular function? | Renal failure, due to the damaged glomerular trying to be exposed of by the immune system |
| The principle mechanism of Type IV Hypersensivity involves a response against _____, ______, _____ and ______. | Bacteria, viruses, fungi, and protozoa. |
| Direct Cell-mediated Cytotoxicity involves what type of cells? | Cytotoxic T-cells |
| How is delayed hypersensitivity mediated? | By excess cytokine release by the T-cells. |
| Contact dermatitus, poison ivy, and latex allergies are all examples of what type hypers. | IV |
| Blood transfusion mis-match 2 is what type of hypers. reaction | II |
| A person with blood type A has what type of antigens and antibodies? | Antigen A and antibodies against antigen B |
| A person with blood type B has what type of antigens and antibodies? | Antigen B and antibodies against antigen A |
| A person with blood type AB has what type of antigen and antibodies? | both A and B and no antibodies against either. |
| A person with blood type O has what type of antigen? | none!! (haha trick question lol) |
| Which blood types are said to be the universal donors? | Type O |
| A person with blood type O has what type antibodies? | antibodies against both antigen A and B |
| What type(s) of blood can a person with 0 type blood receive safely?? | Only O because they have antibodies against A&B |
| Why are persons with Type AB blood are said to be "Universal Recipients"?? | They don't any antibodies against A or B |
| What does AIDS stand for? | Acquired Immunodeficiency Syndrome |
| If a person is anergic they can't do what? | mount an immune response |
| A person that has a lack of white bloods and the inability to produce new lymphocytes is called? | lymphopenic |
| Cytomegalovirus was used to describe what type of patients? | HIV patients in the early to mid 1900's |
| What are the ways that HIV can be transported? | Contact with blood and body fluids, sexual, I.V. drug use, infected blood products, and maternal-fetal transmission |
| HIV is a retrovirus because....? | it must have its RNA genome copied into DNA in order to be replicated. ex: via host cell |
| What are the mechanisms used to attach the HIV cell to a host cell? | spikes or peplomers |
| How does the HIV lipid bilayer help permeability? | The lipid bilayer resembles the human cell membranes and is allowed to pass through. |
| The spike that actually stick out and attaches to the CD4 is? | GP120 |
| What enzyme allows the retrovirus to give the host cell a back copy of the virus DNA ? | reverse transcriptase |
| What type of virus is covered by a lipid bi-layer? | enveloped virus |
| What is made up of the glycoproteins gp120 and gp41? | peplomers , "spikes" |
| Which enzyme intergrates the HIV genome into the host cell? | HIV Integrase |
| Which enzyme is necassary to complete maturation of the HIV ? | HIV Protease |
| The action of reverse transcriptase takes RNA and copies it into a single DNA strand forming a _____ complex. | DNA-RNA |
| What are the eight steps in the life cycle of HIV? | Binding, fusion, reverse transcriptase, integration, transcription, translation, new virus assembly & budding, and maturation |
| As the HIV cell fuses to the host cell what is dissolved exposing the HIV cell inside of the host cell? | the lipid bi-layer |
| What falls apart and allows the hIV RNA to b released into the host cell? | protein capsid |
| How does the new HIV cell obtain the viral lipid bilayer? | The HIV cell performs a "budding" process out of the host cell and takes some of the membrane with it and it alo has peplomers. |
| How is the virus able to leave the host cell? | The proteases do cutting and cleaving |
| The drug AZT(Zidovudine) acts by? | Inhibiting HIV replication |
| What are the three phases of HIV infection? | 1. Primary Infection 2. Chronic Asymptomatic (latency) 3. Over AIDS |
| In which phase of infection do you see very high viral loads | primary infection |
| How long does the primary infection stage usually last? | 2-4 weeks |
| Which phase of HIV infection does the patient experience acute, flu-like syndrome? | primary infection |
| Aggressive treatment during the primary infection phase of infection may yield the best long term outcomes because? | The worst thing you can do is allow the organism to replicate, and mutate into medicine resistant strands |
| What is arthralagia? | joint pain |
| what is myalgia? | muscle pain |
| What is lymphadenopathy? | Abnormal enlargement of the lymph nodes |
| Aspetic meningitis | The lining in the brain become inflammed |
| How long does the latency period typically last and what happens to the viral load and the CD4 numbers? | 8-10 years and the viral load decreases significantly and the CD4 increases |
| Which phase of HIV infection may have possible signs of lymphadenopathy? | Latency |
| What is happening during the latency period? | The virus cell is incorporating is genome into the host cells but no overproduction of the virus |
| What is the CD4 cell count range for overt AIDS? | <200 cell/ul |
| How long does it take a person to die when they reach the overt AIDS stage? | 2-3years w/out treatment |
| The viral load rises during which phases? | primary infection and overt AIDS |
| What are the symptoms of overt AIDS? | opportunistic infection, cancers, and viruses may enter CNS |
| Typical Progressors | Median ten years |
| Rapid Progressors | 2 - 3 years |
| Slow Progressors | 10-13 years |
| Long-term non-progressors | T-cell doesn't drop even though the viral loads remain high |
| Efavirenz, emtricitabine, tenofovir are components of what HIV drug | HAART |
| Why do we give HIV patients three different drugs? | to prevent resistance |
| Why would you give a HIV patient chemotherapy before a bone marrow transplant? | To kill all old bone marrow and replace it with new cells |
| What is the significance of HIV RNA levels? | replication |
| Which gene has a mutation that effects the cobinding receptor on the host cells | CCR-5 (macrophages) CXCR4 (T-cells) |
| Which HIV drug helps in preventing binding to the host cell? | Maraviroc |
| What are two opportunistic infections for the presentation of HIV | Kaposi Sarcoma and Burkitt's lymphoma |
| HIV is a major factor in the resurgence of what disease? | TB (tuberculosis) |
| Candidiasis | yeast (thrush) |
| P. jiroveci pneumonia | fungi in Alveoli |
| ADC is a late stage manifestation that directly effect what organ? | the brain |
| What are symptoms of ADC? | Motor & mental impairment, amnesia, personality disorders |
| What are the current drug targets of HIV drugs and why? | reverse transcriptase because it is not present in normal cell and the inhibitos will not harm normal function |
| Two examples of nucloside analogues non-nucleoside RT inhibitors | Zidovudine (AZT), Nevirapine |
| two Protease inhibitor drugs | Ritonavir, saquinavir |
| Why can't antigens used to make a vaccine against HIV? | You would have to find something that effects the virus the same in every virus which is not easy or very effective |
| What are four purposes of inflammatory responses? | 1. protective response 2. eliminates cause of injury and necrotic cells that come from injury 3. Dilutes, destroys or neatralizes 4. sets stage for healing |
| rubor | redness |
| tumor | swelling |
| calor | heat |
| dolor | pain |
| functio laesa | loss of function |
| The five cardinal signs of inflammation | 1. rubor 2. tumor 3. calor 4. dolor 5. Funcito Laesa |
| What are the two stages of acute inflammation | 1. Vascular Stage 2. Cellular Stage |
| The cellular stage is a response to what? | of immune cells to injury |
| The response of blood vessels to injury is in what stage of acute inflammation? | vascular stage |
| What happens initially in the vascular response? | brief vasconstriction of small vessels which is due to a neutogenic reflex |
| After vasconstriction there is rapid dilation of local _____ and ________, which can be characterized by redness & warmth | arterioles and venules |
| Increased Capillary Permeability during vascular response can lead to....? | edema, pain, impaired tissue function |
| What three purposes does increased capillary permeability serve? | 1. Stagnation of blood flow limits the spread of toxins and bacteria and increases blood clotting 2.exudates dilute toxin concentration 3. facilitates WBC movement out of blood vessel |
| Which two white blood cells are involved in cellular response? | granulocytes (granules) monocytes |
| Three types of granulocytes? | 1. neutrophil 2. basophils 3. eosinophils |
| Which granules are the first responders, generate free radicals, and have a life span of 10 hrs? | neutrophils (phagocytic) |
| _____ release histamine and other inflammatory mediators. | basophils |
| ______ "regulate inflammation", toxic to parasites | Eosinophils |
| _____ are long lived white blood cells. | monocytes |
| Monocytes migrate into tissues (24- 48 hrs) and become ________. | macrophages |
| What is the order of white blood cell response? | 1. margination 2. transigration 3. chemotaxis 4. phagocytosis |
| Macrophages are phagocytic cells that migrate to ______ and _______. | lymph nodes, tissues |
| The granules in basophils contains ______. | histamine |
| These white blood cells increase with parasitic infections | eosinophil |
| Which cells are immature neutrophils? | band cells |
| What are PMN cells characterized by? | multi morphed shaped nucleus, segmented |
| What is the ahesion molecule that initiates rolling? | selectins |
| Which adhesion molecules promote firm adhesion? | B1, B2, integrins |
| Transmigration is promoted by the ________ molecule | PCAM-1 |
| Increased "leakiness" of the blood vessels = the increased _________ of blood. | viscosity |
| TNF | tumor necrosis factor |
| Mast cells are widely distributed in ______ tissues throughout the body. | connective |
| Mast contains _______ with numerous inflammatory mediators that are released when tissues are injured. | granules |
| three inflammatory mediators | 1. histamines 2. leukotrienes 3. prostaglandins |
| "sensitized" mast cells play a key role in _______ and ________ reactions. | allergic + hypersensitivity |
| Degranulation is activated upon _______. | injury |
| What are two platelet activating factors | prostaglandins, leukotrienes |
| What is used to synthesized prostaglandins and leukotrienes? | archidonic acid |
| Arachidonic acid is a 20 carbon fatty acid found in ________ _________, that is released by cell injury or inflammation. | cell membranes |
| What contricts pulmonary airways | Leukotrienes (LTC4, LTD4, LTE4) |
| What do prostaglandins ( PGI2, PGF2a) induce? | vasodilation and bronchoconstriction |
| Which mediatort causes bronchoconstiction promotes platelet function | Thromboxan (TxA2) |
| Corticosteroids inhibit the formation of what four mediators? | 1. leukotrienes 2. proataglandins 3. thromboxanes 4. arachidonis acid |
| _______ is an extension of the inflammatory reponse. | tissue repair |
| Name two types of tissue repair | 1. regeneration 2. scar tissue replacement |
| Regeneration occurs in _______ cells. | parenchymal ( functional cells) |
| Name 2 cell types capable of regeneration capacity | 1. Liabile cells 2. stable cells |
| ______ cells continue to divide throughout life | Labile |
| Skin, oral cavity, vagina & cervix, G.I. epithelium, urinary tract are what type of cells? | labile cells |
| To regenerate the stroma connective tissues and blood vessels must be _____ | in-tact |
| Which cells have stopped growing but can regenerate if needed? | stable cells |
| Name examples of stable cells | hepatocytes, alveolar cells, epithelium of kidney tubules |
| When repair cannot be accomplished by regeneration alone it results in a lost od liver function and disorganized regeneration known as _________. | Metathesis |
| _______ are not capable of regeneration | Permanent or fixed cells |
| When cells that cannot divide are destroyed they are replaced with ______ tissue. | scar |
| Name examples of fixed cells | nerve cells, cardiac muscle, skeletal muscle |
| Hemostasis, vascular & cellular inflammatory responses that occur within 24-48 of tissue damage is apart of which phase of tissue repair? | Inflammatory Phase |
| The proliferative Phase begins in ____ days, and may last ______. | 2-3, 3 weeks |
| Which cells are responsible for the production of collagen, releasing growth factors, proliferation of vascular endothelium and epithelial cells at edges | fibroblasts |
| The phase of repair that can occur for 3 weeks to 6 months post injury | Maturational ( remodeling) phase |
| You can obtain 70-80% of tensile strength of unwounded skin at 3 months, continue activation of fibroblasts & collagen, and remodeling of repaired tissue to give maximal strength all occur during which phase of repair? | Remodeling Phase |
| A small wound that repairs quickly and completely are said to heal by | primary intention |
| Secondary intention heal larger wounds that require longer to heal and often have significant ________. | scar tissue |
| Keloids are abnormal formation of scar tissue during wound repair and are geneticallycharacterized by...? | Abnormal proliferation, apoptosis, or expression of growth factors and extracellular matrix proteins by fibroblast. |
| _______ is a factor effecting wound healing that can be characterized by Kwashiokor, cachexia, and G.I. Disease. | Malnutrition |
| Malnutrition effecting wound repair includes the lack of these three things. | 1. proteins & A.A.'a - collagen 2. CHO's - energy for WBC's 3. Vitamins - co-enzymes for many synthetic enzymes |
| What are three treatments for keloids? | 1. surgical, laser removal 2. radiation 3. corticosteroids |
| What are prevention methods for keloids? | 1. minimize sun exposure 2. Avoid injuries |
| A lack of blood blow can effect wound healing because it will cause a lack of _______ and ______. | nutrients and oxygen |
| WBC's require oxygen to generate free radicals for what? | destroying foreign organisms |
| Sometimes ______ oxygen is used for wounds that wont heal | hyperbaric |
| What are some examlpes of conditions that limit blood flow and oxygen delivery during wound repair? | PVD, CHF, ANemia, diabetes, shock |
| _______ and _______ by immune cells are vital for tissue repair. | inflammation, infiltration |
| What are some examples of condition that cause an impaired immune or inflammatory response? | HIV, Immunossupression, Diabetes, other genetic disorders of WBC's |
| Infection, Wound Seperation and foreign bodies all ________ inflammation, _______ activity of fibroblasts, and ________ contact of wound edges (epithiliazation) | prolong, inhibit, prevents |
| How do sutures enhance wound healing? | It boost proliferation and closes the wound so it becomes easier to fill in the gap |
| As you age the skin decreases in thickness and _______. | elasticity |
| Fibroblast activity and collagen synthesis, WBC activity & number, and re-epithialization decreases with ______. | age |
| A mature red blood cell is called an ________. | erythrocyte |
| The concave sructure of the RBC's allows for? | Increased surface area and facilitates gas exchange |
| What two types of polypeptide chains are in hemoglobin? | 2 alpha, and 2 beta |
| The production of each polypeptide chain in hemoglobin is controlled by individual genes with ______ different loci. | five |
| A heme units function is to ______ to the iron. | bind |
| Each subunit of the polypeptide chain has ____ iron-containing heme unit | 1 |
| Long ______ attach the membrane to support and anchor the protein on the other side, and allow the RBC the ability to move to move bend and stretch. | helices |
| The rate of hemoglobin synthesis by RBC's depend upon the availability of _____ for heme synthesis | iron |
| Where does iron come from? | diet |
| What are some conditions that can cause a person to become iron-deficient? | Vegetarians, females during menstartion, teenagers, bleeding patients |
| _______ is a plasma protein that helps transport iron throughout the blood to the tissues. | transferrin |
| Where does extr iron not needed by the bone marrow goes in the body? | liver |
| Ferritin stores ______ | iron |
| Hemoglobin is released when what happens? | RBC's die |
| _______ is the process by which new RBC's are made and occurs in the bone marrow. | erythropoiesis |
| Erythropoietin is produced by the _______. | kidney |
| Erythropoietin stimulates the production of _______. | RBC's with oxygen |
| This organ is a long term regulator of BP, filtration, and oxygen sensors. | kidney |
| Reticulocytes | immature red blood cell |
| Maturing red blood cells in the bone marrow release _____ to become reticulocytes outside of the bone marrow | nucleus |
| The reticulocytes loose _____ and change _____ to mature into RBC's. | granules, shape |
| The RBC's do what two things at the end of their life cycle. | Metabolic activity decreases, membrane thins & weakness |
| RBC's lyse as they travel through the narrow vessels in the _____. | spleen |
| After a RBC dies ______ is releases and recycled. | hemoglobin |
| The _______ serves as a proving ground for RBC's | spleen |
| The spleen can hold up to _____ mL of blood | 100 |
| _____ is a machanism in which it can take the heme protein and remove it from the blood. | Bilirubin |
| The combinationof bilirubin and the heme goes to the ______ and secretes into the ______, then travels through the ________ to be released in the feces. | liver, bile, intestines |
| When the liver cannot eliminate the bilirubin the patient can then develop _______ | jaundice |
| Percent of RBC's in 100mL plasma | hematocrit |
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