Pathophysiology Exam #1 – Porth Questions and Complete Solutions

Pathophysiology Exam #1 – Porth Questions and Complete Solutions Purpose and function of the mitochondria - Ans: Machine for cellular energy. Transform food energy into ATP Major components of the cell (3 components) - Ans: Plasma/Cell Membrane Nucleus Cytoplasm Plasma/Cell Membrane - Ans: The cell membrane encloses the cell and provides for intracellular and intercellular communication, transport of materials into and out of the cell, and maintenance of the electrical activities that power cell function. Nucleus - Ans: The nucleus is the control center for the cell. It also contains most of the hereditary material. Cytoplasm - Ans: Contain organelles. They include the mitochondria, which supply the energy needs of the cell; the ribosomes, which synthesize proteins and other materials needed for cell function; and the lysosomes and proteosomes, which function as the cell's digestive system. 4 Tissue Types - Ans: - Epithelial - 3 distinct surfaces, closely joined by cell adhesion molecules, and are attached firmly to a basement membrane. - Connective - most abundant tissue in the body, holds tissues together. - Muscle - responsible for movement and changes in size and shape of internal organs - Nervous - integrated communication system Active transport - Ans: Any type of transport across the cell membrane that REQUIRES energy as it moves material against the concentration gradient. Passive transport - Ans: Any type of transport across the cell membrane that does NOT require energy. Facilitated diffusion - Ans: Type of Passive Transport in which Molecules hitch a ride on transport proteins Hypercalcemia - Ans: Occurs in normal tissues as the result of increased serum calcium levels 6 Major causes of Hypercalcemia - Ans: - Hyperparathyroidism - Phosphate retention in renal failure - Increase release of calcium from bone as in immobilization - Paget's disease - disorder that involves abnormal bone destruction and regrowth - Cancer with metastatic bone lesions - Vitamin D intoxication Hypercalcemia causes and its relationship to metastatic calcifications - Ans: Almost any condition that increases the serum calcium level can lead to calcification in inappropriate sites such as the lung, renal tubules, and blood vessels. Compensatory Mechanisms of Tissues - Ans: -Cells may adapt by undergoing changes in: Size, Number, Type -Cellular stresses also include intracellular accumulations and storage of products in abnormal amounts Atrophy - Ans: -Change in size (decrease) -Decreased work demands or adverse environmental conditions -Lower more efficient level of functioning compatible with survival Hypertrophy - Ans: -Change in size (increase) Increase in amount of functioning components in the tissue mass -Can be result of normal physiologic or abnormal pathologic conditions Hyperplasia - Ans: -Change in number of cells (increase) -Stimuli to increase number may be physiologic (compensatory) or nonphysiologic (excessive hormone) -Physiologic- breast & uterine enlargement with pregnancy -Hormonal- BPH (androgen); endometrial (estrogen) -Different process than hypertrophy - but often occur together Metaplasia - Ans: -Represents reversible change - one adult cell type is replaced by another cell type -In response to chronic irritation and inflammation -Allows for substitution of cells that are better able to survive Conditions in which metaplasia can take place - Ans: -Excessive drinking of alcohol -Smoking Dysplasia - Ans: -Deranged cell growth of specific tissue -Results in cells that vary in size, shape and organization -Minor degrees associated with irritation or inflammation -Adaptive and potentially reversible if cause eliminated -Strongly implicated as a precursor of cancer Intracellular Accumulations - Ans: -Represent the build-up of substances that cells cannot immediately use or eliminate -Grouped into 3 categories 1) Normal body substances (lipids, proteins, carbohydrates, melanin and bilirubin)- fatty liver 2) Abnormal endogenous products (inborn errors of metabolism) 3) Exogenous products such as environmental agents and pigments that cannot be broken down- jaundice Gram-negative bacteria harms cells, how? - Ans: They release endotoxins from lipopolysaccharides that cause cell injury and increased capillary permeability. Cardinal Signs of Inflammation - Ans: 1. Rubor or redness 2. Tumor or swelling 3. Calor or heat 4. Dolor or pain 5. Functio laesa or loss of function Systemic manifestations ,such as fever, that may occur as chemical mediators, cytokines, produced at the site of inflammation lead to increased levels in the plasma. Cells associated with Acute Inflammation - Ans: Neutrophils - first to appear at site Cells associated with Chronic Inflammation - Ans: Macrophages, lymphocytes, eosinophils, mast cells Cells associated with Allergic Disorders - Ans: Basophils are most prominent, mediated by immunoglobulin E (IgE). Binding with IgE triggers release of histamine an vasoactive agents from the their basophil granules. Mast cells also release histamine. Cells associated with Immediate Hypersensitivity Reactions (Type I) - Ans: 1. Type 2 Helper T cells 2. Granule containing cells, such as mast cells and/or basophils Phases of Acute Inflammation - Ans: Vascular Phase - leads to changes in blood flow and changes in the small blood vessels of the microcirculation. Cellular Phase - leads to the migration of leukocytes from the circulation and their activation to eliminate the injurious agent. Inflammation: Acute - Ans: -Edema and Neutrophils -Triggered by noxious stimuli (injury; infection) -Rapid in onset -Relatively short duration (minutes to days) -Exudate of fluid and plasma proteins & emigration of leukocytes Inflammation: Chronic - Ans: -Lymphocytes & macrophages, proliferation of blood vessels, fibrosis -Longer duration - days to years -Associated with proliferation of blood vessels (angiogenesis) -Tissue necrosis -Fibrosis (scarring) Why is it that sometimes a healthy patient who has a sudden heart attack does not survive, but a patient with longstanding atherosclerosis will survive? - Ans: Person with long standing atherosclerosis builds collateral pathways -new pathways for blood to flow-. This gives them a higher chance of survival than a healthy person with a sudden attack, who does not have other pathways. Vascular Phase - Ans: - vasoconstriction followed by vasodilation - vasodilation causes increased blood flow that leads to heat, and redness - Increase in vascular permeability, outpouring of exudate - Increased pressure in capillaries causes outflow of fluid from capillaries and accumulation in tissues, causing swelling, pain, and impaired function. - stagnation of flow and clotting of blood occurs Cellular Phase - Ans: - neutrophils are delivered to site of injury for defense - Adhesion & margination - leukocytes accumulate and blood flow slows down. Leukocytes adhere to endothelium. - Transmigration - endothelial cell separates, leukocytes cross vessel wall - Chemotaxis - allows leukocytes to migrate to tissue spaces - Activation & phagocytosis - engulf debris Cellular phase chemical mediators - Ans: mast cells and macrophages Vascular phase chemical mediators - Ans: histamine and nitric oxide Plasma-Derived Mediators - Ans: Contribute to the inflammatory process by: -Causing vasodilation and increasing vascular permeability -Promoting leukocyte activation, adhesion and chemotaxis -Augmenting phagocytosis Cell-Derived Mediators - Ans: Released from cells that are present at sites of inflammation -Histamine and Serotonin -Arachidonic Acid Metabolites -Omega-3 Polyunsaturated Fatty Acids -Platelet-Activating Factor -Cytokines and Chemokines -Nitric Oxide -Reactive Oxygen Species Types of Immunity - Ans: -First line of defense mechanical chemical -Second line of defense inflammatory response -Third line of defense specific immune responses First line of defense - Ans: Barriers to portal of entry: -Intact skin -Mucous membranes -Normal microbiota -Ciliated epithelium Second line of defense - Ans: -Inflammatory response will act when the 1st line of defense has been circumvented -This is a non-specific response to cellular damage -The response is immediate after the cellular injury occurs Third line of defense - Ans: -Provides long-term immunity -Highly specific -Acquired on an individual basis -Involves: cellular immunity & humoral immunity Humoral Immunity - Ans: Third line of defense: -Controlled by B lymphocytes made in Bone Marrow -Uses antibodies (immunoglobulins) for long-term recognition and rapid activation of inflammation Vaccinations depend on which type of immunity? - Ans: Humoral immunity because it produces antibodies to produce other cell types to actively kill microbes and other foreign tissues B cells differentiate into what? - Ans: Plasma cells, but need a first exposure Cell-mediated Immunity - Ans: Third line of defense: -Does not use antibodies, but does release cytokines to influence other cells. -Activates macrophages, Natural Killer cells, and antigen-specific T cells made in the Thymus What immunity is useful in controlling microbes surviving in phagocytes, those infecting non-phagocytic cells (especially viruses) and abnormal cells. - Ans: Cell-mediated immunity because it recognizes abnormal cells from cancers, virus infections, and transplanted tissues Which type of immunity is activated in delayed hypersensitivity (type IV) responses. - Ans: Cell-mediated immunity Innate Immunity - Ans: First line of defense against microbial agents, can distinguish from self and non-self but not among specific pathogens. Adaptive immunity - Ans: Involves humoral and cell-mediated immune responses that react to a unique antigen, can distinguish self from non-self, and develop immunologic memory, allowing a prompt and heightened response on subsequent encounters with the same antigen Cells involved in Innate Immunity responses - Ans: - phagocytic granulocytes - neutrophils, basophils, eosinophils - macrophages - engulf and kills invading microbes, are antigen presenting cells - dendritic cells - antigen-presenting cells - natural killer cells - first line of defense against viral infections Cells involved in Adaptive Immunity responses - Ans: - B lymphocytes - make antibodies - T lymphocytes - include helper T cells that help B celss make antibodies and help phagocytic cells destroy ingested pathogens and cytotoxic t cells that kill intracellular microbes Apoptosis - Ans: Programmed cell death. Highly selective process that eliminates injured and aged cells, thereby controlling tissue regeneration. Necrosis - Ans: Cell death in an organ or tissue that is still part of a living person. Apoptosis vs. Necrosis - Ans: Necrosis differs from apoptosis in that it involves unregulated enzymatic digestion of cell components, loss of cell membrane integrity with uncontrolled release of the products of cell death into the extracellular space, and imitation of the inflammatory response. Necrosis interferes with cell replacement and tissue regeneration. 4 stages of fever - Ans: 1. Prodrome - nonspecific complaints 2. Chill - during which temperature rises - cold, shaking 3. Flush - cutaneous vasodilation makes skin warm, red 4. Defervescence - sweating Not all have to be present. Common manifestations of fever - Ans: -Are worse when fever rises rapidly or exceeds 39.5 ⁰ C (103.1 F) -increased HR -increased Resp -Dehydration (vapor losses/ sweating) -Chills coincides with the introduction of pyrogen into circulation (blood cultures drawn here) -Body switches from glucose metabolism to protein and fat breakdown (prolonged/rapid- metabolic acidosis -Headache - vasodilation of cerebral blood vessels -Confusion/agitation- hypoxemia Management of fever - Ans: -Modification of external environment, such as Cooling measures -Support of hyper-metabolic state- prevent tissue breakdown -Adequate fluids and simple carbohydrates -Protection of vulnerable body organs and systems with use of Antipyretic drugs - reset the hypothalamic temperature control center by blocking the activity of cyclooxygenase (conversion of arachidonic acid to prostaglandin E2) -Treatment of infection or condition causing the fever Fever in very young children - Ans: -Approach varies based on age of child -Infants & young children have decreased immunologic function -More common infection with virulent organisms -Worry when over 103 and rising rapidly Fever in adults - Ans: -Headache is common -Delirium possible when over 104F. Fever in older adults - Ans: -Have lower baseline -Serious infections may go unrecognized -Lack of perception -Bodies don't have ability to raise their temperature so indication of fever may be about 2 degrees above baseline. -Infections most often caused by bacteria -Worry when over 101 Intermittent Fever - Ans: -Temperature returns to normal at least once every 24 hrs. -Commonly associated with diseases caused by gram-negative bacteria, sepsis, abscesses and acute bacterial endocarditis. Remittent fever - Ans: Temperature doesn't return to normal and varies a few degrees in either direction Sustained or continuous fever - Ans: The temperature remains above normal with minimal variations (< 1 F), is a drug induced fever. Recurrent/Relapsing fever - Ans: -There is one or more episodes of fever, each as long as several days with one or more days of normal temperature between episodes. -Diseases causing it are TB, fungal infections, malaria, Lyme disease. Type I reactions - Ans: -"Immediate hypersensitivity reactions" -IgE-mediated response that leads to release of histamine and other inflammatory mediators from mast cells and basophils. Type II reactions - Ans: -(cytotoxic hypersensitivity reactions) -involve immunoglobulin G (IgG) or immunoglobulin M (IgM) antibodies bound to cell surface antigens, with subsequent complement fixation. Type III reactions - Ans: -(immune-complex reactions) -involve circulating antigen-antibody immune complexes that deposit in post-capillary venules, with subsequent complement fixation. Type IV reactions - Ans: -(delayed hypersensitivity reactions, cell-mediated immunity) -are mediated by T cells rather than by antibodies. Example of Type I Reactions - Ans: anaphylactic shock, hay fever, and bronchial asthma - Can also be latex gloves (deadly) Example of Type II Reactions - Ans: -antibody-mediated cell destruction (e.g., transfusion reactions and hemolytic anemia), -complement and antibody-mediated inflammation (e.g., some forms of glomerulonephritis), -antibody-mediated cell dysfunction (e.g., Graves disease and myasthenia gravis); Example of Type III Reactions - Ans: -responsible for the vasculitis (seen in SLE or acute glomerulonephritis), -systemic immune complex disease (serum sickness), -local immune complex disease (Arthus reaction); Example of Type IV Reactions - Ans: -Cell-mediated response - TB and T-cells, viruses, fungi, protozoa, parasites -Hepatitis (virus) -Contact dermatitis (latex gloves) -Hypersensitivity Pneumonitis 5 Stages of disease - Ans: 1) Incubation Period 2) Prodromal Stage 3) Acute Stage 4) Convalescent Stage 5) Resolution Stage Incubation Period - Ans: -Pathogen begins active replication without producing recognizable symptoms in the host -May be short or prolonged -Can be influenced by the general health of the host, portal of entry and the infectious dose of the pathogen Prodromal Stage - Ans: -Initial appearance of symptoms in the host -May be only vague sense of malaise -Mild fever, myalgia, headache, fatigue -Varies from host to host Acute Stage - Ans: -Host experiences maximum impact of the infectious process -Corresponding to rapid proliferation and dissemination of the pathogen -Toxic by-products of microbial metabolism, cell lysis, and the immune response mounted by the host -Production of tissue damage and inflammation Convalescent Period - Ans: -Characterized by containment of infection -Progressive elimination of the pathogen -Repair of damaged tissue -Resolution of associated symptoms -May be short or prolonged -Depends on pathogen and its virulence Resolution Period - Ans: Total elimination of the pathogen from the body without residual signs or symptoms of disease Generating virulence factors - Ans: Substances or products generated by infectious agents that enhance their ability to cause disease 4 types of virulence factors - Ans: 1) Toxins (endotoxins and exotoxins) 2) Adhesions Factors- ability to attach to host 3) Evasion Factors- ability to evade host's immune defenses 4) Invasion Factors- ability to penetrate barriers of host IgG (hint* G is for Great number& Gestation) - Ans: -Most abundant antibody (80%) in serum -During inflammatory process, can cross vascular walls & move into tissue space -Maternal antibodies cross placenta -75% IgM (hint, alphabetical order, "MN") - Ans: -"M" for macro - it is the largest antibody -Predominant antibody involved in ABO incompatibility -Appears 1st in a primary infection -1st antibody made by newborn -10% IgA (think of an A on both nipples, haha!) - Ans: -Found in mucous membranes & secretions (mucus, tears, breast milk) -Most abundant in body (IgG most abundant in serum) -Help prevent attachment of microbes to cell surface, especially in mucosal tissues -15% IgE (E for Bee sting) - Ans: -Binds to mast cells and basophils -Involved in parasitic infections and allergic reactions -Involved in Type I hypersensitivities reactions -0.004% IgD (D is for differentiation) - Ans: -Found in blood, lymph, & surface of B cells -Needed for maturation of B cells -0.2% Serum Sickness - Ans: -Type III systemic immune complex disorder triggered by deposition of insoluble antigen-antibody (IgM, IgG, and occasionally IgA) complexes in blood vessels, joints, and heart and kidney tissue. -These activate complement, increase vascular permeability, and recruit phagocytic edema. -Most common causes of this allergic disorder include antibiotic and other drugs, various foods, and insect venoms. "Trigger Events" of an Autoimmune Disease - Ans: -Infections -Environmental -May be genetic Who is most likely to develop Atelectasis? - Ans: People who just had surgery, patients who have had tumors that might cause compression atelectasis, anyone with broken ribs Atelectasis - Ans: Refers to an incomplete expansion of the lung or portion of the lung. When compression atelectasis occurs, which way does the mediastinum and trachea shift? - Ans: The mediastinum/trachea shift AWAY from the affected lung. Clinical manifestations of atelectasis? - Ans: -tachypnea, tachycardia, dyspnea, cyanosis, signs of hypoxemia, diminished chest expansion, absence of breath sounds, and intercostal retractions. COPD (Chronic Obstructive Pulmonary Disease) - Ans: Refers to a group of respiratory disorders characterized by chronic and recurrent obstruction of airflow in the pulmonary airways. -Airflow obstruction is usually progressive, may be accompanied by airway hyperreactivity, and may be partially reversible. -Most common cause of COPD is smoking (85-90% of patients have smoking history). Emphysema - Ans: -Loss of lung elasticity -Increased CO2. -"Pink Puffers" - Pink because alveoli are getting oxygen but can't breathe CO2 out. -Air becomes trapped in the alveoli and lungs -Barrel chest Chronic Bronchitis - Ans: -"Blue Bloaters" - a reference to cyanosis and fluid retention -Digital clubbing -Edema or crackling in lungs -Productive cough. Muscles that control respiration in nervous system? (Respiratory Center) - Ans: -Pons -Medulla