Cell Biology: Membranes, Communication, and Immune Response, Study Guides, Projects, Research of Pathophysiology

Download Cell Biology: Membranes, Communication, and Immune Response and more Study Guides, Projects, Research Pathophysiology in PDF only on Docsity! 1 / 24 Pathophysiology- Exam 1 Study guide Questions 1.What are the functional components of the cell? And what are each respon- sible for?: 1. Cell Membrane: Regulates substance passage, provides support. 2.Cytoplasm: Houses organelles for cellular activities. 3.Nucleus: Holds DNA, controls cellular activities. 4.Rough ER: protein protection Smooth ER: lipid production and detoxification 5.Ribosomes: Protein synthesis. 6.Golgi Apparatus: Modifies, packages, transports. 7.Mitochondria: Produces ATP. 8.Lysosomes: protein destruction 9.Peroxisomes: lipid destruction also contains oxidative enzymes 2.What are the 7 functions of the cell?: -Transport (active vs passive) -Metabolism (catabolic vs anabolic) -Movement -Absorption -Conduction (pain, heat, pressure, etc) 2 / 24 -Protection (skin, mucous membrane) -Reproduction (mitosis) 3.Describe catabolism and anabolism. What do they do? How are they dif- ferent?: Catabolism- breaks down complex compounds to smaller molecules to produce energy (energy releasing) Anabolism-builds simple compounds to make complex compounds (energy using) 4.Compare and contrast anaerobic and aerobic metabolism. When do they occur? Where do they occur?: Aerobic (with O2) is more efficient and occurs in the cell's mitochondria (citric acid cycle and electron transport chain). Anaerobic (without O2) occurs in the cytoplasm and is less efficient. Allows us to create energy for cells with low to no oxygen by using glucose. Lactic acid is formed with anaerobic metabolism 5.How do cells communicate? What are the different types of signals and how do those work?: Cell Communication- multistage process that includes the following: Sending the chemical signal Receiving the signal at the target cell's outer membrane receptor Relaying the signal into the target cell's interior Changing the target cell's behavior 6.What are the different types of communication signals and how do those work?: Autocrine- cells release chemicals into the extracellular fluid that 5 / 24 3.Osmosis- Movement of water down a concentration gradient - from an area of higher water concentration to lower water concentration 11.How does active transport work? What does it require (2 things)?: Trans- membrane proteins move substances against the concentration gradient. - Energy expenditure required - ATP - Protein carrier required 12.Explain endocytosis and exocytosis. What is the difference in pinocytosis and phagocytosis?: Endocytosis- Plasma membrane engulfs substances from the outside cell a.Pinocytosis - drinking fluids and solutes b.Phagocytosis - eating - bacteria Exocytosis- Discharge (secretion) of material from intracellular vesicles 13.How do cells respond/adapt to stimuli? How does it affect their function- ing?: When cell integrity is threatened, it reacts by drawing on reserves or by undergoing adaptive changes 1.adapt by changing in size, number, or structure. 2.Cellular adaptation is not a normal cellular state, but also is not necessarily a state that is considered to be cellular injury. - Cells adapt to stimuli by hypofunctioning or hyperfunctioning 6 / 24 14.Does all cellular adaptation only occur with cellular injury? What is the benefit of adaptation? What is the problem with ongoing adaptation?: -In early stages of disease, cellular adaptation can improve cellular function -Ongoing cellular adaptation can cause or contribute to disease states Cellular adaption is not bad like growing muscles is hypertrophy 15.Compare the 5 types of adaptive cellular changes. What are they and what occurs?: -Atrophy- Decrease in cell size -Hypertrophy- Increase in cell size -Hyperplasia- Increase in cell number -Metaplasia- Reversible replacement of one mature cell type by another less mature cell type -Dysplasia- Deranged cellular growth 16.What is the significance of dysplasia?: Dysplasia is deranged cellular growth within a specific tissue, often as a result of chronic inflammation or a precancerous condition. 17.How does reversible cell injury differ than cell death?: Reversible Cell Injury: 1.Cell function is impaired 2.Does not result in cell death Cell Death: 1.Irreversible 2.Apoptosis 7 / 24 3.Oncosis 4.Necrosis 18. Discuss the causes of cell injury and give examples of each type.: 1. Physical/Mechanical 2.Radiation 3.Chemical 4.Biological 5.Nutritional imbalances Can also be infectious, inflammatory, immunologic 19.Distinguish between hypoxia, anoxia, and ischemia.: a. Hypoxia- decreased oxygen in blood b. Anoxia- abrupt/sudden absence of oxygen c. Ischemia- decreased oxygenation of tissue due to compromised blood flow 20.When a cell experiences hypoxia, it will decrease ATP production. Order the following responses to cellular hypoxia:: 1. Increased anaerobic metabolism 2.Decreased glycogen stores and increased lactic acid 3.Decreased intracellular pH 4.Cell membrane becomes hyperpermeable, and the cells shrink 21.What is infarction? When and why does this occur?: Infarction, also called ischemic necrosis, is the death of tissue as a consequence of prolonged ischemia. 10 / 28. What role does ischemia have in increasing calcium? Why is cellular accumulation of calcium harmful?: 1. Ischemia injury can cause increased influx of calcium into the cells and release of stored intracellular Ca. 2. Calcium accumulates in the mitochondria of the damaged or dying cells; increased acid build up inside the cell; causes the Ca++ to become rock hard; mitochondria begin to die; cell death 29.Compare and contrast apoptosis to oncosis. Which one generally leads to healthy cell growth?: Apoptosis- Programmed cell death -The cell shrinks, and forms blebs that break off and are phagocytized by macrophages, generally leads to new healthy cell growth Oncosis- Cell death from inflammation & swelling -Accidental or passive cell death. The process is characterized by mitochondrial, nuclear and cytoplasmic swelling generally followed by bursting. 30.What is necrosis? Why is it harmful?: Necrosis is irreversible cell death caused by overwhelming stressors, leading to membrane disintegration, chromatin fragmentation, and lysosomal activation. It releases digestive enzymes, causing autolysis and potential harm to surrounding tissues. 31.Blunt force trauma: injury caused by a blow that does not penetrate the skin or other body tissues 32.Abrasion: Scrape of the skin due to something abrasive 11 / 33.contusion: bruise, injury 34.Hematoma: a solid swelling of clotted blood within the tissues. 35.laceration: a cut, tear 36.Avulsion: An injury in which soft tissue is torn completely loose or is hanging as a flap. 37.Oncosis: cellular swelling 38.How does stress affect well-being?: A person experiences stress when a demand exceeds a person's coping abilities. Resulting in reactions that can adversely affect well-being, especially significant with long-term stress 1.Cognition 2.Emotion 3.Behavior Stress response is designed to be a short-term/acute response. Long-term re- sponse can cause long-term impacts on the body. 39.How does coping impact stress? What are examples of healthy versus un- healthy coping?: Managing stressful demands and challenges that are appraised as taxing or exceeding the resources of the person ii. Coping mechanisms 40.Explain the GAS, including of the stages. Discuss what happens at each stage and how a person moves to the next stage. What stage is associated with the onset of disease and why?: Stress is a threat to homeostasis that provokes a coordinated, adaptive reaction called the general adaptation syndrome. 12 / Three Possible Stages i.Alarm stage 1.Triggered by stressor 2.Starts in hypothalamus 3.Begins with arousal of sympathetic branch of ANS and pituitary gland (recognition by a person/animal that something is not normal) 4.Stressor triggers the hypothalamic-pituitary-adrenal axis (see diagram) ii.Stage of resistance or adaptation 1.Coping mechanisms are used If stress comes to an end, the body should return to a normal state, leading to recovery. OR Person will not cope and advance to Stage 3 Stage of Exhaustion: 1. Exhaustion marks the onset of disease. The body can no longer produce the alarm stage hormones. Continued stress breaks down compensatory mechanisms- organ damage begins 41. What stage is associated with the onset of general adaptation syndrome and why?: Stage of Exhaustion: 1. Exhaustion marks the onset of disease. The body can no longer produce the alarm stage hormones. 15 / -Mechanical, biochemical, and biologic barriers in our body -Skin, epithelial layers, cilia, normal flora of the skin, GI tract Second Line of Defense; The Inflammatory Response -How we first respond to pathogenic invasion Third Line of Defense: Adaptive Immunity - The Immune Response 50.What are the purposes of inflammation? How does it protect the body?- : Inflammation enhances leukocyte migration and blood flow to aid tissue repair, especially when first-line defense barriers are damaged, triggering the release of histamines from injured cells. Its purposes include facilitating immune responses, minimizing injury effects, neutralizing harmful agents, clearing damaged tissue, generating new tissue, and promoting healing. 51.What are endothelial cells?: Endothelial cells, which line blood vessels, play several roles in the inflammatory response. They act as a barrier to both internal and external inflammatory stimuli, control the movement of white blood cells, release mediators to regulate inflammation, and secrete factors that stimulate the production of specific white blood cells. These functions collectively contribute to the body's defense and healing processes during inflammation. 52.What are platelets?: Platelets- Thrombocytes- clotting are activated by injury to the blood vessels, when these cells become activated, they release inflammatory mediators that further increase 16 / the inflammatory response 53.They are five basic types ofWBCs:: 1. neutrophils 2.lymphocytes 3.eosinophils 4.basophils 5.monocytes 54.What are leukocytes and what do they do?: Neutrophils, a type of granu- locyte, are the most abundant white blood cells in circulation. They are the first responders to acute inflammation, drawn to the site of injury or infection through chemotaxis. Specialized in phagocytosis, neutrophils target bacteria and cellular debris, utilizing cytoplasmic granules for degradation. With a short lifespan, they are removed by apoptosis. Neutrophilia, an increase in neutrophil count, is commonly associated with bacterial infections. 55.What are esinophils?: Eosinophils- Allergic & parasitic Eosinophils have a slower reaction time than neutrophils, arriving at the site of inflammation 2-3 hours after neutrophils. 56.What is the role of eosinophils in the immune system, and in which conditions is an increase in eosinophils commonly observed?: The granules released by eosinophils carry proteins that are toxic to parasites that are too large to be phagocytized. Increase in eosinophils is also seen in allergic reactions, like hay fever and bronchial asthma. 57.How do the life spans of eosinophils compare to neutrophils, and what role do eosinophils play in chronic inflammation?: They have longer life spans than neutrophils and are generally still present during chronic 17 / inflammation 58.How does the prevalence of neutrophilia and eosinophilia differ in re- sponse to various types of infections and allergens?: In general, neutrophilia is more commonly seen in bacterial and viral infections vs eosinophilia, which is more commonly seen with parasitic infections and in reaction to allergens 59.In what type of immune reactions are basophils most prominently involved, and how is their activity influenced by immunoglobulin E (IgE)?: Most promi- nent in allergic reactions mediated by immunoglobulin E (a type of antibody that reacts to allergens) 60.What role do basophils play in allergic reactions, and how is their activity influenced by immunoglobulin E (IgE)?: when the basophil binds with the IgE, it releases histamine and vasoactive agents (affects diameter of blood vessels) 61.Describe the roles of granulocytes and agranulocytes in inflammation, including their triggers, targets, and durations of activity.: Granulocytes and agranulocytes play distinct roles in the inflammatory process. Granulocytes, includ- ing neutrophils, respond rapidly to bacterial infections, with a short lifespan of a few hours to days. Agranulocytes, such as monocytes and lymphocytes, respond to viral infections and have a longer duration, persisting for days to years. 62.What is the role of mast cells in inflammation?: During acute inflammation, mast cell degranulation releases multiple cytokines, enzymes, and histamine, con- tributing to various inflammatory responses, including allergic reactions. 20 / of fluids, white blood cells (WBCs), and platelets. The increased capillary permeability allows leukocytes to migrate out of the blood vessel toward the injury site. Protein-rich plasma also leaks from the blood vessel. 69.What are the five non-specific cardinal manifestations of inflammation, and how do they relate to the underlying pathophysiological processes?: 5 Cardinal Signs of Inflammation: Redness, heat, swelling, pain, loss of function 70.Compare the types of exudate.: -Purulent: pus (WBC, proteins, debris) -Serous: watery-plasma -Hemorrhagic: RBCs 71.What manifestations would you expect with a systemic inflammatory re- sponse?: i. Extreme fever or very low temp ii.Elevated heart rate iii.Elevated respiratory rate iv. Excessively high or low WBC 72.What are the consequences of chronic inflammation? How does it affect the body?: Tissue damage -Atherosclerosis -Chronic lung disease 21 / -Arthritis -Inflammatory bowel disease Susceptibility to cancer -Cervical (HPV) -Liver (Hepatitis B & C) -Stomach (H pylori) -Gall bladder (cholecystitis/cholelithiasis) 73.What are common causes of chronic inflammation?: Persistent infections or irritants -Environmental agent exposure -Pathogens- Viruses, Bacteria Tissue injuries -Excessive immune response- Autoimmunity -Obesity- Proinflammatory mediator 74.What are the properties of the immune response? Why are these im- portant?: 1. Specificity: This refers to the immune system's ability to produce a particular antibody tailored for a specific antigen. 2.Memory: The immune system can remember an antigen, enabling a faster and more robust response upon subsequent encounters. 3.Self-recognition: In an adaptive state, the immune system distinguishes the body's own tissues from foreign substances. 22 / 4.Self-limitation: The immune response diminishes once the antigen is eradicated. 5.Specialization: The immune system deploys distinct responses to different anti- gens or microorganisms. 75.Discuss cytocines and why they are important in immunity. Where do they come from?: Cytokines: proteins, peptides or glycoproteins that are secreted by specific cells of immune system. Cytokines are a category of signaling molecules that mediate and regulate immunity, inflammation and hematopoiesis - Primary mechanism for innate and adaptive immunity to communicate - Provides information about invasion - Responsible for directing leukocytes to area of injury and immune responses - Interferon, Interleukin, Growth factor 76.Review the cells that play a role in the immune response. What are their functions?: Immune System Cell: Phagocytes a.Agranulocytes Monocytes -> macrophages b.Granulocytes Neutrophils, Basophils, Eosinophils Dendritic Cells- serve as communication between innate and adaptive 25 / 79.What is adaptive immunity?: the body's ability to recognize and defend itself against distinct invaders and their products Adaptive Immunity 1.Immunity acquired through prior exposure 2.Ability to distinguish self from foreign matter 3.Ability to destroy foreign agents based on their antigenic properties 4.Creates memory for future invasions 5.Involves T-lymphocytes and B-lymphocytes 6.Includes humoral and cell-mediated immunity 80.How does humoral immunity differ from cell-mediated? What cells are involved?: Humoral Immunity: - Mediators: Antibodies from B cells. - Targets: Extracellular pathogens. - Mechanism: Antibodies circulate, neutralize pathogens, and mark them for destruc- tion. - Primary Cells: B cells and plasma cells. Cell-Mediated Immunity: - Mediators: T cells. - Targets: Infected host cells. - Mechanism: T cells directly attack and destroy infected cells. - Primary Cells: T cells, including cytotoxic and helper T cells. Humoral immunity involves antibodies defending against extracellular 26 / threats, while cell-mediated immunity uses T cells to eliminate infected host cells. 81.What are the lines of defense?: First Line of Defense (Innate Immunity): Mechanical barriers: Skin, epithelial layers, intestinal movement, and broncho-pul- monary cilia. Biochemical barriers: Sweat, tears, saliva, and nasal secretions. Biological barriers: Normal flora of the skin and GI tract. Second Line of Defense- The Inflammatory Response Third Line of Defense- Adaptive Immunity - The Immune Response 82.How does adaptive immunity develop actively and passively, and what are the key mechanisms involved in each process?: Methods of Developing of Adaptive Immunity: Active- Produced by individual after natural exposure to antigen or immunization Passive- Antibodies or T-lymphocytes are transferred from donor to recipient i.Placenta ii.Breast milk 83.What are common antibodies?: Common antibodies include IgG, IgA, IgM, IgE, and IgD. 84.What are hypersensitivities? What are the 4 types? H: Hypersensitivities are exaggerated immune responses causing tissue damage. There are 27 / four types: 1.Type I: Immediate hypersensitivity, involving IgE antibodies and mast cell activa- tion. 2. Type II: Antibody-mediated hypersensitivity, with antibodies targeting specific cells or tissues. 3.Type III: Immune complex-mediated hypersensitivity, where immune complexes deposit in tissues, causing inflammation. 4.Type IV: Delayed-type hypersensitivity, involving T cells and delayed responses. Types I-III share immune system involvement and antibody-mediated mechanisms, while Type IV is T cell-mediated and has a delayed response. 85.What are the mediators (think etiology) for each type of hypersensitivity?: 86.Discuss Type I hypersensitivity. What are the properties (think timing and location of response).: Type I Hypersensitivity 1.Can be immediate or delayed a. Immediate reactions occur seconds to minutes, delayed takes up to 2- 3 days 2.Can be local or systemic a.Local - only in certain area, systemic - widespread throughout entire body 87. Describe the two-stage reaction process in Type I.: The reaction process involves two stages: 30 / 2.Type B: Can receive type B or type O blood. 3.Type AB: Can receive type A, B, AB, or O blood (universal recipient). 4.Type O: Can receive type O blood only (universal donor). If the wrong blood type is administered, it can lead to a severe immune response, known as a hemolytic reaction. This occurs when the recipient's immune system at- tacks and destroys the transfused blood cells. Hemolytic reactions can be life-threat- ening, causing complications such as kidney failure, shock, and even death. 95. Describe Type III hypersensitivity and examples of this.: Immune- Complex Mediated Hypersensitivity: 1.Cause: Formation of insoluble antigen-antibody complexes. 2.Effect: Induces localized inflammation. 3.Specificity: Not organ/tissue specific. 4.Outcome: Results in severe inflammation in blood vessels and target organs. 5.Examples: - Vasculitis - Acute glomerulonephritis - Lupus - Serum sickness - Response to foreign proteins or components in the serum, resembling an allergic reaction. 96. Describe Type IV hypersensitivity: Cell-Mediated Hypersensitivity: 31 / 1.Cause- Cell-mediated response to microorganisms (only type that is cell mediat- ed) 2.Does not involve antibody- all T cell mediated 3.Results a.Contact sensitivity- producing skin reactions, autoimmune responses, or graft rejections. b.Direct- Kills both infected and non-infected cells in tissue or organ 97.What is alloimmunity? What does the body attack? How is this different than autoimmunity?: Alloimmune: a. Immune response to non-self antigens from members of the same species b.Body creates antibodies against alloantigens c.Attacks transfused blood, transplanted tissue, fetus d.Includes: i. Transient neonatal disease- occurs during fetal development when the maternal immune system becomes sensitized against antigens expressed by the fetus 98.What is the difference between a transplant reaction and a transfusion re- action? What type immune response do these fall under?: Transplant Reaction vs. Transfusion Reaction: 1.Transplant Reaction: - Definition: Occurs when the recipient's immune system targets human leukocyte antigens (HLA) in transplanted tissue. Type of Immune Response: Alloimmune response due to 32 / histoimmcompatibility between donor and recipient HLA. 2.Transfusion Reaction: - Definition: Occurs when the recipient's red blood cells express surface antigens, eliciting an alloimmune response during a blood transfusion. Type of Immune Response: Alloimmune response against surface antigens on red blood cells. 35 / 103. What are the manifestations and consequences of HIV?: Manifestations and Consequences of HIV: HIV often leads to various manifestations and consequences, including oppor- tunistic infections such as Pneumocystis jiroveci (PCP), tuberculosis (TB), cy- tomegalovirus (CMV), and Clostridium difficile (C- diff). Additionally, individuals with HIV may experience neurologic complications like HIV-Associated Neurocognitive Disorders (HANDS) and encephalopathy. The risk of malignancies, including cancer, is heightened, and there can be associated wasting and metabolic syndromes. 104. Describe the mutual microorganism-human relationship.: The mutual re- lationship involves normal microflora, known as commensals, and opportunistic organisms that usually cause little harm unless in immunocompromised hosts. 105. What are the types of infectious diseases?: bacteria, viruses, fungi, para- sites 106. Define each of the following and provide examples of each 1. Commensals 2. Opportunistic organisms 3. Colonization 4. Obilgate pathogen 5. Nosocomial infection: Commensals: Microorganisms living on/in the 36 / body with- out harm. Example: Normal bacteria in the gut. Opportunistic organisms: Usually harmless but cause illness in weakened immunity. Example: Candida in immunocompromised. Colonization: Microorganisms establishing in an environment. Example: Skin bacte- ria. Obligate pathogen: Causes disease in healthy individuals. Example: Tuberculosis bacteria. 37 / Nosocomial infection: Acquired in healthcare settings. Example: Hospital-acquired infections. 107. Discuss the 4 modes of transmission and give examples of each.: a. Penetration- needle b.Direct Contact- skin to skin c. Ingestion- eating d.Inhalation-breathing in 108. What are the stages of infection? Relate these to symptoms and conta- giousness: 1. Incubation - microorganisms replicate without producing symptoms, potentially contagious. 2.Prodromal - initial appearance of symptoms, highly contagious. 3.Acute - full-blown disease with rapid pathogen proliferation, still contagious. 4.Convalescent - the body contains and eliminates the infection, duration varies. 5.Resolution - total elimination of the pathogen from the body. 109. Describe viral properties and defense mechanisms. Why are viruses so hard to kill?: Virus Defense Mechanisms ÏViruses ÏSurface 40 / ÏMRSA - methicillin resistant staph aureus ÏVRE - vancomycin resistant enterococci ÏMulti-drug resistant TB ÏC-diff - clostridium difficile ÏAcinetobacter baumannii ÏCRE— carbapenem resistant enterobacteriaceae ÏWorried about drug resistant gonorrhea, malaria, and more extremem staphylococ- cal infections 115. Discuss the development of superbugs. Why do these occur? How can we prevent these? Give some common superbugs.: -Using antibiotics too often -not finishing full dosage 41 / 1.MRSA - methicillin resistant staph aureus 2.VRE - vancomycin resistant enterococci 3.Multi-drug resistant TB 4.C-diff - clostridium difficile 116. What is a fungal infection and how do we treat? Are they easily treated?- : Fungal Infections a.Disease caused by fungi are called mycoses b.Examples -yeast candidiasis, tinea capitus, tinea corporis c.Pathogenicity i. Thick cell walls, ability to adapt to host environment d.Some can release mycotoxins that cause systemic infections i. Example: Aspergillus (mold) Treated with antifungals 117. Give examples of parasitic infections.: Parasite infections a. An organism that lives in or on another organism (its host) and benefits by deriving nutrients at the host's expense 118. What are the non-specific manifestations of infectious diseases. How are these tied to the immune and inflammatory response (think about how the body reacts).: Variable depending on pathogen: 1.Fatigue 2.Malaise 3.Loss of appetite 42 / 4.Fever 5.Swelling 6.Inflammation 7.Discharge 8.Congestion 119. Discuss laboratory tests/changes associated with infections. What types of WBC changes do you expect with bacterial, viral, parasitic, and fungal infections?: WBC count: 4,500 - 10,000 / mm3 (normal) i.Neutrophils - percent of neutrophils 55 - 70% ii.Lymphocytes - percent of lymphocytes 20 - 40% iii.Monocytes, eosinophils, and basophils are also given in a differential 120. What is a culture and sensitivity?: Sampling a bacterial site, growing it in the laboratory, testing different antibiotics on the sample, if the bacteria is resistant to an antibiotic, it will not be used. If the bacterial sample is sensitive to the antibiotic it might be used to treat the bacteria in question. 121. What does a titer measure? What is the significance of this?: Titers- can tell us if immunization or past infection 122. What is bactermia? Sepsis?: Bactermia refers to viable bacteria in the blood; sepsis is an inflammatory response in a person that has known bacteremia 123. What is the significance of septic shock?: Septic Shock 1.Occurs when infection is so widespread and the reaction mounted by the body is on such a scale that the response itself starts to cause harm 2.Triggers inflammatory response, complement system,