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Patho Midterm
Nightingale Pathophysiology Midterm Study
| Question | Answer |
|---|---|
| Define Pathophysiology: | The study of the underlying changes in the body's physiology that result from disease or injury. (molecular, cellular and organ systems) |
| Define Pathology: | The investigation of structural alterations in cells, tissues and organs, which can help identify the cause of a particular disease. |
| Define Diagnosis: | The naming or identification of a disease. This is made from evaluating the evidence accumulated from the presenting signs and symptoms, health and medical history, physical exam, and testing. |
| Define Etiology: | The study of the CAUSE of disease. |
| Define Epidemiology: | The study of the frequency and patter, and causes and risk factors of health-related states and events. |
| Describe Nucleus: | Membrane-bound organelle that contains the cell's chromosomes. Controls and regulates the activities of the cells |
| Describe Cytoplasm: | Gelatinous liquid that fills the inside of the cells. Composed of water, salts, and various organic molecules. Medium for chemical reactions. |
| Describe Ribosomes: | Particle consisting of RNA and associated proteins found in large numbers in the cytoplasm of the living cells. Bind mRNA and tRNA to synthesize polypeptides and proteins. |
| Describe Endoplasmic Reticulum: | Network of membranous tubules in the cytoplasm of eukaryotic cells, continuous with nuclear membrane. Has ribosomes attached. Is involved in protein and lipid synthesis |
| Describe Golgi Apparatus: | Responsible for transporting, modifying and packaging proteins and lipids into vesicles for delivery to target destinations and proteins to be exported from the cell. |
| Describe Lysosomes: | Membrane-bound cell organelle that contains digestive enzymes. Involved in degrading and recycling cellular waste, cellular signalling and energy metabolism. |
| Describe Peroxisomes: | Membrane-bound organelle occurring the in the cytoplasms of eukaryotic cells. Contain enzymes that oxidize certain molecules, these reactions produce hydrogen peroxide. |
| Describe Mitochondria: | Power house of the cell. Site of ATP (energy) production |
| Describe Cytoskeleton: | Microscopic network of protein filaments and tubules in the cytoplasm of many living cells, giving them shape and coherence. |
| Describe Plasma Membrane: | Also known as cytoplasmic membrane, biologic membrane that separates the interior of all cells from the outside environment and protects the cell from its environment |
| Signalling Process 1: | 1. They display plasma membrane bound signaling molecule (receptors) that affect the cell itself and other cells in direct physical contact. |
| Signalling Process 2: | 2. They affect receptor proteins inside the target cell. The signal molecule has to enter the cell to bind to them. |
| Signalling Process 3: | 3. They form protein channels (gap junctions) that directly coordinate the activities of adjacent cells. |
| Adaptive Cellular Mechanism - Atrophy: | Decrease in cell size |
| Adaptive Cellular Mechanism - Hypertrophy: | Increase in cell size |
| Adaptive Cellular Mechanism - Hyperplasia: | Increase in Cell Number |
| Adaptive Cellular Mechanism - Metaplasia: | Reversible replacement of one mature cell type by another; less mature cell type or a change in cell phenotype |
| Adaptive Cellular Mechanism - Dysplasia: | Deranged cellular growth. Not considered a true cellular adaptation but instead, atypical hyperplasia |
| Define DNA: | DNA, or deoxyribonucleic acid is the hereditary material in humans and almost all other organisms. Directs the synthesis of all the body's proteins |
| Define DNA Structure: | A molecule of DNA consists of two strands that form a double helix structure. 1. Five-carbon monosaccharide deoxyribose. 2. Phosphate molecule. 3. Four types of nitrogenous bases. |
| Define Mutations: | Any alteration to genetic material. |
| Define Genotype: | The genetic constitution of an individual organism. Three types: PP(homozygous dominant), Pp(heterozygous), pp(homozygous recessive). |
| Define Phenotype: | Set of observable characteristics of an individual resulting from the interaction of its genotype with the environment. |
| Define Alleles: | One of two or more alternative forms of a gene that arise by mutation and are found at the same place on a chromosome. Different forms of a gene. |
| Define Genes: | Basic physical and functional unit of hereditary transmission. Made up of DNA. |
| Define Heterozygous: | Having two different alleles of a particular gene or genes. The alleles are not identical. |
| Define Homozygous: | Having two identical alleles of a particular gene or genes. |
| Define Dominant: | The allele whose effects are observable. |
| Define Ressesive: | The allele whose effects are hidden. |
| Epigenetics | The study of how your behaviors and environment can cause changes that affect the way your genes work. Reversible. Can change how your body reads a DNA sequence. |
| Understanding Genetic Mechanisms - Down Syndrome: | Trisomy of Chromosome 21, best known disease caused by a chromosome aberration. Affects 1 in 800 to 1 in 1000 live births. |
| Understanding Genetic Mechanisms - Gaucher's Disease: | Missing the enzyme that breaks down fatty substances called lipids. Lipids start to build up in certain organs such as the spleen and liver. |
| Understanding Genetic Mechanisms - Zellweger Disease: | Caused by defects in any of 13 genes, termed PEX genes, required for the normal formation and function of peroxisomes. |
| Understanding Genetic Mechanisms - Turner Syndrome: | Presence of a single X chromosome and no homologous X or Y chromosome. Individual has a total of 45 chromosomes (45 X karyotype) |
| Understanding Genetic Mechanisms - Kleinfelter Syndrome: | There are at least two X chromosomes and one Y chromosome in each cell. (47 XXY karyotype) |
| Understanding Genetic Mechanisms - Spinal Muscular Atrophy | Mutation or deletion of the telomeric copy of the survival motor neuron gene (SMN1), which encodes a protein known as survival motor neuron (SMN). All patients retaining at least one copy of the centromeric form of the gene SMN2. T |
| Impact of Alcohol Use During Pregnancy: | Culturing neural stem cells in the presence of alcohol leads to dense methylation and inactivation of loci typically active in neurons. Alters the fetal expression of the DNA methyltransferases (DNMTs). |
| Table 4.8: Asphyxiation | Caused by the failure of cells to receive or use oxygen. Deprivation of oxygen can be partial (hypoxia) or total (anoxia). |
| Table 4.8: Asphyxial Injury, Suffocation | Process of dying as a result of lack of oxygen. Can result from either a lack of oxygen in the environment or from respiratory airway blockage |
| Table 4.8: Asphyxial Injury, Strangulation | Caused by compression of the blood vessels and air passages from external pressure on the neck. The compression causes hypoxia from impaired blood flow to the brain |
| Table 4.8: Asphyxial Injury, Asphyxiants | Chemicals that prevent the delivery of oxygen to the tissues or block oxygen utilization. Examples: CO2, cyanide, hydrogen sulfide, methane |
| Table 4.8: Asphyxial Injury, Drowning | Death from inhalation and suffocation from a liquid. Most often water. |
| Pathophysiology: Clinical Manifestation of Alterations in Water Movement | Edema caused by: 1. increased capillary hydrostatic pressure. 2. decreased plasma oncotic pressure. 3. increased capillary membrane permeability. 4. lymphatic channel obstruction |
| Compensatory Mechanisms for Metabolic Acidosis | Respiratory CO2 Elimination, hyperventilation |
| Compensatory Mechanisms for Metabolic Alkalosis | Respiratory CO2 Retention, hypoventilation |
| Compensatory Mechanisms for Respiratory Acidosis | Renal bicarbonate retention and hydrogen elimination |
| Compensatory Mechanisms for Respiratory Alkalosis | Renal bicarbonate elimination and hydrogen retention |
| Major Components of the Innate Response: Physical | 1. Physical Barriers; tight junctions in the skin, epithelial and mucous membrane surfaces, mucous itself. |
| Major Components of the Innate Response: Anatomical | 2. Anatomical Barriers; epithelial and phagocytic cell enzymes, phagocytes, inflammation-related serum proteins |
| Major Components of the Innate Response: Immune | 2. Immune: cells that release cytokines and inflammatory mediators (macrophages, mast cells, natural-killer cells) |
| Role of Histamine: | Induces vasodilation and increased capillary permeability |
| Role of Proinflammatory Cytokines | Have a key role in the destruction of many pathogenic microorganisms |
| Systemic Manifestations of Acute Inflammation | Fever, swelling, pain, loss of function, redness, leukocytosis, increased plasma protein synthesis |
| Phases of Wound Healing: 1. Hemostasis | 1. Hemostasis (coagulation) - platelet activation and fibrin clot. Stops bleeding and allows the body to start repairs on the injury. |
| Phases of Wound Healing: 2. Inflammation | 2. Inflammation - Macrophages, cytokines, neutrophils and lymphocytes. Injured blood vessels leak transudate and causes localized swelling. Controls bleeding and prevents infections |
| Phases of Wound Healing: 3. Proliferation | 3. Proliferation/Tissue Formation - Angiogenesis, fibroblast activation, granulation tissue formation, cytokines.Wound is rebuilt with new granulation tissue comprised of collagen and extracellular matrix. New network of blood vessels develop. |
| Phases of Wound Healing: 4. Remodeling | 4. Remodeling and Maturation - Fibroblasts. Occurs with granulation tissue formation. Formation of new epithelium and new scar tissue. Can take up to a year or longer to complete. |
| Identify the various types of scars in dysfunctional wound healing: | Keloid scars, hypertrophic scars, contractures, adhesions, pitted or sunken scars. |
| Primary Immune Response: | Reaction of the immune system when it contacts and antigen for the first time. Can take up to 14 days to resolve and leads to generation of memory cells with high specificity for inducing antigen. |
| Secondary Immune Response: | Reaction of the immune system when it contacts and antigen for the second and subsequent times. Can eliminate the antigen encountered during primary invasion more rapidly and efficiently. |
| Identify examples of the different types of hypersensitivities and the immunoglobulin associated with each response: Type I | Type I hypersensitivities, (IgE). Examples: seasonal allergic rhinitis, asthma |
| Identify examples of the different types of hypersensitivities and the immunoglobulin associated with each response: Type II | Type II hypersensitivities, (IgG, IgM). Examples: autoimmune thrombocytopenic purpura, Graves disease, autoimmune hyemolytic anemia |
| Identify examples of the different types of hypersensitivities and the immunoglobulin associated with each response: Type III | Type III hypersensitivities, (IgG, IgM). Examples: Systemic lupus erythematous |
| Identify examples of the different types of hypersensitivities and the immunoglobulin associated with each response: Type IV | Type IV hypersensitivities, (no immunoglobulin associated, it is a cell-mediated reaction). Examples: contact sensitivity to poison ivy, metals, and latex |
| Differentiate the various types of transplant rejection: Hyperacute Rejection | 1. Hyperacture Rejection - immediate, rare, and occurs because of the presence of pre-existing antibodies. Type II reaction to HLA antigens on the vascular endothelial cells in the grafted tissue. |
| Differentiate the various types of transplant rejection: Acute Rejection | 2. Acute Rejection: cell-mediated immune response that occurs within days to months after transplant. This rejection occurs when the recipient develops an immune response against unmatched HLA antigens after transplantation |
| Differentiate the various types of transplant rejection: Chronic Rejection | 3. Chronic Rejection: May occur after a period of months or years of normal function. Characterized by slow, progressive organ failure. Occurs in recipients who were poorly match to a donor, have co-morbidities, received a graft that was damaged, etc |
| Describe the clinical manifestations of combined deficiencies | May include bleeding secondary to thrombocytopenia (low platelet counts), eczema, and recurrent infections. (otitis media, pneumonia, herpes simplex, cytomegalovirus) |
| Identify major manifestations of sepsis and bacteremia. | Bacteremia: occurs when bacteria in blood. Sepsis: occurs when bacteria in blood releases toxins. Fever, rapid heart rate, shaking chills, low blood pressure, GI symptoms, rapid breathing, confusion |
| Major Functions of Midbrain: | Relay center for motor and sensory tracts. Also center for auditory and visual reflexes |
| Major Functions of Spinal Cord: | Connection of the brain and the body through a long nerve cable, somatic and autonomic reflexes, motor pattern control, and sensory and motor modulation |
| Major Functions of Forebrain: | Telencephalon(two cerebral hemispheres). Allows conscious perception of internal and external stimuli, thought and memory processes, voluntary control of skeletal muscles. Diencephalon (deep portion of forebrain) processes incoming sensory data |
| Major Functions of Hindbrain: | Allows sampling and comparison of sensory data received from the periphery and motor impulses of the cerebral hemispheres for the purpose of coordination and refinement of skeletal muscle movement. |
| Identify the major clinical manifestations of disorders of temp regulation: Hyperthermia | 1. Hyperthermia - can produce nerve damage, coagulation of cell proteins, and death. At 41C (105.8F), nerve damage produces convulsions in the adult. Death results at 43C (109.4F) |
| Identify the major clinical manifestations of disorders of temp regulation: Hypothermia | 2. Hypothermia - core body temp less than 35C (95F). Produces depression of the CNS and respiratory system, vasoconstriction, alterations in the microcirculation and coagulation and ischemic tissue damage |
| Identify the major clinical manifestations of disorders of temp regulation: Major Body Trauma | 3. Major Body Trauma - Damage to the CNS, inflammation, increased intracranial pressure, or intracranial bleeding can produce a body temp of greater than 39C (102.2F). Sustained noninfectious fever, central fever, appears with or w/out bradycardia. |
| Define Hyposmia: | Impaired sense of smell |
| Define Ansomia: | Complete loss of sense of smell |
| Define Parosmia: | Abnormal or perverted sense of smell |
| Define Olfactory Hallucinations: | Smelling odors that are not really presents |
| Define Hypogeusia: | Decrease in taste sensation |
| Define Ageusia: | Absence of the sense of taste |
| Define Dysgeusia: | perversion of taste in which substances possess an unpleasant flavor (i.e. metallic) |
| Describe outcomes of the various alterations in arousals: Brain Death | Brain death (total brain death) - when the brain is damaged beyond so completely that it can never recover (irreversible) and cannot maintain the body's internal homeostasis |
| Describe outcomes of the various alterations in arousals: Cerebral Death | Cerebral Death (irreversible coma) - death of the cerebral hemispheres exclusive of the brainstem and cerebellum. Brain damage is permanent and the individual is forever unable to respond behaviorally in any significant way to the environment. |
| Describe outcomes of the various alterations in arousals: Persistent vegetative state | Persistent vegetative state: complete unawareness of the self or surrounding environment and complete loss of cognitive function. Recovery is unlikely if the state persists for 12 months. |
| Describe outcomes of the various alterations in arousals: Minimally conscious state | Minimally conscious state (MSC, minimally preserved consciousness) - may follow simple commands, manipulate or reach for objects, gesture or give yes/no response, etc. May remain permanently in this state or progress to minimal ability |
| Describe outcomes of the various alterations in arousals: Locked-in syndrome | Locked-in syndrome: complete paralysis of voluntary muscles with the exception of eye movement |
| Decorticate Posture/Rigidity: | Upper extremity flexion, lower extremity extension. Response: slowly developing flexion of arm, wrist and fingers w/ adduction in the upper extremity and extension, internal rotation and plantar flexion of lower extremity |
| Decerebrate Posturing/Rigidity: | Upper and lower extremity extensor responses. Response: hyperextension of vertebral column w/ clenching of teeth; extension, abduction and hyperpronation of arms and extension of lower extremities. |
| Major characteristics of expression disorders: Hypermimesis | Commonly manifests as pathologic laughter or crying. Pathologic laughter is associated w/ right hemisphere injury and pathologic crying is associated w/ left hemisphere injury |
| Major characteristics of expression disorders: Hypomimesis | Manifests as aprosody (loss of emotional language). Receptive involves inability to understand emotion in speech and facial expressions. Expressive involves inability to express emotion in speech & facial expression. Associated w/ right hemisphere damage. |
| Major characteristics of expression disorders: Apraxia/Dyspraxia | Disorder of learned skilled movements w/ difficulty planning and executing coordinated motor movements. Often used interchangeably with dyspraxia. Can be developmental or associated with vascular disorders. |
| Identify clinical manifestations of spinal cord and vertebral injury | Extreme back pain or pressure in neck, head or back. Weakness, numbness, loss of bladder or bowel control, exaggerated reflex activities, changes in sexual function, pain or intense stinging sensation, difficulty breathing |
| Risk factors for cerebrovascular disease (CVD) | Hypertension, smoking, insulin resistance, diabetes, atrial fibrillation, polycythemia, high cholesterol, congestive heart disease, obesity, sleep apnea, physical inactivity, family history of ischemic stroke, high sodium intake, etc. |
| Clincal Manifestations of Multiple Sclerosis (MS) | Paresthesias of the face, trunk or limbs. Weakness, impaired gait, urinary incontinence. Visual impairment, cerebellar and corticospial involvement presents as nystagmus, ataxia and weakness, slurred speech, tremor. |
| Clinical Manifestations of Subarachnoid Hemorrhage (SAH) | If only in the subarachnoid space, there may be no local signs. If bleeding has spread; hemiparesis, paralysis, dysphasia, homonymous hemianopia |
| Clincal Manifestations of Different Types of Headaches: Migraine w/out Aura | Vomiting |
| Clincal Manifestations of Different Types of Headaches: Migraine w/ Aura | Vomiting. Visual, sensory, language and motor disturbance |
| Clincal Manifestations of Different Types of Headaches: Cluster Headache/Proximal Hemicrania | Lacrimation, rhinorrhea, horner syndrome |
| Clincal Manifestations of Different Types of Headaches: Tension-type | Dull and aching head pain, sensation of tightness across forehead and sides of head, tenderness in scalp, neck and shoulders |
| Pathophysiology of neuromuscular joint disorders | Results from a defect in nerve impulse transmission at the neuromuscular junction. Post-synaptic AChRs on the muscle cell's plasma membrane no longer recognized and elicit T Cell dependent formation of IgG autoantibodies. Blocks binding of acetylcholine |
| Positive Feedback System: | Enhance or amplify changes; this tends to move a system away from its equilibrium state and become more unstable |
| Negative Feedback System: | Dampen or buffer changes; tends to hold a system to equilibrium state making it more stable. Homeostatic |
| Evaluation of Addison Disease | Serum and urine levels of cortisol are depressed w/ primary hypocortisolism, and ACTH levels increase. Blood urea nitrogen levels may increase from dehydrations. Serum Glucose level is low. Eosinophil and lymphocyte count is elevated. |
| Treatment of Addison Dease | Lifetime glucocorticoid and mineralocorticoid replacement therapy, together with dietary modifications and correction of any underlying disorders |
| Clinical Manifestations fo Diabetes Insipidus | Polyuria, nocturia, continuous thirst, polydipsia |
| Clinical Manifestations of hyperthyroidism | Thin hair, exophthalmos, enlarged thyroid, heart failure (tachycardia), weight loss, diarrhea, warm skin, sweaty palms, hyperreflexia, pretibial edema |
| Clinical Manifestations of hyperaldosteronism | Thinning of scalp hair, emotional instability, acne, moon face, increased facial hair, buffalo hump, osteoporosis, cardiac hypertrophy, hypertension, obesity, striae of skin, easy bruising, muscle wasting, DM |
| Events that lead to a thyroid storm | TH levels rise dramatically and death can occur w/in 48 hours w/out treatment. May develop spontaneously but usually occurs in uncontrolled Graves Disease or those subjected to physiologic stress. |
| An individual who is heterozygous for a gene has: | Alleles at a given locus that are different from one another. |
| When an infant has been identified as having had fetal exposure to alcohol, which assessment parameters should be considered WHEN A MOTHER PRESENTS>>>>> | ALL OF THE ABOVE. low birth weight, mental retardation, facial abnormalities |
| A nurse documents "tattooing and stippling" in a trauma patient. Which type of injury does this patient have? | Gunshot wounds |
| A Nurse recalls that adaptive cellular mechanisms function to | protect cells from injury |
| When the clinician is discussing the DNA helix, which information should be included? In the DNA helix, guanine pairs with | cytosine and guanine |
| Which of the following statements by a clinician about mutations is correct? | Mutations are alterations in a normal sequence |
| The nurse is caring for a new mother who just gave birth to a baby with Down Syndrome. The nurse explains that this syndrome is a result of trismony with which chromosome? | Trisomy 21 |
| The patient is having a reaction to a bee sting. Which type of hypersensitivity reaction does the nurse expect to see documented in the patient's chart | Type 1 |
| Peanut allergy | Type 1 |
| A patient with cancer sustains an excessive amount of Tumor Necrosis Factor-Alpha. Which condition should the nurse be particularly alert for? | Cachexia |
| Among the many innate defenses the body has to pathogens, the first line of defense is the: | skin and mucous membranes. |
| A patient with a spinal cord injury at T7 level reports a headache. The patient's blood pressure is 296 systolic and the patient is sweating. Which intervention is most appropriate? (Worded a little different) | Autonomic Hyperreflexia |
| A nurse is describing the pathophysiology of Myasthenia Gravis. Which information should the nurse include? | This is an autoimmune disease mediated by antibodies against the acetycholine receptors, resulting in defective nerve impulses. |
| The nurse is assessing the patient for menigitis the nurse bends the patients neck and the patient expereinces neck pain and rigidity. How would the nurse chart this? | Positive Brudzinski Sign |
| The nurse on a neurological unit is caring for several patients . Which patient is at highest risk for a cerebral vascular accident? | Hypertension and Diabetes |
| brown urine/rotten eggs | hydrogen sulfide |
| Addisons disease | autoimmune damage |
| A patient with a combined immune deficiency lacks: | T and B lymphocytes |
| Among the many innate defenses the body has to pathogens, the first line of defense is the: | skin an mucous membranes |
| If a patient has liquefactive necrosis, which organ should the nurse assess first? | Brain |
| The outward manifestation of a disease, often influenced by both genes and the environment, is called the disease: | Phenotype |
| Cellular atrophy is: | A decrease in cell size |
| Process by which cells program themselves to die: | Apoptosis |
| Most commonly reported symptom associated with cancer is: | fatigue |
| Which term is used to describe cancer that extends to organs or tissues distant from the site of origin? | Metastasis |
| For metastasis to occur, tumor cells must be capable of: | surviving in the blood stream |
| A patient is experiencing leukopenia from cancer and chemotherapy treatment. Which condition should you assess for in this patient? | Infection |
| During a myasthenic or cholinergic crisis, a patient is in danger of: | Respiratory arrest |
| A herniated disk allows the gelatinous material (the nucleus pulposus) to: | Extrude and compress the nerve root |
| During your assessment of a patient with meningitis, you want to test for nuchal rigidity. Which test will you implement? | Kernig |
| Term used to describe the loss of reflex function below the level of injury/lesion? | Spinal Shock |
| The eukaryotic cell consists of three general components | Plasma membrane, the cytoplasm, and the intracellular organelles |
| Genes, the basic units of inheritance, are composed of: | deoxyribonucleic acid (DNA) |
| An inherited alteration of genetic material is called: | a mutation |
| The reversible replacement of one mature cell type by another less mature cell type is called: | Metaplasia |
| A problem of fluid distribution that results in accumulation of fluid within interstitial spaces: | Edema |
| Waterbalance is regulated by: | Sensation of thirst and antidiuretic hormone (ADH) |
| What is regulated by the kidney, by aldosterone and insulin secretion, and by changes in pH? | Potassium balance |
| The second line of defense is: | The inflammatory response |
| What are molecules that bind and react with components of the immune response, such as antibodies and receptors on B and T cells? | antigens |
| What enters host cells and uses the metabolic processes of host cells to proliferate and cause disease? | viruses |
| A propensity to unusual or recurrent severe infections is a clinical hallmark of: | immunodeficiency i |
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