Final Exam Study Guide PDF

Preview

Summary

Final Exam Study Guide - summary of everything on the final exam ...

Description

N310 Pathophysiology - Final Exam Study Guide  -

The final exam will have 4 or 5 questions from each of the 21 lectures for a total of 100 questions. The final exam covers the information listed below. Not all of the exam topics were covered in the review session, so be sure to follow the study guide. But also carefully review your notes from the review session.

 ** there are 100 questions on the study guide: so everyone please fill out like 16 ish** - Mia → 1-17 - Hannah→ 18- 34 - Tommy → 35-51 - Mia→ 52-68 - Adi→ 69-85 - Marissa→ 86-100 9/04 Principles of Cellular Function and Nutrition 1. Define passive transport and identify the types of passive transport. - Passive transport = areas of higher concentration → areas of lower concentration - Does not require energy - Types: - Simple diffusion: through membrane down concentration gradient - Facilitated diffusion: passing through a transporter - Osmosis: diffusion of water molecules - •From areas of higher WATER concentration → areas of lower WATER concentration - Aka water follows solutes - Ion channels: leakage and gated - Potassium can leak out with difference in concentration gradient - Test Question: - Name 3 types of passive transport - A: Diffusion, filtration and osmosis 2. Identify and define the types of cellular adaptations. - Atrophy- Smaller size → lower & more efficient level of function - Hypertrophy: - ↑ cell size due to ↑ workload - -Physiologic – cardiac, skeletal muscle from exercise - -Compensatory – loss of kidney → ↑ nephron size - -Pathophysiologic – cardiac from ↑ blood pressure - Hyperplasia- -Increased number of cells (so not the size of the physical cells just the AMOUNT of them) - -Epidermis, intestine glands (cells with mitotic division) - Metaplasia: -Change from one cell type to another 1

- -Reversible - -Ex – smoking changes cells in airway - Dysplasia: -Deranged cell growth - -Varied size, shape, organization - -Cervical dysplasia (Pap test) - -Can return to normal or lead to cancer - Test Question: - Which type of cell adaptation is occuring in a smoker when normal columnar cells of the bronchial lining have been replaced by stratified squamous epithelial cells? - A: Metaplasia 3. Define the types of cell death: apoptosis and necrosis -

Programmed cell death: apoptosis or “cell suicide” - Physiologic: restructures tissues during development, replaces cells, immune function - Like removing webbing of feet in embryo - Pathologic - •Too little apoptosis → cancer - Too much apoptosis → neurodegenerative disease - Alzheimer’s, Huntington’s, Parkinson’s diseases - Start to lose your neurons - •Necrotic cell death - Unregulated death caused by injuries to cells - Cells swell and rupture → inflammation - Inflammation causes damage to surrounding cells - Ex. blood clot in the heart - cells swell and rupture → longer hypoxia stays → the more the injury spread to more surrounding tissue - Test Question: - A patient has a heart attack that leads to progressive cell injury that causes cell death with severe cell swelling and breakdown of organelles. What is the term that defines this process? - A: Cell necrosis 4. Define obesity as a disorder of altered metabolism, and identify hormonal dysfunctions related to the development of obesity. Causes of Obesity -

•Interaction of peripheral (adipocytes) and central (neuroendocrine) pathways and includes multiple inflammatory proteins (cytokines), hormones, and neurotransmitters •Adipocytes (fat cells) don’t just store fat – they have endocrine functions → secretion of hormones, cytokines, and adipokines that regulate (or dysregulate) many physiologic processes

2

-

•These mediators have multiple effects that contribute to obesity - Insulin resistance, inflammation, increased appetite - Leptin - Acts on hypothalamus to suppress appetite - Functions to regulate body weight within a narrow range - Leptin resistance in  obesity: - Promotes overeating and excessive weight gain (satiety signaling in hypothalamus is lost - no longer feel full) - Associated with insulin resistance - Related to cardiovascular complications of obesity 5. Describe how cells communicate and explain the role of second messengers in signal transduction. - When a ligand binds to a cell-surface receptor, the receptor’s intracellular domain (part inside the cell) changes in some way. Generally, it takes on a new shape, which may make it active as an enzyme or let it bind other molecules. - The change in the receptor sets off a series of signaling events. For instance, the receptor may turn on another signaling molecule inside of the cell, which in turn activates its own target. This chain reaction can eventually lead to a change in the cell's behavior or characteristics  9/09 Genetics and Oncogenesis 6. Define genotype and phenotype and explain the relationship between them.  -

•Genotype: a person’s genetic material •Phenotype: a person’s physical characteristics •Expressivity: manner in which gene is expressed (mild severe) •Penetrance: ability of a gene to express its function 

 Test Question - The DNA sequence and composition at a given locus is known as the: - A: Genotype 7. Define epigenetics and identify the effects of increased/decreased DNA methylation on gene expression. - Epigentics = Changes in gene expression caused by mechanisms OTHER THAN changes in DNA sequence - Lots of cells with SAME DNA have DIFFERENT functions - able to do this because of epigenetics - •Environmental factors (diet, chemical exposure) can→ epigenetic modifications - Ex. high fat diet - •Maintained in successive mitotic cell divisions - Daughter cells will have the same makeup due to epigenetics unless something is done to change them 3

-

Histone methylation – turns genes off - CH3 Add a methyl group and turn the gene off - Test Question: - Why are epigenetic modifications important? - A: They change DNA structure in future generations - control access to DNA for transcription (can turn it off or on, tighter chromatin ex) 8. Identify the characteristics of benign and malignant tumors. - Benign - Cells still look like original cells - liver cell - Grows slowly  - Encapsulated- stays in one place - Malignant - Cells are undifferentiated - no longer look/act like liver cells - Grows very fast - Spreads / invaded to other places - metastasis 9. Define proto-oncogene, oncogene, and tumor suppressor gene.  -

•Proto-oncogenes – normal genes that become cancer-causing genes if mutated - Encode for normal cell proteins that generally regulate growth, cell cycle, and apoptosis - Normal gene (proto-oncogene) → gets mutated (now oncogene) → contributes to the development of cancer - •Oncogene – mutated gene that causes cancer - Turn it ON to promote cancer - •Tumor-suppressor genes – when inactivated create an environment in which cancer is promoted - Turn it OFF to promote cancer - Ex. p53 9/11 Inflammation and Cell Proliferation, Immunity 10. Describe the effects of hypoxia in reversible cellular injury and ischemia in irreversible cell injury. - If ischemia or hypoxia is for short period of time, the cell can be reverting back to its normal condition - Decrease supply of oxygen, decreases cells aerobic respiration by mitochondria due to decrease ATP generation. - To maintain the supply of energy to the cell anaerobic glycolysis takes place to generate ATP. - Decreases glycogen level. This results in increased accumulation of lactic acid. Thus, decreases intracellular pH. - hypoxia continues, intracellular protein synthesis decreases due to damage to ribosomes and polysomes.

4

-

**hypoxia causes ATP depletion → so this can no longer power the pumps → therefore increased intracellular sodium → cell swells with water ** - 2 main problems: - Accumulation of lactic acid - Loss of ATP - Also cell has too much calcium in it→ which is bad because it can activate too many things - Test Question: - A 72 year old patient demonstrates left-sided weakness of upper and lower extremities. The symptoms lasted less than an hour and resolved with no evidence of infarction. What did the patient most likely experience? - A: Transient ischemic attack 11. Identify the cells involved in the inflammatory response. -

•Neutrophils - •Most numerous leukocytes in blood - •First cells to arrive at site of inflammation** - •Phagocytosis of bacteria and cellular debris - •Release enzymes and other antibacterial substances - •Short life span - So fastest responders but shortest lifespan- get in and get out- to not damage tissue further - •Eosinophils - •Release of granules kills parasitic worms - •Play a role in allergic reactions - •Basophils - •Circulating cells that play a role in allergic reactions - •Mast cells - •Reside in tissues, such as mucosal surfaces - •Involved in acute and chronic inflammation – prominent role in allergic reactions → these are what release the histamine - •Monocyte/macrophage - •Monocytes are circulating cells that become macrophages when they enter the tissues. - •Phagocytosis – eat more and last longer than neutrophils 12. Define oxidative stress and reactive oxygen species (ROS). Explain the role ROS play in cellular injury. -

Oxidative Stress - Imbalance between production of reactive oxygen species (ROS) and antioxidant defenses

5

- Reactive oxygen species - •Released by multiple immune cells and produced during phagocytosis - •Amplifies inflammation, increases inflammatory cytokines 13. Identify and describe the cardinal signs of inflammation.



-

Cardinal signs of inflammation: - •Rubor – redness - •Tumor – swelling - •Calor – heat - •Dolor – pain - •Functio laesa – loss of function - Temporary 14. List and describe the cellular and vascular stages of the inflammatory response. Vascular Phase: -

•Changes in small blood vessels at the site of injury •*Momentary* vasoconstriction then rapid vasodilation •Vasodilation → increase in capillary blood flow → heat and redness •Increased capillary permeability → fluid and proteins into tissue→ swelling, pain, loss of function - So now fluid / proteins that were in the blood can flow into the tissue **purpose: draw all materials to site of injury so that they can reach the tissue

 Cellular Phase: -

•Delivery of leukocytes (neutrophils) to the site of injury 4 steps: - 1.Adhesion and margination - •Blood flow slows so neutrophils can creep along wall of blood vessel and adhere to endothelial cells - *they get off the highway, slow down, and stick to the wall - 2.Transmigration - •Extravasation of neutrophil across endothelial lining - When white blood cells squeeze through the vascular lining 6

-

3.Chemotaxis - •Migration toward site of injury along a chemical gradient (chemokines) - 4. Leukocyte activation and phagocytosis - •Opsonization – coating of a microbe to make it more appealing for phagocytosis - Proteins get candy coated so that they look more appealing to the macrophages to enhance phagocytosis 9/16 Innate and Adaptive Immunity 15. Identify and define the components of the innate immune system - Innate Immunity: -

•Always present •Attacks non-self microbes •Does not distinguish b  etween different microbes - Attacks everything the same way - inflammatory response •Mechanisms include: - •Epithelial barriers – skin and mucous membranes - •Phagocytic cells – neutrophils, macrophages - •Plasma proteins – complement system - •Cell messenger molecules – cytokines - •Natural killer (NK) cells – specialized lymphocytes Innate Immunity

Activated immediately after injury or insult Rapid response Similar response regardless of cause of tissue damage or whether the inflammatory site is sterile or contaminated with infectious microorganism Mediators must be removed quickly to limit damage to surrounding healthy tissue and allow healing  Aka short lived Response to both recurrent tissue damage and infection is identical

Test Question: - The major cells of the INNATE immune response are primary phagocytic cells. These include what 2 cells?

7

- A: Neutrophils and macrophages 16. Explain the process of antibody production. -

B cells → produce antibodies - Antibodies are made in response to antigens - Test Question: - What cells produce antibodies? (be specific) - A: B lymphocytes that have differentiated into plasma cells -  17. Identify and define the components of the adaptive immune system. -Adaptive Immunity:

-

-

•Attacks s pecific microbes (antigens) •Develops after exposure to specific antigen (specific protein that is recognized by microbe) •Mechanisms include: - •Humoral immunity – Antibodies from B cells - •Cell-mediated immunity – T cells  Adaptive Immunity

Inducible; effectors do not preexist – must be produced in response to infection

Slow response Extremely specific to the invader (or perceived invader)

Long-lived and systemic, providing long-term protection against specific infections  Aka inducible- the cells must be created in response Memory – provides permanent long-term protection against infection.



8

18. Differentiate between passive and active immunity. - Passive immunity - Breastfeeding – IgA is transferred to infant in breast milk - Pregnancy – IgG can cross the placenta to provide immunity to fetus - Passive immunotherapy - Preformed antibodies - Human immunoglobulin for hepatitis - Immunoglobulin and monoclonal antibodies for rabies - Monoclonal antibody for RSV - Active Immunity - Get the disease - Vaccines - Induction of long-lasting protective immune responses that will not result in disease in a healthy recipient - Biologic preparations of weakened (attenuated) or dead pathogens or recombinant viral protein - Long-lasting immunity-Reluctance to vaccinate but complications rare 19. Define antigen and describe the role of antigens in the immune response. - Adaptive Immunity - Attacks specific microbes (antigens) - Develops after exposure to specific antigen - Mechanisms include: - Humoral immunity – Antibodies from B cells - Cell-mediated immunity – T cells - 1.APC (antigen presenting cell) ingests antigen - 2.Antigen is paired with MHC II molecule - This MHC-antigen combo is brought to the surface of the APC (antigen presenting cell) - Must be MHC-II - 3.MHC II-Antigen duo is presented to TCR of TH (helper t cell) cell (CD4+) → TH cell is activated - Talks to T-cell receptor of CD4 cell - Sends cytokines - 4.Activated TH cell then talks to B cell and CTL (CD8+) - Turns them both on to create an immune response - All make memory cells also - Leads to T-cell activation - 5. Once activated. The CD4+ helper T cell the communicates with B cells and CD8+ cytotoxic T cells - This activates cytotoxic T cells to:

9

-

-

Become effector cells that eliminate antigen by killing our cells who display the antigen on the MHC I molecules (so infected cells) - Become memory CD8+ T cells This activates the B cells to: - Become plasma cells to produce antibodies - Become memory B cells

 9/18 Disorders of Immune System 20. List and define the 4 types of hypersensitivity reactions - Characterized by the immune mechanism: - Type I - IgE mediated - Against environmental antigens (allergens) - IgE binds to the Fc receptors on the surface of mast cells—“sensitized” - Histamine release from mast cell degranulation - H1 and H2 receptors - Antihistamines - Sensitizing happens first: - Antibodies are made in response to allergen exposure - IgE binds to the Fc receptor on mast cell - Now you have a sensitized mast cell - Re-exposure – allergen binds to IgE on sensitized mast cell allergic response - Some reactions are 2-phase responses - Asthma - 1. Primary early response - 2. Secondary late response - Type II - Tissue-specific reactions → antibody mediated (IgG or IgM) - Specific cell or tissue (tissue-specific antigens) is the target of an immune response - Whereas in type I er eere responding to environmental allgeron, now in type II we are responding to our own cells - Mediated by IgG or IgM antibodies directed against target antigens on cell surfaces or connective tissues - 3 mechanisms: - Complement- and antibody-mediated cell destruction - Complement- and antibody-mediated inflammation - Antibody-mediated cellular dysfunction - Complement-mediated cell destruction 10

-

-

-

-

Antibody-mediated cell-mediated cytotoxicity (ADCC) MAC – membrane attack complex Examples: ABO or Rh incompatibility Drug reactions RBC or WBC lysis Complement and antibody-mediated inflammation Deposition of antibodies in cellular matrix inflammation Antibody-mediated cellular dysfunction Antibody binds to specific target cell receptors that lead to change in cell function but not death - Examples: Graves disease, myasthenia gravis Type III - Immune complex mediated - **Antigen-antibody complexes** are formed in the circulation and are later deposited in vessel walls or extravascular tissues - Causes localized inflammation where the antibody complex is deposited - Large release of lysosomal enzymes - Example - glomerulonephritis - Systemic reaction: Serum sickness - Some antibiotics, drugs, food, insect venoms - Urticaria, rash, edema, fever Type IV - Cell mediated - **Does not involve antibody** - Cytotoxic T lymphocytes or lymphokine-producing Th1 and Th17 cells - Direct killing by CTL or recruitment of phagocytic cells by Th1 and Th17 cell - •Examples: - Graft rejection - Tuberculosis skin test - Allergic reactions from poison ivy or metals - Cell-mediated - Cytotoxic T cells - Delayed-type hypersensitivity - Takes 24-72 hours - Ex – Tb test - Contact dermatitis - Poison ivy or oak Test Question:

11

-

In type I Hypersensitivity, which antibody isotype plays primary role - IgE - Test Question: - could also work for antigen question - What is the primary function of cytotoxic T lymphocytes (CD8+) - A: To kill virally infected cells and cancer cells - adaptive immune cells- specific 21. Define immunodeficiency and how it would present clinically. Distinguish between primary and secondary immune deficiency. - Immunodeficiency - means not enough of the immune response - Abnormality in one or more components of the immune system that makes a person susceptible to diseases normally prevented by an intact immune system - Primary – genetic defects - B cell, T cell deficiencies - Severe combined immunodeficiency disorder (SCID) – deficiency in both T cell and B cell function - - Secondary – acquired - AIDS - Seroconversion – infected person now is positive for HIV antibodies in blood – generally within 1-3 months - Window period – time after infection and before seroconversion - Will test HIV negative, but can still transmit virus - Generally about 3-4 weeks, but varies by individual - 1. Acute stage – acute clinical syndrome (primary infection)- - 1-4 weeks after exposure - Flu-like symptoms - Increase in viral replication high viral load and decrease CD4 count - Eventually the immune system can control viral replication set point of stable level of lower viral load that can last years - 2. Latent period – no signs or symptoms of illness (~10 years) - Stable viral load with gradual loss of CD4 T cells - 3. AIDS - AIDS-defining illness or CD4 T cell count < 200 cells/μL 22. Define autoimmunity and identify autoimmune disorders based on that definition. - Autoimmunity - Distu...