Patho-Exam1 - Exam 1 PDF

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PATHOPHYSIOLOGY: EXAM 1 STUDY GUIDE WEEKLY OBJECTIVES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

Introduce pathophysiologic concepts and principles. Understand and use medical terminology when discussing pathophysiologic conditions. Discuss normal cell and tissue development and disease progression. Explain carcinogenesis, risk factors, stages of tumor development, and preventive strategies. Describe the process of cellular development and alterations based on external environmental and genetic factors. Explain how fluids and electrolytes are used by the body to adapt and maintain physiologic homeostasis. Apply growth and development principles as they relate to the impact of aging on normal pathophysiologic changes. Discuss the role genetics and aging plays in the process of cellular adaptation, mutation, and dysplasia. Understand inflammation, healing, infection, immunity, and neoplasms and cancer. Apply growth and development principles as they relate to the impact of aging on the pathophysiologic changes. Compare and contrast processes of inflammatory and healing processes, alterations in immune responses, and pathological processes of the immune system. Apply understanding of alterations in inflammatory and healing processes and across the lifespan to formulate care priorities. Describe how genetics influence pathophysiological alterations in healing, immunologic responses, and integumentary system. Explain carcinogenesis, risk factors, stages of tumor development, and preventive strategies.

CHAPTER OBJECTIVES 1. Explain the role of Pathophysiology in the diagnosis and treatment of disease  Pathophysiology is the study of physical and biological abnormalities occurring due to disease. It is important to the diagnosis and treatment of a disease because you can easily see the clinical manifestations, easily diagnose, and the risk factors. 2. Use appropriate terminology for pathophysiology 3. Describe common cellular changes and adaptations with possible reasons for occurrence  Atrophy: decrease in cellular size  Hypertrophy: increase in cell size  Hyperplasia: increase in cell number  Metaplasia: one mature cell is replaced by different another mature cell  Dysplasia: abnormal change in size, shape, and organization of mature cells, cells vary in size and shape  Neoplasia: new tumor growth 4. List common causes of cell injury  Ischemia  Physical agents: excessive temperatures, radiation exposure  Mechanical agents: pressure/tearing of tissue  Chemical toxins 5. Define Apoptosis and Necrosis

Apoptosis: programmed cell death Necrosis: group of cells die and cause further damage due to cellular disintegration Describe common types of cell necrosis  Coagulative: sever ischemia or hypoxia caused by chemical injury  Caseous: results from tuberculous pulmonary infection, form of coagulative, dead cells disintegrates, but the debris is not completely digested by the hydrolases  Gangrenous: death of tissue from severe hypoxic injury because of arteriosclerosis, or blockage, of major arteries  Liquefactive: mainly seen in brain cells are rich in digestive hydrolytic enzyme, dead cells liquefy under the influence of certain cell enzymes  Fat: injury to fatty tissue and fat being replaced with oily contents of fat cells Explain how fluids and electrolytes are used by the body to adapt and maintain physiologic homeostasis  Fluid & Electrolyte Imbalances  Acid-Base Balance Explain the role of normal defenses in prevention of disease (3 lines of defense)  First line: nonspecific, innate, natural immunity. Consist of saliva, skin, stomach acid, tears, mucus, “good” gut  Second line: inflammation, non-specific response to innate immunity, granulocytes, macrophages, mast cells  Third line: specific defense, agranulocytes, T and B lymphocytes, production of specific antibodies or cell-mediated immunity Define the pathophysiology of inflammatory response  

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10. Describe local and systemic signs/effects of inflammation  Local (physical): Erythema, warmth, pain, impaired function  Systemic (affecting the whole body): fever, leukocytosis, malaise, headache, anorexia, sepsis 11. Explain the causes of acute and chronic inflammation and complications of both  Acute: develops immediately but only lasting for a short amount of time. It may have delayed onset (sunburn) or may be more severe and prolonged.  Chronic: develops after an acute inflammation, can develop from smoking, certain bacteria, or long termed immune responses. 12. Define passive, active natural, and artificial immunity (in chapter 7)

13. List the elements of the immune system and purpose of each  Antigens o Self: HLA proteins label cells of the individual, immune system ignores self-cells o Non-self: immune system recognizes specific non-self-antigens as foreign, development of a specific response to that particular antigen (what we develop an immunity against), memory cells produced to respond quickly to antigen o Usually exogenous substances, proteins polysaccharides, glycoproteins (cell surface antigens), MHC= genes inherited from parents that code selfantigens on plasma membranes, activate and regulate the immune response  Cells o Macrophages: initiation of immune response, develop from monocytes, part of the mononuclear phagocytic system, engulf foreign material, secrete chemicals (monokines, interleukins), present throughout the body 14. Explain the four methods of acquiring immunity(SEE 12) 15. Describe the mechanism and clinical effects of each of the four types of hypersensitivity reactions  Type I Hypersensitivity—allergic reactions i. Most Common 1. Caused by allergen 2. Skin rashes 3. Hay fever (allergic rhinitis) ii. Causative mechanism 1. Exposure to allergen 2. Development of IgEs after 1st exposure 3. Mast cells (histamine rxn) iii. Complications 1. Mild to severe 2. Anaphylaxis a. Highly sensitized b. Systemic reaction 3. Treat the clinical manifestations  Type II Hypersensitivity i. Antigen is present on cell membrane a. May be normal body component or exogenous ii. Circulating IgGs react with antigen a. Destruction by phagocytosis or cytolytic enzymes

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Example a. Response to incompatible blood transfusion  Type III Hypersensitivity i. Antigen combines with antibody a. Forms immune complexes, deposited in tissue b. Activation of complement system c. Involves IgG & IgM d. Antigen = Antibody ii. Process causes inflammation and tissue destruction iii. Examples: a. Glomerulonephritis b. Rheumatoid arthritis  Type IV Hypersensitivity i. Delayed response by sensitized T lymphocytes a. Delayed response of immune system ii. Release of lymphokines iii. Inflammatory response iv. Destruction of the antigen v. Examples: a. Tuberculin test b. Contact dermatitis c. Allergic skin rash 16. Discuss the mechanism of autoimmune disorders  Development of antibodies against own cells or tissues.  Autoantibodies are antibodies formed against self-antigens- loss of self-tolerance  Disorder can affect single organs or tissues or can be generalized  Ex: hashimoto’s thyroiditis, rheumatic fever, systemic lupus erythematosus 17. Explain the effects of anaphylaxis  Severe, life threatening  Systemic hypersensitivity reaction  Decreased blood pressure caused by release of histamine  Airway obstruction  Severe hypoxia

18. Review of normal cell behaviors  Require growth factors: grow and repair  Contact inhibition allows them to be orderly  Require firm surface attachment to grow (petri dish)

 Limited life span 19. Distinguish between benign and malignant tumors, their characteristics, and medical terminology Benign (-oma) Malignant (-carcinoma) Grow slowly Frequently encapsulated Not invasive Well differentiated

Grow rapidly No capsule INVASIVE Poorly differentiated

Mitosis normal Do not metastasize (remains local)

Mitosis increased and atypical Metastasis through blood and lymph vessels

20. Explain carcinogenesis, metastasis, and stages of tumor development  Carcinogenesis: the process by which normal cells are transformed into cancer cells.  Metastasis: spread to distant sites by blood or lymphatic systems.  Stages of Tumor Development o Stage I: no metastasis o Stage II: local invasion o Stage III: spread to regional structures such as lymph nodes o Stage IV: Distant metastasis 21. Identify risk factors, clinical manifestations of cancer and possible complications Local Effects of Tumors

Systemic Effects

PAIN: LATE symptom, now advanced Obstruction: tumor compress a duct/passageway Tissue Necrosis/ulceration: *lead to infection or bleeding around tumor

Weight loss (cachexia) Anemia Severe Fatigue Infections Bleeding Paraneoplastic syndromes

22. Discuss possible treatment measures including surgery, radiation, chemotherapy, and nutrition  Depends on specific cancer o Surgery, chemotherapy, immunotherapy, radiation o Combination of the above  Chemotherapy o Induction: shrinkage of tumor o Adjuvant: after sx to eliminate micro metastasis o Neoadjuvant: before localized (surgical or radiation) to convert large tumor into smaller- allowing for improved excision

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May be used alone or combined with other therapies Ionizing radiation damages cell o Causes mutations or alterations in target DNA o External sources or brachytherapy o Damages blood vessels that supply tumor  Damage normal “healthy” cells Most effective in rapidly dividing cells Some types of cancers are radioresistant. May be used as an adjuvant therapy prior to surgery to shrink tumor Preventative: colon polyps Dx: biopsy & staging Debulking surgery o Remove as much as possible chemo/radiation to work o Palliative Removal of tumor and surrounding tissue Lymph node sampling o Sentinel nodes Removal of adequate surrounding tissue may result in changes in function. Radiofrequency ablation (RFA) o Alternative surgery for small single tumors in solid or fluid-filled organs, but not the lungs Nutrition o Advanced CA  Malnourished  Change in taste sensation  Anorexia  Vomiting/diarrhea  Sore mouth/loss of teeth  Pain/fatigue  Malabsorption caused by inflammation in digestive tract...