Patho Exam 1 Study Guide PDF

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Exam 1 Pathophysiology study guide Cohort 10 KU Nursing ABSN Cellular injury causes enzyme release that leads to cellular self- destruction. Apoptosis-programmed cell death Hypoxia- oxygen deprivation Hypoxic injury- Single most common cause of cellular injury, results from: reduced amount of oxygen in the air, loss of hemoglobin or decreased efficacy of hemoglobin, decreased production of red blood cells, diseases of the respiratory and cardiovascular systems, poisoning of the oxidative enzymes (cytochromes) within the cells.  

Ischemia- most common cause of hypoxia Ischemia-reperfusion injury- Additional injury that can be caused by restoration of blood flow and oxygen

Hydropic Degeneration steps Hypoxia ATP production decreased Sodium and water move into cell, potassium moves out of cell Osmotic pressure (force caused by a solution passing through a semi permeable surface by osmosis, which is equal to the force required to resist the solution from passing back through the surface) increases Cisternae of ER ruptures and from vacuoles Extensive vacuolation End result is cell swelling Cellular injury mechanisms Free radicals and reactive oxygen species- uncharged atom or molecule having unpaired electron damages:    

Lipid peroxidation: destruction of polyunsaturated lipids- leading to membrane damage and increased permeability Alternation of proteins: loss of protein function Alternation of DNA: mutation Mitochondria: disrupt function

Necrosis-cell death from injury 

Liquefactive: cells digested by their own hydrolases (liquefies) mostly in neurons and glial cells in brain

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Coagulative: from hypoxia, effects kidneys heart and adrenal gland. Protein denaturation Caseous: tuberculosis, combination of coagulative and liquefactive necrosis. Cheese like debris Gangrene: gas gangrene forms bubbles of gas from hypoxia due to infection Fat necrosis: cellular dissolution caused by power enzyme lipases

Transcription- the process of making an RNA copy of a gene sequence. This copy, called a messenger RNA (mRNA) molecule, leaves the cell nucleus and enters the cytoplasm, where it directs the synthesis of the protein, which it encodes. Cancer cell sustained proliferative signaling pathways Pg. 103-104 in textbook Tumor suppressor genes inhibit the proliferation of cells in a tumor. When this type of gene is inactivated, a genetic signal that normally inhibits cell proliferation is removed, thereby causing unregulated growth to begin. point mutation in RAS gene (GTPase) converts GTP to GDP, thus initiating the signaling pathways. The DNA repair genes affect cell proliferation and survival indirectly through their ability to repair damage in proto-oncogenes, genes impacting apoptosis, and tumor suppressor genes. A common way in which cancer cells gain autonomous growth is through mutations in genes that control growth factor signaling pathways. These signaling pathways connect the growth factor receptors to their nuclear targets. Uncontrolled cellular proliferation is known as the “Hallmark of cancer.” Proliferative signaling is the process where a cell receives a signal and acts on it by initiating cell division. Cancer cells use autocrine signaling to stimulate their survival and proliferation. (Slide 49 the first set of power points, chapters 1,2,3,9) Punnett Square – autosomal recessive Both parents of affected individuals are heterozygous carriers. Sharp force injuries- Incised wound- longer than deep, Stab Wound- penetrating sharp force injury deeper than it is long. Puncture wound –nail in foot instrument or objects with sharp points but without sharp edges produce puncture. Chopping wound- heavy- edged instrument, ie axe, hatchet – produce wounds with a combo of sharp and blunt force characteristics. Cell Death Apoptosis – programmed cellular death. Heat loss mechanisms- Radiation – heat loss through electromagnetic waves emanating from surfaces with temperature higher than surrounding air. Conduction- Heat loss by direct molecule to molecule transfer from one surface to another- so that warmer surface loses heat to cooler surfaces. Convection – transfer of heat through currents of gases or liquids; exchanges warmer

air at body’s surface with cooler air in surrounding space. Vasodilation – diverts core-warmed blood to surface of body, heat lost through conduction. Evaporation – body water evaporates from surface of skin and linings of mucous membranes; major source of heat reduction connected with increased sweating in warmer surroundings. Increased respirations- air is exchanged with environment through normal process. Voluntary measures - “slowing down” in response to high body temps. Dressing in loose-fitting garments. Bacterial virulence and infectivity – sepsis Bacteremia (present in the blood) or septicemia (growth in the blood) - A result of a failure of the body’s defense mechanisms, Usually caused by gram-negative bacteria, Endotoxins released into the blood activate the complement and clotting systems, leading to a degree of capillary permeability sufficient to permit escape of large volumes of plasma into surrounding tissue, contributing to hypotension and, in severe cases cardiovascular shock—Endotoxic shock=up to 50% mortality (slide 62 of week 4) Body temperature regulation- Peripheral and central thermoreceptors trigger hypothalamus to cause heat production and conservation. Thermoregulation –balancing of heat production – heat conservation and heat loss. Chemical reactions of metabolism – ingestion and metabolism of food. - Skeletal muscle contraction – gradual increase in muscle tone or rapid muscle oscillations (shivering) - Chemical thermogenesis- epinephrine release leads to heat production through increase in basal metabolic rate. Vasoconstriction. Infants- produce sufficient body heat but are unable to conserve heat produced- small body size and high body surface to weight ratio, thin subcutaneous layer Elderly- slow blood circulation, vasoconstrictive response, and decreased metabolic rate. Decreased sweating, shivering, and perception of heat and cold

Membrane transport (e.g. active transport, osmosis, diffusion, etc.) (The following can be reviewed on pgs 22-25 textbook) Active Transport: Molecules move up a concentration gradient, this requires ATP. Uses ATP, uses pumps endocytosis exocytosis. Osmosis: The movement of water across a semipermeable membrane from a region of higher water concentration to one of lower concentration. The movement of water continues until the concentration of substances on either side of the membrane is equally diluted, or until the osmotic pressure opposes the flow of water. Diffusion: The movement of a solute molecule from an area of greater solute concentration to an area of lesser solute concentration resulting in an equal distribution across the cell membrane. Hydrostatic Pressure: The force of fluid against a cell membrane. Within the vascular system, this pressure is the blood pressure.

Facilitated Diffusion: The passive movement of molecules across the cell membrane via the aid of a membrane protein. -Substances move across the cell membrane with the help of transport proteins. Passive Transport: transport substances across the cell membrane influenced by chemical or electrical gradients and does not require an input of energy. Cortisol secretion - secretion during stress (week 4 slide 12) Epigenetic modifications- Stable and heritable alterations in gene expression and cellular function without changes to the original DNA sequence. Ex: In utero exposure to chemicals may lead to similar epigenetic modifications (week 3 slide 76) Therapeutic hypothermia - used to slow metabolism and preserve ischemic tissue during surgery or limb reimplantation. May lead to ventricular fibrillation and cardiac arrest. (week 2 Slide 215) General adaptation syndrome - Dr. Selye termed this general stress response the general adaptation syndrome (GAS), he perceived it as primarily physiologic (week 4, slides 4,5) 

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Alarm stage- stressor triggers the hypothalamic-pituitary-adrenal (HPA) axis o Activates sympathetic nervous system o Arousal of body defenses Resistance/adaptation stage o Begins with the actions of adrenal hormones o Mobilization contributes to fight or flight Exhaustion stage (allostatic overload) o Occurs only is stress continues and adaption is not successful o Leads to stress-related disorders

T cell function and activation Activation: Binding antigen to specific T cell receptors. Allows: Direct killing of foreign or abnormal cells. Assistance or activation of other cells. T regulatory of cells (Tregs): Regulate the immune response to avoid attacking “self”. Memory T cells Eukaryotic organelles - Ribosomes. RNA protein complexes, synthesized in nucleolus, Sites for cellular protein synthesis. -- Endoplasmic reticulum – synthesis and transport of protein and lipids Golgi Complex – network of smooth membranes, processing and packaging of proteins, secretory vesicles, cytoskeleton. Lysosomes – Originate from the Golgi- contain enzymes for digestion, cellular injury causes enzyme release that leads to cellular self-destruction. Peroxisomes – contain oxidative enzymes, break substances down into harmless products. Mitochondria – cellular energy metabolism, ATP generation. Has role in osmotic regulation – ph control – calcium homeostasis, cell signaling. Cytoskeleton – bones and muscles of cell – helps maintain – protein filaments –forms cell extensions.

Benign vs. Malignant Tumors- Benign – ending in OMA (lipoma fat cells – leiomyoma – smooth muscle of uterus – meningioma – membranes surrounding the brain and spinal cord) Grow slowly, well defined capsule, not invasive, well differentiated, low mitotic index, do not metastasize. Malignant – Grow rapidly, not encapsulated, Invasive, poorly differentiated, high mitotic index, can spread distantly (metastasis) Carcinoma – epithelial tissue, adenocarcinomafrom ductal or glandular tissue. Sarcoma- mesenchymal tissue, Lymphoma – lymphatic tissue, Leukemia- blood forming cells. Wound healing phases- Regeneration –replacement of damaged tissue with healthy tissue. Resolution – Returning injured tissue to the original structure and function. Repair-replacement of destroyed tissue with scar tissue. Scar tissue – Composed primarily of collagen to restore the strength of the tissue but not its function. Healing – Filling in the wound – Sealing the wound (epithelialization) Shrinking the wound (contraction). Primary intention – wounds that heal under conditions of minimal tissue loss. Secondary intention – wounds that require a great deal more tissue replacement aka open wound. Inflammation phase- coagulation, infiltration of wound-healing cells. Angiogenesis- formation of a new blood supply. Proliferative phase – Granulation – Epithelialization – requires fibroblast proliferation, collagen formation, wound contraction. Remodeling and maturation phase – continuation of cellular differentiation, scar tissue formation – scar remodeling. Dysfunctional wound healing- may occur during any phase of wound healing – ie ischemiaexcessive bleeding – excessive fibrin deposition- predisposing disorders ie diabetes, obesity, wound infection, inadequate nutrients, numerous drugs, tobacco smoke. Dysfunction during reconstructive phase—dysfunctional collagen synthesis- ie keloid scar. Hypertrophic scar – Wound disruption – dehiscence (increases risk of infection). Starling Forces- as plasma flows from the arterial to the venous end of the capillary, four forces determine if fluid moves out of the capillary and into the interstitial space (filtration) OR if fluid move back into the capillary from the interstitial space (reabsorption). Genetic terminology (e.g. Locus, allele, genotype, phenotype, etc.)- Locus- position of a gene along a chromosome. Allele – a different form of a particular gene at a given locus. Polymorphism – locus that has two or more alleles that occur with appreciable frequency. Homozygous- Loci on a pair of chromosomes have identical genes. Heterozygous- Loci on a pair of chromosomes have different genes. Genotype- (what they have) The composition of genes at a given locus. Phenotype (what they demonstrate)- The outward appearance/physical of the genetics of an organism. Viral replication - Not capable of independent reproduction, copies genetic material made (week 4 Slides 65-73) 

Need permissive host cell  Attachment- to a receptor on the target cell  Penetration – entrance into the cell by endocytosis or membrane fusion

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Uncoating – release of viral nucleic acid from the viral capsid by viral or host enzymes Replication - synthesis of mRNA and viral protein Assembly - formation of new virions Release - exit from the cell by lysis or budding

ABG interpretation ABG= arterial blood gas, tests measures oxygenation and blood acid level Normal Range PH: 7.35-7.45

Less= acid Greater=Base

PaCO2: 35-45

(Opposite) Less=base greater= Acid

HCO3: 22-26

Less=acid Greater= base

PaCO2= respiratory (partial pressure of carbon dioxide) the more CO2 in our blood the more acidic the blood is. Levels controlled by lungs HCO3=bicarbonate, metabolic, levels controlled by kidneys Respiratory acidosis: High CO2=hypoventilating, hypoxia Respiratory alkalosis: Low CO2= hyperventilating, deep rapid breathing Metabolic Acidosis: Low HCO3. too much acid secretion or low base secretion Metabolic alkalosis: High hCO3= too much base secretion or low acid secretion

Compensation in ABG -Body's ability to correct acidosis or alkalosis Compensation is present if PH is normal but HCO3 and CO2 is abnormal Partial compensation: Ex. PH is 7.6-basic PaCO2 is 29-basic HCO3 is 30- acidic Since PH level and CO2 are basic, then respiratory alkalosis is in effect. HCO3 is trying to bring the PH to level by becoming more acidic, since the PH is still not in normal range, this means there is partial compensation

HIV therapy – not curative but death reduced significantly; current medications decrease the amount of virus in the body but do not eradicate HIV; antiretroviral therapy (ART) -combination of the following: •Reverse transcriptase inhibitors; inhibit RNA virus replication by reversible inhibition of viral HIV enzyme •Protease inhibitors; block an enzyme known as protease (break down proteins into peptides) •Integrase inhibitors; block integrase which HIV uses to insert its viral DNA into CD4 cell •Fusion inhibitors; prevent HIV from fusing with and infecting it •CCR5 antagonist; prevent HIV from entering and infecting immune cells by blocking CCR5 cell-surface receptor Prokaryotes and Eukaryotes- Prokaryotes – no distinct nucleus (single, circular chromosome) lack histones, organelles – Cyanobacteria, bacteria, and rickettsia (nonmotile, gram neg, nonspore forming, highly pleomorphic bacteria that can be present as cocci, rods, or thread like). Eukaryotes – complex cellular organization, Membrane-bound organelles, well-defined nucleus with several chromosomes, higher animals, plants, fungi, protozoa, and algae. --- Differences in biochemical activity: protein synthesis, transport across outer cell membrane, enzyme content. Cellular adaptations (e.g. atrophy, hypertrophy, etc.) a. Atrophy i. Decrease in cellular size; ex: immobile leg in cast b. Hypertrophy i. Increase in cellular size; ex: gym junkie c. Hyperplasia i. Increase in number of cells; ex: tumor d. Dysplasia i. Deranged cellular growth; ex: cancer cells in cervix during pap smear e. Metaplasia i. Replacement of one type of cell with another; ex: scar tissue

Antibodies[immunoglobulins]{Highly specific protein secreted by B lymphocytes following exposure to an antigen. (Pgs 246-247 in textbook).

Antibodies bind antigens by a lock and key mechanism to produce antigen/antibody complexes. these are a key feature of the specific immune system, which stimulates the nonspecific system and inflammation. Fungal infection -- Fungus infections occur when an invading fungus takes over an area of the body and is too much for the immune system to handle. Fungi can live in the air, soil, water, and plants. Genomic imprinting- For some human genes, a given gene is transcriptionally inactive on only one copy of a chromosome. - ex. Copy inherited from father is active while copy inherited from mother is inactive (silenced). transcriptionally silenced genes are said to be “imprinted” Biallelic expression- maternal and paternal inherited genes contribute to offspring phenotype. Monoallelic expression – maternal copy randomly chosen for inactivation in some cells, paternal copy in others. Imprinted Copy inherited through sperm or egg is inactivated and remains inactive for life. Prader-Willi and Angelman syndromes. - deletion of 4 million base pairs of long arm of chromosome 15. Manifestations of Prader-Willi syndrome if inherited from Father- Short stature, hypotonia, small hands and feet, obesity – mentally challenged. Manifestations of Angelman syndrome if inherited from mother – Severely mentally challenged, seizures, ataxic gait. Indistinguishable at DNA sequence level. Beckwith-Wiedmann syndrome – 20-30% caused by inheritance of two copies of a chromosome from father and no copies from mother. Overexpression of active insulin-like growth factor 2 (IGF-2). Manifestations present at birth – Large for gestational age, neonatal hypoglycemia, large tongue, creases on earlobe, omphalocele. Hypersensitivity reactions Hypersensitivity – abnormal and excessive response of the activated immune system that causes injury and damage to host tissues. Disorders caused by immune responses are collectively referred to as Hypersensitivity reactions. Hypersensitivity reactions are classified as one of four types: Type 1, IgE-mediated disorders; type II antibodymediated disorders; type III complement-mediated immune disorders; and type IV cell-mediated disorders. (A lot of info on this on pages 275-282 in the textbook) Exudative fluids - Serous – watery; indicates early inflammation. Fibrinous: Thick –Clotted: indicates more advanced inflammation. Purulent (suppurative): Pus- indicates a bacterial infection. Hemorrhagic –contains blood indicates bleeding. Innate Immunity – First line of Defense- Physical, mechanical, biochemical barriers. SKIN – linings of the Gastrointestinal, genitourinary, and respiratory tracts. Sloughing off of cells, coughing and sneezing, flushing-urine, vomiting, mucus and cilia.

Cellular necrotic pathways Sum of cellular changes after local cell death and the process of cellular auto digestion (autolysis)

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Coagulative- results from hypoxia caused by severe ischemia or hypoxia caused by chemical injury  Kidney, heart, and adrenal glands  Protein denaturation- causes the protein albumin to change from a gelatinous, transparent state to a firm opaque state Liquefactive Most common in neurons and glial cells of the brain  Hydrolytic enzymes- cells are digested by their own hydrolases, so the tissue becomes soft, liquefies, and segregates from healthy tissue  Bacterial infection- Staph, strep, E.coli Caseous  Tuberculous pulmonary infection, caused by mycobacterium tuberculosis  Combination of coagulative and liquefactive necrosis Fat- cellular dissolution caused by the powerful enzyme lipases found in:  Breast, pancreas, and other abdominal organs  Lipases break down triglycerides, releasing free fatty acids that then combine with calcium, magnesium, and sodium ions, creating soaps (saponification) Gangrenous- death of tissue from severe hypoxic injury (arteriosclerosis)  Common in the feet and toes Gas gangrene- caused by infection by a species of clostridium, these anaerobic bacteria produce hydrolytic enzymes and toxins that destroy connective tissue and cause bubbles of gas to form

Chromosomal aberrations Abnormalities in the structure and number of chromosomes resulting in developmental delay. (Examples: Trisomy 21 Down Syndrome, XXY male Kli...